PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18084321-4 2008 We report that nanomolar concentrations of all-trans retinoic acid (ATRA) amplify TNFalpha-induced apoptosis in APL cells expressing a specific repressor of NF-kappaB activation. Tretinoin 53-66 tumor necrosis factor Homo sapiens 82-90 18571505-5 2008 Adding AG1296 with RA increased secretion of TNF-alpha, IL-8, and MMP-9 expression. Tretinoin 19-21 tumor necrosis factor Homo sapiens 45-54 18084321-4 2008 We report that nanomolar concentrations of all-trans retinoic acid (ATRA) amplify TNFalpha-induced apoptosis in APL cells expressing a specific repressor of NF-kappaB activation. Tretinoin 68-72 tumor necrosis factor Homo sapiens 82-90 18084321-10 2008 This study also suggests that inclusion of nanomolar doses of ATRA could be clinically beneficial in amplifying TNFalpha-induced antitumor signals. Tretinoin 62-66 tumor necrosis factor Homo sapiens 112-120 17313834-0 2006 [Retinoic acid inhibits tumor necrosis factor-alpha induced injury in human lung epithelial cells]. Tretinoin 1-14 tumor necrosis factor Homo sapiens 24-51 18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 47-70 tumor necrosis factor Homo sapiens 184-193 18416830-1 2008 BACKGROUND: We have recently demonstrated that all-trans-retinoic acid (ATRA) and 9-cis-retinoic acid (9-cis RA) promote IL-4, IL-5 and IL-13 synthesis, while decreasing IFN-gamma and TNF-alpha expression by activated human T cells and reduces the synthesis of IL-12p70 from accessory cells. Tretinoin 72-76 tumor necrosis factor Homo sapiens 184-193 17253143-0 2007 Retinoic acid enhances the production of IL-10 while reducing the synthesis of IL-12 and TNF-alpha from LPS-stimulated monocytes/macrophages. Tretinoin 0-13 tumor necrosis factor Homo sapiens 89-98 17253143-8 2007 In contrast, the addition of atRA inhibited the LPS-induced TNF-alpha and IL-12p40 mRNA expression, and the number of ELISPOT positive cells for TNF-alpha. Tretinoin 29-33 tumor necrosis factor Homo sapiens 60-69 17253143-8 2007 In contrast, the addition of atRA inhibited the LPS-induced TNF-alpha and IL-12p40 mRNA expression, and the number of ELISPOT positive cells for TNF-alpha. Tretinoin 29-33 tumor necrosis factor Homo sapiens 145-154 17253143-11 2007 While atRA downregulated the proinflammatory cytokines, e.g., IL-12 and TNF-alpha, the production of an immune modulating cytokine, IL-10 was enhanced by atRA. Tretinoin 6-10 tumor necrosis factor Homo sapiens 72-81 17313834-7 2006 RA alone did not significantly promote the proliferation of the A549 cells, but weakened the inhibitory effect of TNF-alpha on the proliferation of the A549 cells. Tretinoin 0-2 tumor necrosis factor Homo sapiens 114-123 17313834-9 2006 CONCLUSION: RA relieves the injury of alveolar epithelial cells and protects the pulmonary surfactant by inhibiting the destruction of TNF-alpha to type II lung alveolar epithelial cells. Tretinoin 12-14 tumor necrosis factor Homo sapiens 135-144 18039708-0 2008 Retinoic acid modulates chromatin to potentiate tumor necrosis factor alpha signaling on the DIF2 promoter. Tretinoin 0-13 tumor necrosis factor Homo sapiens 48-75 16292516-7 2006 In contrast, ATRA suppressed the production of IFN-gamma and TNF-alpha significantly. Tretinoin 13-17 tumor necrosis factor Homo sapiens 61-70 16292516-9 2006 CONCLUSIONS: ATRA was demonstrated to affect the cytokine production of IFN-gamma and TNF-alpha. Tretinoin 13-17 tumor necrosis factor Homo sapiens 86-95 15256426-0 2004 Combination of retinoic acid and tumor necrosis factor overcomes the maturation block in a variety of retinoic acid-resistant acute promyelocytic leukemia cells. Tretinoin 102-115 tumor necrosis factor Homo sapiens 33-54 15946654-6 2005 We showed that both MMP-1 and MMP-13 mRNA expression, protein production and enzyme activity induced by either IL-1 or TNF-alpha were suppressed by t-RA or different retinoid derivatives. Tretinoin 148-152 tumor necrosis factor Homo sapiens 119-128 15946654-9 2005 Furthermore, we showed that t-RA could reduce IL-1-induced TNF-alpha production in chondrocytes. Tretinoin 28-32 tumor necrosis