PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7645423-11 1995 Growth inhibition by RA may be mediated through the cytokine transforming growth factor-beta (TGF-beta), a potent inhibitor of epithelial cell proliferation. Tretinoin 21-23 transforming growth factor beta 1 Homo sapiens 94-102 7645423-13 1995 Also, Northern blot analysis of mRNA isolated from HKc/HPV16 demonstrated that RA treatment induced TGF-beta 1 and TGF-beta 2 expression about 3- and 50-fold, respectively. Tretinoin 79-81 transforming growth factor beta 1 Homo sapiens 100-110 7813633-4 1995 The effects of LPA are compared with all-trans-retinoic acid (RA), a structurally unrelated lipid that has previously been shown to induce both TGF alpha and TGF beta and have pronounced effects on keratinocyte proliferation and differentiation. Tretinoin 62-64 transforming growth factor beta 1 Homo sapiens 158-166 7813633-8 1995 LPA and RA also induced both the active and latent forms TGF beta from cultured keratinocytes. Tretinoin 8-10 transforming growth factor beta 1 Homo sapiens 57-65 7817811-4 1994 Furthermore, TGF-beta 1 decreased osteocalcin synthesis modulated negatively by dexamethasone or positively by retinoic acid. Tretinoin 111-124 transforming growth factor beta 1 Homo sapiens 13-23 7943653-3 1994 This study demonstrates that therapeutic doses of RA (0.1-10 microM) significantly increase transforming growth factor-beta (TGF beta) production both in THP-1, human myelomonocytic cells, and in human peripheral blood monocytes. Tretinoin 50-52 transforming growth factor beta 1 Homo sapiens 92-123 7519122-10 1994 These results indicate that in both U937 and NB4 cells high level PML/RAR alpha expression inhibits the monocytic terminal differentiation program triggered by D3 or D3 plus TGF-beta 1, whereas RA treatment effectively antagonizes this inhibitory PML-RAR alpha action and restores the D3 differentiative effect. Tretinoin 70-72 transforming growth factor beta 1 Homo sapiens 174-184 7943653-3 1994 This study demonstrates that therapeutic doses of RA (0.1-10 microM) significantly increase transforming growth factor-beta (TGF beta) production both in THP-1, human myelomonocytic cells, and in human peripheral blood monocytes. Tretinoin 50-52 transforming growth factor beta 1 Homo sapiens 125-133 7943653-5 1994 Combination of RA stimulation with acute in vitro ethanol treatment, however, resulted in significantly lower M theta TGF beta production than TGF beta levels induced by RA alone (p < 0.003). Tretinoin 15-17 transforming growth factor beta 1 Homo sapiens 118-126 7943653-5 1994 Combination of RA stimulation with acute in vitro ethanol treatment, however, resulted in significantly lower M theta TGF beta production than TGF beta levels induced by RA alone (p < 0.003). Tretinoin 170-172 transforming growth factor beta 1 Homo sapiens 143-151 7943653-6 1994 Down-regulation of M theta TGF beta production by ethanol was tested at the concentration range of 25-150 mM and occurred both at high and low RA concentrations (10-0.1 microM). Tretinoin 143-145 transforming growth factor beta 1 Homo sapiens 27-35 7943653-7 1994 In contrast to its inhibitory effect on RA-induced M theta TGF beta production, ethanol augmented TGF beta production induced by muramyl dipeptide (20 micrograms/ml), suggesting that ethanol can either up- or down-regulate M theta TGF beta production, depending on the costimulatory factors. Tretinoin 40-42 transforming growth factor beta 1 Homo sapiens 59-67 8125154-9 1994 TGF-beta treatment was able to at least partially overcome the inhibitory effects of retinoic acid. Tretinoin 85-98 transforming growth factor beta 1 Homo sapiens 0-8 8163572-0 1994 Inhibition of the chondrocyte phenotype by retinoic acid involves upregulation of metalloprotease genes independent of TGF-beta. Tretinoin 43-56 transforming growth factor beta 1 Homo sapiens 119-127 8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 320-333 transforming growth factor beta 1 Homo sapiens 28-61 7504151-5 1993 In cells in which TGF beta inhibited DNA synthesis, it also inhibited RA-induced granulocytic differentiation of APL cells and, to a greater degree, granulocytic differentiation induced by RA plus G-CSF. Tretinoin 70-72 transforming growth factor beta 1 Homo sapiens 18-26 8100485-0 1993 Interactions between interferon gamma and retinoic acid with transforming growth factor beta in the induction of immune recognition molecules. Tretinoin 42-55 transforming growth factor beta 1 Homo sapiens 61-92 8100485-15 1993 In contrast to IFN gamma-induced ICAM-1 expression, retinoic-acid-induced ICAM-1 expression was inhibited by TGF beta on two of the three responsive lines. Tretinoin 52-65 transforming growth factor beta 1 Homo sapiens 109-117 8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 320-333 transforming growth factor beta 1 Homo sapiens 63-73 8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 335-337 transforming growth factor beta 1 Homo sapiens 28-61 8218938-1 1993 Previously we reported that transforming growth factor-beta 1 (TGF-beta 1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1 alpha,25-dihydroxyvitamin D3 (VD3) and also that it induced Fc receptor for immunoglobulin G (Fc gamma R), type IIIB, in the presence of retinoic acid (RA). Tretinoin 335-337 transforming growth factor beta 1 Homo sapiens 63-73 8476634-0 1993 Retinoic acid and calcium regulation of p53, transforming growth factor-beta 1, and transforming growth factor-alpha gene expression and growth in adenovirus 12-SV40-transformed human tracheal gland epithelial cells. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 45-78 1531473-6 1992 These results indicated that TGF-beta 1 could induce phosphatidylinositol-glycan-linked Fc gamma RIII (Fc gamma RIII-I) in THP-1 cells in the presence of RA. Tretinoin 154-156 transforming growth factor beta 1 Homo sapiens 29-39 1334692-0 1992 Retinoic acid induces secretion of latent transforming growth factor beta 1 and beta 2 in normal and human papillomavirus type 16-immortalized human keratinocytes. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 42-73 1334692-2 1992 We investigated the ability of RA to modulate the production of TGF-beta in normal human keratinocytes (HKc) and HKc lines immortalized by transfection with human papillomavirus type 16 DNA (HKc/HPV16). Tretinoin 31-33 transforming growth factor beta 1 Homo sapiens 64-72 1334692-3 1992 RA treatment of both normal HKc and HKc/HPV16 resulted in a 2-3-fold induction in secreted levels of latent TGF-beta. Tretinoin 0-2 transforming growth factor beta 1 Homo sapiens 108-116 1334692-4 1992 The induction in TGF-beta secretion by RA was dose dependent, with significant increases observed with RA concentrations as low as 1-10 nM, and time dependent, with maximal induction occurring about 3 days after initiation of RA exposure. Tretinoin 39-41 transforming growth factor beta 1 Homo sapiens 17-25 1334692-4 1992 The induction in TGF-beta secretion by RA was dose dependent, with significant increases observed with RA concentrations as low as 1-10 nM, and time dependent, with maximal induction occurring about 3 days after initiation of RA exposure. Tretinoin 103-105 transforming growth factor beta 1 Homo sapiens 17-25 1334692-4 1992 The induction in TGF-beta secretion by RA was dose dependent, with significant increases observed with RA concentrations as low as 1-10 nM, and time dependent, with maximal induction occurring about 3 days after initiation of RA exposure. Tretinoin 103-105 transforming growth factor beta 1 Homo sapiens 17-25 1334692-5 1992 In addition, RA induced intracellular levels of TGF-beta almost 5-fold. Tretinoin 13-15 transforming growth factor beta 1 Homo sapiens 48-56 1334692-8 1992 Northern blot analysis of mRNA isolated from HKc/HPV16 demonstrated that RA treatment induced specific transcripts for TGF-beta 1 and TGF-beta 2 about 3- and 50-fold, respectively. Tretinoin 73-75 transforming growth factor beta 1 Homo sapiens 119-127 1334692-8 1992 Northern blot analysis of mRNA isolated from HKc/HPV16 demonstrated that RA treatment induced specific transcripts for TGF-beta 1 and TGF-beta 2 about 3- and 50-fold, respectively. Tretinoin 73-75 transforming growth factor beta 1 Homo sapiens 134-142 1334692-11 1992 These studies indicate that RA may regulate growth control in both normal HKc and HKc/HPV16 by enhancing TGF-beta 1 and TGF-beta 2 production, which, after activation at the cell surface, could inhibit cellular proliferation in an autocrine and/or paracrine manner. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 105-113 1334692-11 1992 These studies indicate that RA may regulate growth control in both normal HKc and HKc/HPV16 by enhancing TGF-beta 1 and TGF-beta 2 production, which, after activation at the cell surface, could inhibit cellular proliferation in an autocrine and/or paracrine manner. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 120-128 1372988-1 1992 Retinoic acid (RA) exerts potent suppressive and upregulatory effects on human immunodeficiency virus (HIV) expression in mononuclear phagocytes, strikingly similar to the effects of the cytokine transforming growth factor beta (TGF-beta). Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 229-237 1734039-8 1992 Our results indicate a complex pattern of regulation of the different TGF-beta genes by themselves as well as by PDGF, EGF, IL-1, dexamethasone, TPA, and retinoic acid in chicken embryo cells. Tretinoin 154-167 transforming growth factor beta 1 Homo sapiens 70-78 1734039-0 1992 Differential regulation of the expression of transforming growth factor-beta mRNAs by growth factors and retinoic acid in chicken embryo chondrocytes, myocytes, and fibroblasts. Tretinoin 105-118 transforming growth factor beta 1 Homo sapiens 45-76 1734039-7 1992 Retinoic acid also has contrasting effects on chondrocytes and myocytes either increasing or decreasing, respectively, expression of TGF-beta s 2 and 3 mRNAs and TGF-beta 2 protein. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 133-141 1728634-0 1992 Differential modulation of transforming growth factor-beta 1 expression and mucin deposition by retinoic acid and sodium lauryl sulfate in human skin. Tretinoin 96-109 transforming growth factor beta 1 Homo sapiens 27-60 1728634-3 1992 The modulation of transforming growth factor-beta 1 expression by retinoic acid occurred in the absence of any change in its mRNA level. Tretinoin 66-79 transforming growth factor beta 1 Homo sapiens 18-51 1728634-5 1992 Similar changes in TGF-beta 1 and TGF-beta 2 immunoreactivity and mRNA levels, as observed in retinoic acid-treated skin, were observed in skin following topical application of the irritant sodium lauryl sulfate, indicating that the alterations induced by retinoic acid were not specific. Tretinoin 94-107 transforming growth factor beta 1 Homo sapiens 19-29 1728634-5 1992 Similar changes in TGF-beta 1 and TGF-beta 2 immunoreactivity and mRNA levels, as observed in retinoic acid-treated skin, were observed in skin following topical application of the irritant sodium lauryl sulfate, indicating that the alterations induced by retinoic acid were not specific. Tretinoin 256-269 transforming growth factor beta 1 Homo sapiens 19-29 1728634-8 1992 Treatment of keratinocytes with retinoic acid resulted in a 50% induction of transforming growth factor-beta 1 protein, without any detectable change in transforming growth factor-beta 2. Tretinoin 32-45 transforming growth factor beta 1 Homo sapiens 77-110 1728634-10 1992 Whereas alterations in transforming growth factor-beta 1 expression were observed in both retinoic acid- and sodium lauryl sulfate-treated skin, accumulation of mucin was specific to retinoic acid-treated skin. Tretinoin 90-103 transforming growth factor beta 1 Homo sapiens 23-56 1847657-6 1991 TGF-beta was synergistic with retinoic acid, a known anti-tumor promoter, in inhibiting the PMA-induced transformation of JB6 cells. Tretinoin 30-43 transforming growth factor beta 1 Homo sapiens 0-8 1848114-0 1991 Induction of transforming growth factor-beta 1 (TGF-beta 1), receptor expression and TGF-beta 1 protein production in retinoic acid-treated HL-60 cells: possible TGF-beta 1-mediated autocrine inhibition. Tretinoin 118-131 transforming growth factor beta 1 Homo sapiens 85-95 1848114-0 1991 Induction of transforming growth factor-beta 1 (TGF-beta 1), receptor expression and TGF-beta 1 protein production in retinoic acid-treated HL-60 cells: possible TGF-beta 1-mediated autocrine inhibition. Tretinoin 118-131 transforming growth factor beta 1 Homo sapiens 85-95 1848114-3 1991 Although TGF-beta 1 alone had little effect on proliferation or differentiation of HL-60 cells, addition of TGF-beta 1 to HL-60 cells treated with a suboptimum concentration of RA (1.0 nmol/L) resulted in a marked decrease in proliferation with no effect on granulocytic differentiation. Tretinoin 177-179 transforming growth factor beta 1 Homo sapiens 108-118 1848114-4 1991 Studies of the mechanism of RA-induced TGF-beta sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-beta 1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 39-47 1848114-4 1991 Studies of the mechanism of RA-induced TGF-beta sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-beta 1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 127-137 1848114-4 1991 Studies of the mechanism of RA-induced TGF-beta sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-beta 1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Tretinoin 235-237 transforming growth factor beta 1 Homo sapiens 39-47 1848114-5 1991 Maximum induction was achieved after treatment with 10 nmol/L RA and consisted predominantly of the 65-Kd TGF-beta 1 receptor type. Tretinoin 62-64 transforming growth factor beta 1 Homo sapiens 106-116 1848114-6 1991 Moreover, RA treatment also resulted in a dose-dependent increase in both TGF-beta 1 steady-state mRNA expression and production of active TGF-beta with maximum induction at 10 nmol/LRA. Tretinoin 10-12 transforming growth factor beta 1 Homo sapiens 74-84 1848114-6 1991 Moreover, RA treatment also resulted in a dose-dependent increase in both TGF-beta 1 steady-state mRNA expression and production of active TGF-beta with maximum induction at 10 nmol/LRA. Tretinoin 10-12 transforming growth factor beta 1 Homo sapiens 74-82 1848114-8 1991 These data suggest that the effects of RA may be mediated by a TGF-beta 1-mediated autocrine antiproliferative loop during differentiation of HL-60 cells. Tretinoin 39-41 transforming growth factor beta 1 Homo sapiens 63-73 1847657-8 1991 TGF-beta, therefore, appears to function as an incomplete antipromoter whose action can be permitted and/or complemented by retinoic acid. Tretinoin 124-137 transforming growth factor beta 1 Homo sapiens 0-8 2371287-8 1990 The presence of retinoic acid was required for maximal PUFA-dependent growth inhibition of A549 or B16 cells by TGF-beta 1 under some, but not all, conditions. Tretinoin 16-29 transforming growth factor beta 1 Homo sapiens 112-122 2337474-0 1990 Transforming growth factor beta (TGF-beta) potentiates the inhibitory effect of retinoic acid on human breast carcinoma (MCF-7) cell proliferation. Tretinoin 80-93 transforming growth factor beta 1 Homo sapiens 0-31 2337474-0 1990 Transforming growth factor beta (TGF-beta) potentiates the inhibitory effect of retinoic acid on human breast carcinoma (MCF-7) cell proliferation. Tretinoin 80-93 transforming