factor Homo sapiens 59-68 15256426-5 2004 Here, we report that combining TNF with RA leads to maturation of several RA-resistant APL cells along a monocytic pathway, whereas UF-1, a patient-derived RA-resistant cell line, showed characteristics of granulocytic differentiation. Tretinoin 74-76 tumor necrosis factor Homo sapiens 31-34 15256426-5 2004 Here, we report that combining TNF with RA leads to maturation of several RA-resistant APL cells along a monocytic pathway, whereas UF-1, a patient-derived RA-resistant cell line, showed characteristics of granulocytic differentiation. Tretinoin 74-76 tumor necrosis factor Homo sapiens 31-34 11470254-5 2001 Furthermore, indomethacin potentiated apoptosis in cells treated with a differentiating agent, all-trans retinoic acid, which induces resistance to TNF-alpha. Tretinoin 105-118 tumor necrosis factor Homo sapiens 148-157 12935977-7 2003 RESULTS: ATRA significantly inhibited TNFalpha-induced TF expression in HMEC-1 as well as HUVEC. Tretinoin 9-13 tumor necrosis factor Homo sapiens 38-46 12935977-8 2003 ATRA increased t-PA antigen without significantly affecting PAI-1 expression, and counteracted the TNFalpha-induced t-PA decrease in both types of EC. Tretinoin 0-4 tumor necrosis factor Homo sapiens 99-107 12935977-10 2003 Finally, ATRA upregulated TM, and prevented TNFalpha-induced TM downregulation. Tretinoin 9-13 tumor necrosis factor Homo sapiens 44-52 12586626-4 2003 Here we show that TNF can synergize with ATRA to induce differentiation, showing monocytic characteristics more typical of differentiation mediated by TNF than by ATRA. Tretinoin 41-45 tumor necrosis factor Homo sapiens 151-154 12586626-4 2003 Here we show that TNF can synergize with ATRA to induce differentiation, showing monocytic characteristics more typical of differentiation mediated by TNF than by ATRA. Tretinoin 163-167 tumor necrosis factor Homo sapiens 18-21 12586626-6 2003 Underlying this response was an increase in TNF-induced nuclear factor-kappaB (NF-kappaB) DNA binding within 2 hours in the presence of ATRA and activation of NF-kappaB DNA binding and transcriptional activity in response to ATRA alone within 48 hours of ATRA treatment. Tretinoin 136-140 tumor necrosis factor Homo sapiens 44-47 12586626-6 2003 Underlying this response was an increase in TNF-induced nuclear factor-kappaB (NF-kappaB) DNA binding within 2 hours in the presence of ATRA and activation of NF-kappaB DNA binding and transcriptional activity in response to ATRA alone within 48 hours of ATRA treatment. Tretinoin 225-229 tumor necrosis factor Homo sapiens 44-47 12586626-6 2003 Underlying this response was an increase in TNF-induced nuclear factor-kappaB (NF-kappaB) DNA binding within 2 hours in the presence of ATRA and activation of NF-kappaB DNA binding and transcriptional activity in response to ATRA alone within 48 hours of ATRA treatment. Tretinoin 225-229 tumor necrosis factor Homo sapiens 44-47 12526099-3 2002 Treatment of cells with TNF in the presence of all-trans-retinoic acid (RA) significantly decreased their ability to produce nitrite and iNOS induction. Tretinoin 47-70 tumor necrosis factor Homo sapiens 24-27 12526099-3 2002 Treatment of cells with TNF in the presence of all-trans-retinoic acid (RA) significantly decreased their ability to produce nitrite and iNOS induction. Tretinoin 72-74 tumor necrosis factor Homo sapiens 24-27 12526099-5 2002 The inhibitory effect of RA on TNF-induced iNOS induction was reversible, completely recovered after 2 days, and was exerted through the inhibition of NF-kappaB activation. Tretinoin 25-27 tumor necrosis factor Homo sapiens 31-34 12526099-7 2002 RA could not reverse the TNF- induced LPL suppression at RA levels causing near complete inhibition of the TNF-induced NO production. Tretinoin 0-2 tumor necrosis factor Homo sapiens 107-110 15469694-5 2004 TNF-alpha or C(2) ceramide, a cell permeable ceramide analog, induced cell death in normal cells, but cell death was largely inhibited by the RA treatment. Tretinoin 142-144 tumor necrosis factor Homo sapiens 0-9 15469694-6 2004 The inhibition of tTGase by the tTGase inhibitors, monodansylcadaverine and cystamine, eliminated the protective role of RA-treatment in the cell death that is caused by TNF-alpha or C(2)-ceramide. Tretinoin 121-123 tumor necrosis factor Homo sapiens 170-179 15469694-9 2004 These results suggest that tTGase expressed by RA treatment plays an important role in the protection of cell death caused by TNF-alpha and ceramide. Tretinoin 47-49 tumor necrosis factor Homo sapiens 126-135 15008977-0 2004 Retinoic acid enhances the gene expression of human polymeric immunoglobulin receptor (pIgR) by TNF-alpha. Tretinoin 0-13 tumor necrosis factor Homo sapiens 96-105 15008977-2 2004 Expression of the pIgR by tumour necrosis factor (TNF-alpha) was enhanced by the addition of all-trans retinoic acid (ATRA) or 9-cis retinoic acid (9CRA). Tretinoin 93-116 tumor necrosis factor Homo sapiens 50-59 15008977-2 2004 Expression of the pIgR by tumour necrosis factor (TNF-alpha) was enhanced by the addition of all-trans retinoic acid (ATRA) or 9-cis retinoic acid (9CRA). Tretinoin 118-122 tumor necrosis factor Homo sapiens 50-59 12586626-9 2003 We propose that ATRA can prime cancer cells for differentiation triggered by TNF and suggest that targeting the TNF pathway in combination with ATRA may represent a novel route to treat leukemias. Tretinoin 16-20 tumor necrosis factor Homo sapiens 77-80 12586626-9 2003 We propose that ATRA can prime cancer cells for differentiation triggered by TNF and suggest that targeting the TNF pathway in combination with ATRA may represent a novel route to treat leukemias. Tretinoin 16-20 tumor necrosis factor Homo sapiens 112-115 11880314-0 2002 Protective role of retinoic acid from antiproliferative action of TNF-alpha on lung epithelial cells. Tretinoin 19-32 tumor necrosis factor Homo sapiens 66-75 11880314-8 2002 Interestingly, we observed that RA abrogated TNF-alpha-induced growth arrest and that this effect was associated with a dramatic decrease in IGFBP-2 expression. Tretinoin 32-34 tumor necrosis factor Homo sapiens 45-54 11880314-9 2002 These results suggest a protective role of RA from TNF-alpha antiproliferative action, through mechanisms involving modulation of IGFBP-2 production. Tretinoin 43-45 tumor necrosis factor Homo sapiens 51-60 10936200-4 2000 This biphasic response may be related to the different expression of TNF-alpha receptors (TNFRs); a significant increase in the density of TNFR1 was in fact observed following RA-induced differentiation. Tretinoin 176-178 tumor necrosis factor Homo sapiens 69-78 11358989-4 2001 In contrast, ATRA treatment induced resistance to TNF-alpha-induced apoptosis. Tretinoin 13-17 tumor necrosis factor Homo sapiens 50-59 10766166-4 2000 The B94 gene (TNFAIP2; Unigene Hs.101382), originally identified as a tumor necrosis factor alpha-inducible gene in endothelial cells, was one of several genes found to be induced by RA specifically in TF1-PR cells, but not in TF1-neo (control) cells. Tretinoin 183-185 tumor necrosis factor Homo sapiens 70-97 10954918-3 2000 Exposure to LPS resulted in the maximum release of soluble TNF-alpha by 2 h. Electrophoretic mobility shift assays (EMSA) using the TAC element as a probe showed a unique pattern for LPS-activated cells: the disappearance of the upper band of a doublet seen in untreated and all-trans retinoic acid (ATRA)-treated cells. Tretinoin 285-298 tumor necrosis factor Homo sapiens 59-68 10954918-3 2000 Exposure to LPS resulted in the maximum release of soluble TNF-alpha by 2 h. Electrophoretic mobility shift assays (EMSA) using the TAC element as a probe showed a unique pattern for LPS-activated cells: the disappearance of the upper band of a doublet seen in untreated and all-trans retinoic acid (ATRA)-treated cells. Tretinoin 300-304 tumor necrosis factor Homo sapiens 59-68 10082656-0 1999 Retinoic acid potentiates TNF-alpha-induced ICAM-1 expression in normal human epidermal keratinocytes. Tretinoin 0-13 tumor necrosis factor Homo sapiens 26-35 10646501-9 2000 The addition of TNFalpha or PMA potentiated RA-induced MMP-9 expression with a synergic maximal effect at day 14 of RA exposure. Tretinoin 44-46 tumor necrosis