growth factor beta 1 Homo sapiens 33-41 2337474-5 1990 These results demonstrate that although TGF-beta does not inhibit the growth of MCF-7 cells, it potentiates the antiproliferative effect of RA, suggesting that it may play a part, albeit indirect, in the regulation of MCF-7 cell growth. Tretinoin 140-142 transforming growth factor beta 1 Homo sapiens 40-48 2295827-0 1990 Trans retinoic acid enhances the growth response of epidermal keratinocytes to epidermal growth factor and transforming growth factor beta. Tretinoin 6-19 transforming growth factor beta 1 Homo sapiens 107-138 2295827-4 1990 Transforming growth factor beta (TGF beta) inhibited the EGF-induced DNA synthesis in a dose-dependent manner, and the inhibition was greatly enhanced by a low dose of RA. Tretinoin 168-170 transforming growth factor beta 1 Homo sapiens 0-31 2295827-4 1990 Transforming growth factor beta (TGF beta) inhibited the EGF-induced DNA synthesis in a dose-dependent manner, and the inhibition was greatly enhanced by a low dose of RA. Tretinoin 168-170 transforming growth factor beta 1 Homo sapiens 33-41 2295827-6 1990 A low concentration of RA also enhanced the inhibitory effect of TGF beta on growth-factor-induced DNA synthesis and cell growth in hKC. Tretinoin 23-25 transforming growth factor beta 1 Homo sapiens 65-73 2613750-6 1989 Similarly, retinoic acid treatment also enhanced in a time- and dose-dependent manner the TGF alpha-dependent response of EGF receptor mRNA and acted synergistically with TGF beta 1. Tretinoin 11-24 transforming growth factor beta 1 Homo sapiens 171-181 2562184-5 1989 We give particular attention to tamoxifen and retinoic acid, since it has been shown that these agents, which are of known efficacy for prevention of cancer, can markedly enhance the secretion of specific isotypes of TGF-beta by several types of cells. Tretinoin 46-59 transforming growth factor beta 1 Homo sapiens 217-225 2558941-6 1989 Furthermore, and again in contrast to murine embryonal carcinoma cells, treatment of the human embryonal carcinoma cells with retinoic acid causes a nearly complete loss of TGF-beta 1 binding sites. Tretinoin 126-139 transforming growth factor beta 1 Homo sapiens 173-183 3191488-5 1988 N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Tretinoin 26-39 transforming growth factor beta 1 Homo sapiens 184-192 3191488-5 1988 N,N-Dimethylformamide and retinoic acid, two other agents associated with induction of a partial differentiation-like response in the MOSER parental cells (similar to that elicited by TGF-beta), inhibited the monolayer proliferation of both the parental cells and the TGF-beta-resistant sublines. Tretinoin 26-39 transforming growth factor beta 1 Homo sapiens 268-276 2886219-4 1987 Treatment of both EC cell lines with retinoic acid leads to the appearance of irreversibly differentiated cells that begin to exhibit receptors for TGF-beta by 48 h. After an additional 3-5 days, the differentiated cells express approximately 6000 high affinity receptors for TGF-beta, with an apparent dissociation constant of 45 PM. Tretinoin 37-50 transforming growth factor beta 1 Homo sapiens 148-156 2886219-4 1987 Treatment of both EC cell lines with retinoic acid leads to the appearance of irreversibly differentiated cells that begin to exhibit receptors for TGF-beta by 48 h. After an additional 3-5 days, the differentiated cells express approximately 6000 high affinity receptors for TGF-beta, with an apparent dissociation constant of 45 PM. Tretinoin 37-50 transforming growth factor beta 1 Homo sapiens 276-284 31880511-4 2019 Our results indicate that ATRA can augment the expression of RARalpha and PHB proteins and reduce the expression of TGF-beta1, FN and Col-IV proteins. Tretinoin 26-30 transforming growth factor beta 1 Homo sapiens 116-125 32104972-0 2020 All-trans retinoic acid regulates TGF-beta1-induced extracellular matrix production via p38, JNK, and NF-kappaB-signaling pathways in nasal polyp-derived fibroblasts. Tretinoin 10-23 transforming growth factor beta 1 Homo sapiens 34-43 32104972-6 2020 TGF-beta1-induced fibroblasts were pretreated with ATRA. Tretinoin 51-55 transforming growth factor beta 1 Homo sapiens 0-9 32104972-12 2020 TGF-beta1-induced cell migration and collagen gel contraction were significantly inhibited by ATRA pretreatment. Tretinoin 94-98 transforming growth factor beta 1 Homo sapiens 0-9 32104972-13 2020 ATRA also significantly inhibited phosphorylation of c-Jun N-terminal kinase (JNK), p38, and p50 in TGF-beta1-induced NPDFs, but did not inhibit phosphorylation of extracellular signal-related kinase (ERK). Tretinoin 0-4 transforming growth factor beta 1 Homo sapiens 100-109 30826380-5 2019 Our experiments revealed that ATRA alone, but also a cocktail of mediators consisting of IL2, TGFbeta and ATRA, upregulate expression of FOXP3 gene in normal and leukemic myeloid cells. Tretinoin 30-34 transforming growth factor beta 1 Homo sapiens 94-101 28620241-0 2017 TGF-beta/atRA-induced Tregs express a selected set of microRNAs involved in the repression of transcripts related to Th17 differentiation. Tretinoin 9-13 transforming growth factor beta 1 Homo sapiens 0-8 27375161-0 2016 ATRA modulates mechanical activation of TGF-beta by pancreatic stellate cells. Tretinoin 0-4 transforming growth factor beta 1 Homo sapiens 40-48 28187790-11 2017 Co-targeting of the retinoic acid and TGF-beta pathways, through RA and kartogenin (KGN; a TGF-beta signalling activating small molecule) combination treatment, induced the loss of viability of MYCN-amplified retinoid-resistant neuroblastoma cells. Tretinoin 20-33 transforming growth factor beta 1 Homo sapiens 91-99 27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 151-170 transforming growth factor beta 1 Homo sapiens 43-51 27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 151-170 transforming growth factor beta 1 Homo sapiens 289-297 27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 172-176 transforming growth factor beta 1 Homo sapiens 43-51 27375161-4 2016 Here we study the mechanical activation of TGF-beta by PSCs in vitro by investigating LTBP-1 organisation with fibrillar fibronectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechanically organise LTBP-1 and activate TGF-beta through a mechanism involving myosin II dependent contractility. Tretinoin 172-176 transforming growth factor beta 1 Homo sapiens 289-297 27375161-5 2016 Therefore, ATRA inhibits the ability of PSCs to mechanically release active TGF-beta, which might otherwise act in an autocrine manner to sustain PSCs in an active state and a tumour-favouring stiff microenvironment. Tretinoin 11-15 transforming growth factor beta 1 Homo sapiens 76-84 26981578-4 2016 Treatment with TGFbeta and retinoic acid (RA) enabled enrichment of this sub-population for therapeutic testing, through which the endoplasmic reticulum (ER) stressor and autophagy inhibitor Thapsigargin was shown to selectively target these cells. Tretinoin 42-44 transforming growth factor beta 1 Homo sapiens 15-22 26018078-0 2015 All-trans-retinoic Acid Modulates the Plasticity and Inhibits the Motility of Breast Cancer Cells: ROLE OF NOTCH1 AND TRANSFORMING GROWTH FACTOR (TGFbeta). Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 146-153 26018078-10 2015 Stimulation of TGFbeta contributes to the anti-migratory effect of ATRA. Tretinoin 67-71 transforming growth factor beta 1 Homo sapiens 15-22 25614514-7 2015 RESULTS: ATRA inhibited TGF-beta-induced collagen gel contraction mediated by HTFs in a concentration- and time-dependent manner. Tretinoin 9-13 transforming growth factor beta 1 Homo sapiens 24-32 25268355-5 2014 All-trans retinoic acid in vitro induced IL-10 in CD4(+)CD25(high)Foxp3(+) T cells; IL-10 and TGF-beta production in CD4(+)CD25-Foxp3- T cells, and IL-10 in monocytes isolated from healthy children. Tretinoin 10-23 transforming growth factor beta 1 Homo sapiens 94-102 25614514-9 2015 ATRA also stimulated TIMP-1 release from HTFs in the presence of TGF-beta. Tretinoin 0-4 transforming growth factor beta 1 Homo sapiens 65-73 25614514-12 2015 CONCLUSIONS: ATRA inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, likely in part by attenuating the production of MMP-1 and MMP-3 and by stimulating the production of TIMP-1. Tretinoin 13-17 transforming growth factor beta 1 Homo sapiens 28-36 25878769-0 2015 Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPbeta. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 63-94 25878769-2 2015 During adult skeletal myogenesis, TGFbeta signaling inhibits the differentiation of myoblasts, and this can be reversed by treatment with retinoic acid (RA). Tretinoin 138-151 transforming growth factor beta 1 Homo sapiens 34-41 24846581-8 2014 Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-beta1 (all p < 0.05). Tretinoin 37-41 transforming growth factor beta 1 Homo sapiens 150-159 24894398-7 2014 RESULTS: All-trans-retinoic acid inhibited TGF-beta-induced collagen gel contraction mediated by HTFs in a concentration- and time-dependent manner. Tretinoin 9-32 transforming growth factor beta 1 Homo sapiens 43-51 24894398-9 2014 All-trans-retinoic acid also inhibited the TGF-beta-induced phosphorylation of the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase (JNK) as well as that of c-Jun and Smad2/3. Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 43-51 24894398-11 2014 CONCLUSIONS: All-trans-retinoic acid inhibited TGF-beta-induced collagen gel contraction mediated by HTFs, most likely by attenuating the formation of actin stress fibers and focal adhesions as well as signaling by MAPKs, c-Jun, and Smads. Tretinoin 13-36 transforming growth factor beta 1 Homo sapiens 47-55 23531410-5 2013 Numerous genes belonging to specific signaling pathways (the Hedgehog, Notch, Wnt, FGF, TGFbeta/BMP, and retinoic acid pathways), and/or to the homeobox gene superfamily, were also uncovered when a less stringent fold change threshold was used. Tretinoin 105-118 transforming growth factor beta 1 Homo sapiens 88-95 24374174-0 2014 Retinoic acid remodels extracellular matrix (ECM) of cultured human fetal palate mesenchymal cells (hFPMCs) through down-regulation of TGF-beta/Smad signaling. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 135-143 24374174-6 2014 Because of the pivotal role of TGF-beta/Smad pathway in palatogenesis we therefore checked the effect of RA on TGF-beta/Smad signaling. Tretinoin 105-107 transforming growth factor beta 1 Homo sapiens 111-119 24374174-9 2014 In conclusion, these findings suggested that RA overexposure inhibited cell proliferation and disrupted the ECM network through down-regulation of TGF-beta/Smad pathway. Tretinoin 45-47 transforming growth factor beta 1 Homo sapiens 147-155 23582512-9 2013 The TGF-beta type II receptor, responsible for binding TGF-beta during neuronal differentiation, was increased 14-fold in NT2 cells treated with RA (P < 0.001). Tretinoin 145-147 transforming growth factor beta 1 Homo sapiens 4-12 23011350-5 2012 RESULTS: This study reveals, for the first time, that activin/TGF-beta signalling blocks pancreatic specification induced by retinoic acid while promoting hepatic specification in combination with bone morphogenetic protein and fibroblast growth factor. Tretinoin 125-138 transforming growth factor beta 1 Homo sapiens 62-70 21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 19-32 transforming growth factor beta 1 Homo sapiens 172-180 21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 49-62 transforming growth factor beta 1 Homo sapiens 103-111 21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 49-62 transforming growth factor beta 1 Homo sapiens 159-167 21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 64-66 transforming growth factor beta 1 Homo sapiens 103-111 21460203-3 2011 We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-beta-dependent Foxp3(+) Treg induction but inhibits TGF-beta-driven Th17 differentiation. Tretinoin 64-66 transforming growth factor beta 1 Homo sapiens 159-167 21352343-5 2011 Cultured skin fibroblasts from patients with scleroderma were treated with RA and their effect on the expression of 5-lipoxygenase (LOX), transforming growth factor (TGF)-beta1, connective tissue growth factor (CTGF), type I and type III collagen was tested by reverse transcription polymerase chain reaction (RT-PCR) and western immunoblotting. Tretinoin 75-77 transforming growth factor beta 1 Homo sapiens 138-176 21352343-8 2011 RA significantly inhibited the expression of 5-LOX and of TGF-beta1, CTGF, type I and type III collagen. Tretinoin 0-2 transforming growth factor beta 1 Homo sapiens 58-67 21352343-10 2011 In vitro, RA reduced 5-LOX expression in scleroderma fibroblasts and downregulated TGF-beta1 and CTGF expression, leading to the inhibition of type I and type III collagen synthesis. Tretinoin 10-12 transforming growth factor beta 1 Homo sapiens 83-92 21352343-11 2011 Our results indicate that the clinical effects of RA on scleroderma are, at least in part, attributable to the reduction of 5-LOX expression and the subsequent suppression of TGF-beta1 and CTGF expression that results in the blockade of collagenogenesis. Tretinoin 50-52 transforming growth factor beta 1 Homo sapiens 175-184 21173077-2 2011 We have shown that retinoic acid (RA), which is known to play a necessary role in early events in pregnancy, can combine with transcriptional activators of VEGF (e.g. TPA, TGF-beta, IL-1beta) to rapidly induce VEGF secretion from human endometrial stromal cells through a translational mechanism of action. Tretinoin 34-36 transforming growth factor beta 1 Homo sapiens 172-180 21173077-5 2011 Importantly, co-treatment of RA with TPA or TGF-beta further stimulated ROS production in a fashion that positively correlated with levels of VEGF secretion. Tretinoin 29-31 transforming growth factor beta 1 Homo sapiens 44-52 21173077-6 2011 The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibited both RA + TPA and RA + TGF-beta-stimulated secretion of VEGF, as well as RA-induced ROS production. Tretinoin 94-96 transforming growth factor beta 1 Homo sapiens 99-107 20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 transforming growth factor beta 1 Homo sapiens 97-128 21287335-4 2011 Furthermore, we also address methods in order to achieve TGFbeta-dependent Treg conversion in vitro, thereby mainly focusing on the role of retinoic acid (RA) to enhance TGFbeta-dependent conversion into Tregs. Tretinoin 140-153 transforming growth factor beta 1 Homo sapiens 170-177 20921526-8 2010 Our in vitro findings support a model in which TGF-beta1-bearing PMVs, released from promonocytic leukemia cells (THP-1) or primary peripheral blood monocytes on exposure to sublytic complement or after treatment with a differentiation therapy agent, such as all-trans retinoic acid, significantly reduce proliferation of THP-1 cells. Tretinoin 269-282 transforming growth factor beta 1 Homo sapiens 47-56 20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 transforming growth factor beta 1 Homo sapiens 130-138 20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 36-49 transforming growth factor beta 1 Homo sapiens 301-309 20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 transforming growth factor beta 1 Homo sapiens 97-128 20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 transforming growth factor beta 1 Homo sapiens 130-138 20870174-1 2010 The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-beta (TGF-beta)-induced Foxp3 transcription and inhibition of the latter by cytokines such as IL-27 were here shown to be related processes involving modifications of baseline (TGF-beta-induced) phosphorylated Smad3 (pSmad3) binding to a conserved enhancer region (enhancer I). Tretinoin 51-53 transforming growth factor beta 1 Homo sapiens 301-309 20643338-3 2010 We showed here that direct stimulation of FDCs by bacterial products and retinoic acid synergistically enhanced the expression of the chemokine CXCL13, the survival factor BAFF, and molecules that facilitate the secretion and activation of the cytokine TGF-beta1. Tretinoin 73-86 transforming growth factor beta 1 Homo sapiens 253-262 20577838-5 2010 These data suggested that miR-146a might influence proliferation of APL cells through TGF-beta1/Smad signal transduction pathway during ATRA induction. Tretinoin 136-140 transforming growth factor beta 1 Homo sapiens 86-95 20421479-3 2010 In this study, we show that Ag-specific memory Th cells were redifferentiated into Foxp3(+) T cells by TGF-beta when stimulated in the presence of all-trans retinoic acid and rapamycin. Tretinoin 157-170 transforming growth factor beta 1 Homo sapiens 103-111 20386594-0 2010 Retinoic acid mediates regulation of network formation by COUP-TFII and VE-cadherin expression by TGFbeta receptor kinase in breast cancer cells. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 98-105 20172853-0 2010 All-trans-retinoic acid promotes trafficking of human concentrative nucleoside transporter-3 (hCNT3) to the plasma membrane by a TGF-beta1-mediated mechanism. Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 129-138 20386594-8 2010 Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Tretinoin 63-65 transforming growth factor beta 1 Homo sapiens 21-28 20386594-8 2010 Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Tretinoin 135-137 transforming growth factor beta 1 Homo sapiens 21-28 20386594-8 2010 Several genes in the TGFbeta signaling pathway were induced by RA, and specific inhibition of the TGFbeta type I receptor blocked both RA-induced VE-cadherin expression and cell fusion. Tretinoin 135-137 transforming growth factor beta 1 Homo sapiens 98-105 20386594-9 2010 Together these data indicate a role for the TGFbeta pathway and COUP-TFII in mediating the endothelial transdifferentiating properties of RA. Tretinoin 138-140 transforming growth factor beta 1 Homo sapiens 44-51 19340880-2 2009 Recent studies have revealed that retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (Treg) cells. Tretinoin 34-47 transforming growth factor beta 1 Homo sapiens 106-143 20197308-0 2010 Proinsulin C-peptide antagonizes the profibrotic effects of TGF-beta1 via up-regulation of retinoic acid and HGF-related signaling pathways. Tretinoin 91-104 transforming growth factor beta 1 Homo sapiens 60-69 20197308-10 2010 We confirmed a role for RA in reversal of TGF-beta1-induced changes associated with epithelial-mesenchymal transition, including expression changes in Snail, E-cadherin, vimetin, and redistribution of beta-catenin. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 42-51 18809338-2 2009 Recently, we described that RA also functions as a key modulator of transforming growth factor-beta (TGF-beta)-driven immune deviation, capable of suppressing the differentiation of interleukin-17 secreting T helper cells (T(H)17) and conversely promoting the generation of Foxp3(+) T regulatory (Treg) cells. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 68-99 19340880-2 2009 Recent studies have revealed that retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (Treg) cells. Tretinoin 49-51 transforming growth factor beta 1 Homo sapiens 106-143 19363708-6 2009 These results indicate that the upregulation of TGF-beta1 pathway plays an important role in NB4 cells differentiation induced by ATRA. Tretinoin 130-134 transforming growth factor beta 1 Homo sapiens 48-57 19371709-0 2009 Retinoic acid can directly promote TGF-beta-mediated Foxp3(+) Treg cell conversion of naive T cells. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 35-43 18809338-2 2009 Recently, we described that RA also functions as a key modulator of transforming growth factor-beta (TGF-beta)-driven immune deviation, capable of suppressing the differentiation of interleukin-17 secreting T helper cells (T(H)17) and conversely promoting the generation of Foxp3(+) T regulatory (Treg) cells. Tretinoin 28-30 transforming growth factor beta 1 Homo sapiens 101-109 18809338-3 2009 This review will focus on the role of RA in the reciprocal TGF-beta-driven differentiation of T(H)17 and Treg and on the importance of such regulatory mechanism to control a functional immune system, in particular at the mucosal interface of the intestine. Tretinoin 38-40 transforming growth factor beta 1 Homo sapiens 59-67 20429413-11 2009 For example, retinoic acid, produced by the dendritic cells and epithelial cells in the intestine, works together with TGF-beta1 and promotes generation of small intestine-homing FOXP3 T-cells by upregulating the expression ofFOXP3 and gut homing receptors. Tretinoin 13-26 transforming growth factor beta 1 Homo sapiens 119-128 19006694-2 2008 Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 29-37 19006694-2 2008 Retinoic acid (RA) increases TGF-beta-induced expression of Foxp3, through unknown molecular mechanisms. Tretinoin 15-17 transforming growth factor beta 1 Homo sapiens 29-37 18248652-13 2008 CONCLUSION: Exposure of leiomyomas to ATRA down-regulated cell proliferation, ECM formation, RA metabolism and TGF-beta regulation, suggesting that RA exposure can alter the leiomyoma phenotype to one that more closely approximates normal myometrium. Tretinoin 40-42 transforming growth factor beta 1 Homo sapiens 111-119 17569825-4 2007 We identified the vitamin A metabolite retinoic acid as a key regulator of TGF-beta-dependent immune responses, capable of inhibiting the IL-6-driven induction of proinflammatory T(H)17 cells and promoting anti-inflammatory Treg cell differentiation. Tretinoin 39-52 transforming growth factor beta 1 Homo sapiens 75-83 18684916-0 2008 Retinoic acid increases Foxp3+ regulatory T cells and inhibits development of Th17 cells by enhancing TGF-beta-driven Smad3 signaling and inhibiting IL-6 and IL-23 receptor expression. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 102-110 17951529-4 2008 Conversely, inhibition of retinoic acid signaling constrains transforming growth factor beta (TGF-beta1) induction of FoxP3. Tretinoin 26-39 transforming growth factor beta 1 Homo sapiens 94-103 18293192-0 2008 Activation of TGF-beta1 through up-regulation of TSP-1 by retinoic acid in retinal pigment epithelial cells. Tretinoin 58-71 transforming growth factor beta 1 Homo sapiens 14-23 18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 9-22 transforming growth factor beta 1 Homo sapiens 54-87 18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 9-22 transforming growth factor beta 1 Homo sapiens 89-98 18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 54-87 18293192-1 2008 PURPOSE: Retinoic acid (RA) affects the activation of transforming growth factor-beta 1 (TGF-beta1) in a variety of cells. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 89-98 18293192-3 2008 Since TSP-1 activates TGF-beta1, we investigated whether RA stimulates the activation of TGF-beta1 through up-regulation of TSP-1 in RPE cells. Tretinoin 57-59 transforming growth factor beta 1 Homo sapiens 89-98 18293192-6 2008 RESULTS: The active form of TGF-beta1 was increased dose-dependently by RA or TSP-1. Tretinoin 72-74 transforming growth factor beta 1 Homo sapiens 28-37 18293192-7 2008 The activation of TGF-beta1 by RA was significantly hampered by an anti-TSP-1 antibody. Tretinoin 31-33 transforming growth factor beta 1 Homo sapiens 18-27 18293192-9 2008 CONCLUSIONS: These findings suggest that, in RPE cells, RA increases the activation of TGF-beta1 via up-regulation of TSP-1, and integrins such as alphavbeta3 and alphavbeta5 are essential in this activation step. Tretinoin 56-58 transforming growth factor beta 1 Homo sapiens 87-96 18157915-0 2007 On the role of transforming growth factor-beta in the growth inhibitory effects of retinoic acid in human pancreatic cancer cells. Tretinoin 83-96 transforming growth factor beta 1 Homo sapiens 15-46 18157915-9 2007 A TGF-beta neutralizing antibody blocked the growth inhibitory effects of retinoic acid in Capan-2 cells and partially inhibitory the effects in Hs766T cells. Tretinoin 74-87 transforming growth factor beta 1 Homo sapiens 2-10 18157915-11 2007 Furthermore, it demonstrates the fundamental role of TGF-beta in growth inhibition in response to retinoic acid treatment is preserved in vitro. Tretinoin 98-111 transforming growth factor beta 1 Homo sapiens 53-61 17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 67-80 transforming growth factor beta 1 Homo sapiens 36-44 17694576-3 2007 We now show that, in the context of TGF-beta signalling, all-trans retinoic acid (ATRA) leads to increased induction of CD4(+) T cells expressing the Treg specification factor forkhead box protein P3 (FoxP3) and decreased frequency of cells expressing IL-17, even in the presence of IL-6. Tretinoin 82-86 transforming growth factor beta 1 Homo sapiens 36-44 17620364-2 2007 New studies support this idea by showing that the catalysis of vitamin A into retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (T reg) cells and also directs T reg cell homing to the gut. Tretinoin 78-91 transforming growth factor beta 1 Homo sapiens 150-187 17620364-2 2007 New studies support this idea by showing that the catalysis of vitamin A into retinoic acid (RA) in gut-associated dendritic cells (DCs) enhances the transforming growth factor (TGF)-beta-dependent conversion of naive T cells into regulatory T (T reg) cells and also directs T reg cell homing to the gut. Tretinoin 93-95 transforming growth factor beta 1 Homo sapiens 150-187 17098229-4 2007 The negative growth factor-transforming growth factor beta (TGFbeta) was secreted by RA and/or tamoxifen treatment and was studies as a potential mediator of the synergistic effects of RA and tamoxifen in apoptosis. Tretinoin 85-87 transforming growth factor beta 1 Homo sapiens 60-67 19262136-4 2007 A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation. Tretinoin 24-37 transforming growth factor beta 1 Homo sapiens 90-97 19262136-4 2007 A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation. Tretinoin 39-41 transforming growth factor beta 1 Homo sapiens 90-97 17098229-4 2007 The negative growth factor-transforming growth factor beta (TGFbeta) was secreted by RA and/or tamoxifen treatment and was studies as a potential mediator of the synergistic effects of RA and tamoxifen in apoptosis. Tretinoin 185-187 transforming growth factor beta 1 Homo sapiens 60-67 16242776-0 2006 Transforming growth factor-beta1 inhibits all-trans retinoic acid-induced apoptosis. Tretinoin 52-65 transforming growth factor beta 1 Homo sapiens 0-32 16242776-2 2006 In this study, we demonstrated that a combination treatment with all-trans retinoic acid (ATRA) and TGF-beta1 led to the enhancement of ATRA-induced suppression of cell proliferation, which is accompanied by inhibition of ATRA-induced apoptosis in human leukemia HL-60 cells. Tretinoin 136-140 transforming growth factor beta 1 Homo sapiens 100-109 16242776-2 2006 In this study, we demonstrated that a combination treatment with all-trans retinoic acid (ATRA) and TGF-beta1 led to the enhancement of ATRA-induced suppression of cell proliferation, which is accompanied by inhibition of ATRA-induced apoptosis in human leukemia HL-60 cells. Tretinoin 136-140 transforming growth factor beta 1 Homo sapiens 100-109 16242776-4 2006 Inhibition of ATRA-induced apoptosis by TGF-beta1 was associated with an increased level of Mcl-1 protein, an anti-apoptotic member of Bcl-2 family, but not with inhibition of mitochondrial membrane depolarization. Tretinoin 14-18 transforming growth factor beta 1 Homo sapiens 40-49 16246418-4 2006 Concomitantly, treatment of HL-60 cells with the combination of TGFbeta1 and the retinoid partially suppresses ATRA-dependent induction of TRAIL. Tretinoin 111-115 transforming growth factor beta 1 Homo sapiens 64-72 15897880-5 2005 In addition to enhanced retinoid signaling, the transforming growth factor-beta (TGFbeta) pathway was strongly activated by ATRA treatment of Wilms tumor cells. Tretinoin 124-128 transforming growth factor beta 1 Homo sapiens 48-79 15897880-5 2005 In addition to enhanced retinoid signaling, the transforming growth factor-beta (TGFbeta) pathway was strongly activated by ATRA treatment of Wilms tumor cells. Tretinoin 124-128 transforming growth factor beta 1 Homo sapiens 81-88 15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 132-145 transforming growth factor beta 1 Homo sapiens 216-224 15988048-5 2005 Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay. Tretinoin 147-149 transforming growth factor beta 1 Homo sapiens 216-224 15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 35-48 transforming growth factor beta 1 Homo sapiens 167-176 15955085-9 2005 After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Tretinoin 13-17 transforming growth factor beta 1 Homo sapiens 29-37 15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 35-48 transforming growth factor beta 1 Homo sapiens 167-176 15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 191-204 transforming growth factor beta 1 Homo sapiens 22-31 15823505-6 2005 While the addition of TGF-beta1 or retinoic acid to monkey normal lung bronchial 12MBr6 cells and human lung cancer NCI-H727 cells increased DENTT protein production, TGF-beta1 together with retinoic acid resulted in a more sustained increase in DENTT production than with TGF-beta1 or retinoic acid alone. Tretinoin 191-204 transforming growth factor beta 1 Homo sapiens 22-31 15823505-7 2005 Transient transfection studies showed that ectopic DENTT expression significantly increased TGF-beta1-responsive 3TP-Lux and CAGA12-Lux reporter transcription in 12MBr6 and NCI-H727 cells with TGF-beta1 addition, while ectopic DENTT expression had no significant effect on the transcription of a retinoic acid-responsive element reporter in the presence of retinoic acid or TGF-beta1. Tretinoin 296-309 transforming growth factor beta 1 Homo sapiens 92-101 15823505-7 2005 Transient transfection studies showed that ectopic DENTT expression significantly increased TGF-beta1-responsive 3TP-Lux and CAGA12-Lux reporter transcription in 12MBr6 and NCI-H727 cells with TGF-beta1 addition, while ectopic DENTT expression had no significant effect on the transcription of a retinoic acid-responsive element reporter in the presence of retinoic acid or TGF-beta1. Tretinoin 357-370 transforming growth factor beta 1 Homo sapiens 92-101 15970678-8 2005 Cotreatment with the RAR-alpha antagonist, Ro41-5253 or pan-TGF-beta neutralizing antibody abolished the phenotypic and antiproliferative effects of all-trans retinoic acid. Tretinoin 159-172 transforming growth factor beta 1 Homo sapiens 60-68 12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 233-246 transforming growth factor beta 1 Homo sapiens 87-94 15727050-3 2005 Components of the TGFbeta signal transduction machinery are discussed in relation to regulation of transcription, cell division and tissue differentiation in developing orofacial tissue, as evidence for a functional linkage between the TGFbeta and retinoic acid signal transduction pathways during orofacial development. Tretinoin 248-261 transforming growth factor beta 1 Homo sapiens 18-25 12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 57-80 transforming growth factor beta 1 Homo sapiens 43-52 12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 57-80 transforming growth factor beta 1 Homo sapiens 278-287 12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 82-86 transforming growth factor beta 1 Homo sapiens 43-52 12393416-4 2003 Simultaneous treatment of these cells with TGF-beta1 and all-trans-retinoic acid (ATRA), which leads to almost equal numbers of granulocytes and monocytes, significantly reduced the level of phospho-Smad2/3 and its nuclear accumulation, compared with that in cells treated with TGF-beta1 alone. Tretinoin 82-86 transforming growth factor beta 1 Homo sapiens 278-287 12393416-6 2003 Addition of the inhibitor-of-protein serine/threonine phosphatases, okadaic acid, blocks the ATRA-mediated reduction in TGF-beta-induced phospho-Smad2 and shifts the differentiation toward monocytic end points. Tretinoin 93-97 transforming growth factor beta 1 Homo sapiens 120-128 12468040-2 2002 SH-SY5Y cells express the intracellular factors activated through the receptors of the TGFbeta superfamily members, Smad1 and Smad4, as in basal conditions or after differentiation with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or retinoic acid (RA). Tretinoin 248-250 transforming growth factor beta 1 Homo sapiens 87-94 12468040-4 2002 Cell differentiation due to TGF-beta1 treatment is accompanied by an increase in tyrosine hydroxylase (TH) expression, more pronounced in the presence of TPA or RA and counteracted by BMP-2. Tretinoin 161-163 transforming growth factor beta 1 Homo sapiens 28-37 12115542-7 2002 Owing to a decrease in the secretion of MCP-1 and transforming growth factor-beta 1 (TGF-beta 1), tumor cells treated with RA were unable to induce peripheral blood monocyte (PBM) chemotaxis. Tretinoin 123-125 transforming growth factor beta 1 Homo sapiens 50-83 12115542-7 2002 Owing to a decrease in the secretion of MCP-1 and transforming growth factor-beta 1 (TGF-beta 1), tumor cells treated with RA were unable to induce peripheral blood monocyte (PBM) chemotaxis. Tretinoin 123-125 transforming growth factor beta 1 Homo sapiens 85-95 11176716-9 2001 Tretinoin-treated keloid-producing fibroblasts secreted more TGF-beta1 than did controls at 120 hours (P<.05). Tretinoin 0-9 transforming growth factor beta 1 Homo sapiens 61-70 11074878-14 2000 Oral all-trans-retinoic acid enhanced collagen deposition, TGF-beta and IGF-I levels over normal chow fed control animals (P<.05). Tretinoin 5-28 transforming growth factor beta 1 Homo sapiens 59-67 10611763-4 1999 In addition, enhanced levels of circulating endogenous TGF-beta appear to be an instrument of suppression during the development of oral tolerance, cyclosporin treatment, and following administration of retinoic acid. Tretinoin 203-216 transforming growth factor beta 1 Homo sapiens 55-63 10938282-10 2000 The TGF-beta-neutralizing antibody blocked the RA-induced as well as TGF-beta2-mediated MUC4 expression. Tretinoin 47-49 transforming growth factor beta 1 Homo sapiens 4-12 10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 90-98 10218988-15 1999 Retinoic acid stimulated TGFbeta3 mRNA expression within 24 h and increased expression of TGFbeta1 and TGFbeta2 after 72 h. Retinol increased expression of TGFbeta1 and TGFbeta2 but not TGFbeta3 after 72 h of treatment. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 156-164 9688937-8 1998 We also showed that RA was able to reduce the decrease in cell number observed when type 2 cells were treated with transforming growth factor (TGF)-beta1. Tretinoin 20-22 transforming growth factor beta 1 Homo sapiens 115-153 9688937-9 1998 These results together with the known stimulatory effect of TGF-beta1 on IGFBP-2 expression led to suggest that RA may be associated with type 2 cell proliferation through mechanisms interfering with the TGF-beta1 pathway. Tretinoin 112-114 transforming growth factor beta 1 Homo sapiens 60-69 9688937-9 1998 These results together with the known stimulatory effect of TGF-beta1 on IGFBP-2 expression led to suggest that RA may be associated with type 2 cell proliferation through mechanisms interfering with the TGF-beta1 pathway. Tretinoin 112-114 transforming growth factor beta 1 Homo sapiens 204-213 9261338-5 1997 The differentiation effects of TGF-beta 1 alone and especially of its combination with MK-886 were most pronounced when the cells were pretreated with dimethyl sulfoxide or all-trans-retinoic acid. Tretinoin 173-196 transforming growth factor beta 1 Homo sapiens 31-41 9649124-9 1998 This regimen of melatonin followed by atRA induced cytocidal effects on MCF-7 cells by activating pathways leading to apoptosis (programmed cell death) as evidenced by decreased ER and Bcl-2 and increased Bax and transforming growth factor beta 1 (TGF-beta1) expression. Tretinoin 38-42 transforming growth factor beta 1 Homo sapiens 213-246 9649124-9 1998 This regimen of melatonin followed by atRA induced cytocidal effects on MCF-7 cells by activating pathways leading to apoptosis (programmed cell death) as evidenced by decreased ER and Bcl-2 and increased Bax and transforming growth factor beta 1 (TGF-beta1) expression. Tretinoin 38-42 transforming growth factor beta 1 Homo sapiens 248-257 9664142-8 1998 The most striking difference between the cell lines was a strong downregulation of transforming growth factor-beta (TGF-beta) expression in cell lines derived from metastases when treated with RA in contrast to cell lines from primary melanomas. Tretinoin 193-195 transforming growth factor beta 1 Homo sapiens 83-114 9664142-8 1998 The most striking difference between the cell lines was a strong downregulation of transforming growth factor-beta (TGF-beta) expression in cell lines derived from metastases when treated with RA in contrast to cell lines from primary melanomas. Tretinoin 193-195 transforming growth factor beta 1 Homo sapiens 116-124 9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 0-23 transforming growth factor beta 1 Homo sapiens 55-63 9262057-11 1997 Together, these data suggested that; 1) retinoic acid has a preferential effect on T cell and Hodgkin"s lymphoma cell lines; 2) autoregulation of RAR-alpha by retinoic acids, and the presence of TGF-beta 1 receptors may be relevant to the response of lymphomas to treatment with retinoic acids. Tretinoin 40-53 transforming growth factor beta 1 Homo sapiens 195-205 9262057-11 1997 Together, these data suggested that; 1) retinoic acid has a preferential effect on T cell and Hodgkin"s lymphoma cell lines; 2) autoregulation of RAR-alpha by retinoic acids, and the presence of TGF-beta 1 receptors may be relevant to the response of lymphomas to treatment with retinoic acids. Tretinoin 279-293 transforming growth factor beta 1 Homo sapiens 195-205 9153223-4 1997 All-trans-retinoic acid (t-RA) increased the levels of TGF-beta2 and IGFBP-3 mRNA and of secreted TGF-beta and IGFBP-3 proteins. Tretinoin 25-29 transforming growth factor beta 1 Homo sapiens 55-63 9639813-7 1996 Addition of suitable amount of anti-TGF-beta 1 monoclonal antibody IgG (TB21) to the culture medium of embryoid bodies of ES-T6 cells could effectively abolish the formation of vessel-like structures induced by retinoic acid. Tretinoin 211-224 transforming growth factor beta 1 Homo sapiens 36-46 8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 46-48 transforming growth factor beta 1 Homo sapiens 119-127 8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 46-48 transforming growth factor beta 1 Homo sapiens 154-162 8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 223-225 transforming growth factor beta 1 Homo sapiens 119-127 8946934-6 1996 Preincubation experiments further showed that RA is capable of sensitizing the progenitors to the inhibitory action of TGF-beta: the inhibitory effect of TGF-beta was significantly increased when cells were pretreated with RA. Tretinoin 223-225 transforming growth factor beta 1 Homo sapiens 154-162 8946934-7 1996 These data show that, in combination with IL-3, RA additionally stimulates quiescent bone marrow progenitors in a simultaneous way, and that it increases sensitivity of the progenitors to the inhibitory action of TGF-beta. Tretinoin 48-50 transforming growth factor beta 1 Homo sapiens 213-221 9627689-6 1996 Retinoic acid, which is known to interfere with vitamin D3 signaling, slightly decreased the levels of secreted TGF-beta 1 protein in BT-20 cells, but did not significantly affect the vitamin D3-induced increase. Tretinoin 0-13 transforming growth factor beta 1 Homo sapiens 112-122 8687982-8 1996 As some RA effects are mediated through increased activity of TGFbeta, a known PPi stimulant, we examined the effect of anti-TGFbeta antibody on RA-induced PPi elaboration. Tretinoin 145-147 transforming growth factor beta 1 Homo sapiens 125-132 8626114-1 1996 The purpose of this study was to determine whether all-trans-retinoic acid (RA) can inhibit the growth of cervical neoplastic cells by inducing differentiation or by increasing the secretion of transforming growth factor-beta (TGF-beta). Tretinoin 51-74 transforming growth factor beta 1 Homo sapiens 227-235 8626114-1 1996 The purpose of this study was to determine whether all-trans-retinoic acid (RA) can inhibit the growth of cervical neoplastic cells by inducing differentiation or by increasing the secretion of transforming growth factor-beta (TGF-beta). Tretinoin 76-78 transforming growth factor beta 1 Homo sapiens 227-235 8626114-9 1996 Secretion of either TGF-beta 1 or TGF-beta 2 is significantly increased (P<0.05) in response to RA, both in RA-sensitive and in RA-resistant cells. Tretinoin 99-101 transforming growth factor beta 1 Homo sapiens 20-30 8564960-0 1996 Effects of endogenously activated transforming growth factor-beta on growth and differentiation of retinoic acid-treated HL-60 cells. Tretinoin 99-112 transforming growth factor beta 1 Homo sapiens 34-65 8564960-4 1996 The role of TGF-beta in RA-dependent differentiation and cessation of growth was examined by adding neutralizing anti-TGF-beta IgG to RA-treated HL-60 cells, followed by assessing cell growth and markers of granulocytic differentiation over 5 days. Tretinoin 24-26 transforming growth factor beta 1 Homo sapiens 12-20 8564960-9 1996 Similar levels of total TGF-beta were observed between control and RA-treated cells. Tretinoin 67-69 transforming growth factor beta 1 Homo sapiens 24-32 8564960-11 1996 Activation of endogenous latent TGF-beta by RA-treated cells occurred through a plasmin-independent mechanism. Tretinoin 44-46 transforming growth factor beta 1 Homo sapiens 32-40 8574976-0 1995 Effect of retinoic acid on expression of transforming growth factor-beta by retinal pigment epithelial cells in culture. Tretinoin 10-23 transforming growth factor beta 1 Homo sapiens 41-72 8557779-1 1996 This report shows for the first time that platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta (TGF-beta) can interact in a synergistic manner with retinoic acid to stimulate the production of tissue inhibitor of metalloproteinases (TIMP) from human skin and synovial fibroblasts. Tretinoin 175-188 transforming growth factor beta 1 Homo sapiens 90-121 8557779-1 1996 This report shows for the first time that platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta (TGF-beta) can interact in a synergistic manner with retinoic acid to stimulate the production of tissue inhibitor of metalloproteinases (TIMP) from human skin and synovial fibroblasts. Tretinoin 175-188 transforming growth factor beta 1 Homo sapiens 123-131 8574976-1 1995 OBJECTIVE: To study the effect of retinoic acid on the expression of transforming growth factor-beta (TGF-beta) by human retinal pigment epithelial (RPE) cells in culture. Tretinoin 34-47 transforming growth factor beta 1 Homo sapiens 69-100 8574976-1 1995 OBJECTIVE: To study the effect of retinoic acid on the expression of transforming growth factor-beta (TGF-beta) by human retinal pigment epithelial (RPE) cells in culture. Tretinoin 34-47 transforming growth factor beta 1 Homo sapiens 102-110 8574976-5 1995 Densitometry showed that retinoic acid reduced the level of TGF-beta 1 mRNA expression by 41% compared with control samples. Tretinoin 25-38 transforming growth factor beta 1 Homo sapiens 60-70 8574976-6 1995 ELISA showed that retinoic acid inhibited TGF-beta expression when compared with the baseline level of TGF-beta in media from RPE cells in culture. Tretinoin 18-31 transforming growth factor beta 1 Homo sapiens 42-50 7757990-0 1995 Induction of transforming growth factor beta 1 and its receptors during all-trans-retinoic acid (RA) treatment of RA-responsive human neuroblastoma cell lines. Tretinoin 76-95 transforming growth factor beta 1 Homo sapiens 13-46 7757990-0 1995 Induction of transforming growth factor beta 1 and its receptors during all-trans-retinoic acid (RA) treatment of RA-responsive human neuroblastoma cell lines. Tretinoin 97-99 transforming growth factor beta 1 Homo sapiens 13-46 7757990-0 1995 Induction of transforming growth factor beta 1 and its receptors during all-trans-retinoic acid (RA) treatment of RA-responsive human neuroblastoma cell lines. Tretinoin 114-116 transforming growth factor beta 1 Homo sapiens 13-46 7757990-1 1995 Recent work on a variety of normal and malignant cell lines has shown that induction and secretion of biologically active TGF-beta may occur after exposure to all-trans-retinoic acid (RA), coincident with decreased growth rate and/or differentiation. Tretinoin 163-182 transforming growth factor beta 1 Homo sapiens 122-130 7757990-1 1995 Recent work on a variety of normal and malignant cell lines has shown that induction and secretion of biologically active TGF-beta may occur after exposure to all-trans-retinoic acid (RA), coincident with decreased growth rate and/or differentiation. Tretinoin 184-186 transforming growth factor beta 1 Homo sapiens 122-130 7757990-4 1995 However, in the RA-resistant line SK-N-AS, TGF-beta 1 is constitutively secreted at levels that are unchanged after RA treatment, and although TBRI and TBRIII mRNA is expressed in untreated SK-N-AS cells, levels of TBRI and TBRIII protein and TBRII mRNA decrease after RA treatment. Tretinoin 16-18 transforming growth factor beta 1 Homo sapiens 43-53 7757990-5 1995 Thus, in RA-sensitive neuroblastoma cells, RA treatment may result in the induction of a negative autocrine TGF-beta 1 growth regulatory loop. Tretinoin 9-11 transforming growth factor beta 1 Homo sapiens 108-118 7873195-4 1995 To test this hypothesis, we determined whether all-trans retinoic acid (RA) and several other retinoid compounds regulate the production of types I and III collagen by unstimulated and TGF-beta 1-stimulated human lung fibroblasts. Tretinoin 72-74 transforming growth factor beta 1 Homo sapiens 185-195 7873195-7 1995 RA preincubation also totally abrogated the collagen inductive effects of TGF-beta 1. Tretinoin 0-2 transforming growth factor beta 1 Homo sapiens 74-84 7873195-8 1995 At 10(-5) M, RA preincubation caused a 97% decrease in the stimulation of type I collagen and a 115% decrease in the stimulation of type III collagen caused by TGF-beta 1. Tretinoin 13-15 transforming growth factor beta 1 Homo sapiens 160-170