factor Homo sapiens 16-24 10022522-6 1999 Tumor necrosis factor-alpha, which enhances the posttranscriptional action of retinoic acid, reduced U1 70K mRNA expression, while an inhibition of retinoic acid action by transforming growth factor-beta was associated with a marked increase in U1 70K mRNA levels. Tretinoin 78-91 tumor necrosis factor Homo sapiens 0-27 10022522-6 1999 Tumor necrosis factor-alpha, which enhances the posttranscriptional action of retinoic acid, reduced U1 70K mRNA expression, while an inhibition of retinoic acid action by transforming growth factor-beta was associated with a marked increase in U1 70K mRNA levels. Tretinoin 148-161 tumor necrosis factor Homo sapiens 0-27 10815802-0 2000 All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-kappaB, activated protein-1 and apoptosis in human lung cancer cells. Tretinoin 0-23 tumor necrosis factor Homo sapiens 36-39 10815802-0 2000 All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-kappaB, activated protein-1 and apoptosis in human lung cancer cells. Tretinoin 0-23 tumor necrosis factor Homo sapiens 66-69 10815802-2 2000 In this study, we investigated the effect of all-trans-retinoic acid (ATRA) on the cell surface expression of TNF receptors and receptor-mediated signaling in various human lung cancer cell lines. Tretinoin 45-68 tumor necrosis factor Homo sapiens 110-113 10815802-2 2000 In this study, we investigated the effect of all-trans-retinoic acid (ATRA) on the cell surface expression of TNF receptors and receptor-mediated signaling in various human lung cancer cell lines. Tretinoin 70-74 tumor necrosis factor Homo sapiens 110-113 10815802-3 2000 ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner. Tretinoin 0-4 tumor necrosis factor Homo sapiens 134-137 10815802-3 2000 ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner. Tretinoin 0-4 tumor necrosis factor Homo sapiens 203-206 10815802-9 2000 Treatment of these cells with as little as 0.5 microM ATRA was effective in converting TNF-resistant cells to TNF-sensitive. Tretinoin 54-58 tumor necrosis factor Homo sapiens 87-90 10815802-9 2000 Treatment of these cells with as little as 0.5 microM ATRA was effective in converting TNF-resistant cells to TNF-sensitive. Tretinoin 54-58 tumor necrosis factor Homo sapiens 110-113 10815802-10 2000 Overall our results indicate that ATRA induces the TNF receptors in human lung cancer cells, which sensitizes them to TNF-induced signaling leading to activation of NF-kappaB, AP-1 and apoptosis. Tretinoin 34-38 tumor necrosis factor Homo sapiens 51-54 10815802-10 2000 Overall our results indicate that ATRA induces the TNF receptors in human lung cancer cells, which sensitizes them to TNF-induced signaling leading to activation of NF-kappaB, AP-1 and apoptosis. Tretinoin 34-38 tumor necrosis factor Homo sapiens 118-121 10414449-5 1999 Our results have shown that ATRA induces an increased expression of IL-8, IL-1beta, TNF-alpha and ICAM-1 in APL cells, which can be amplified by the addition of G-CSF. Tretinoin 28-32 tumor necrosis factor Homo sapiens 84-93 10502453-7 1999 Retinoic acid with TNFalpha and IFN-gamma had a marked inhibitory effect (P<0.05) which was similarly reversed by increasing concentrations of IGFBP-3 antibody. Tretinoin 0-13 tumor necrosis factor Homo sapiens 19-27 10082656-7 1999 RA potentiated the TNF-alpha-induced ICAM-1 response in all Ca2+-concentrations. Tretinoin 0-2 tumor necrosis factor Homo sapiens 19-28 10082656-9 1999 In summary, our results establish retinoic acid as an enhancer of TNF-alpha-induced ICAM-1 levels in NHK. Tretinoin 34-47 tumor necrosis factor Homo sapiens 66-75 16465284-9 1997 Treatment with IFN-gamma+TNF induced GI-LI-N cells to show only a late and remarkable increase of alpha1/beta1 heterodimer; on the contrary, RA treatment caused a decrease in all integrin chains. Tretinoin 141-143 tumor necrosis factor Homo sapiens 25-28 9599015-3 1998 Retinoic acid exerted synergistic effects on AM secretion from THP-1 and HL-60 cells when administered with tumor necrosis factor-alpha, lipopolysaccharide or 12-O-tetradecanoyl phorbol-13-acetate. Tretinoin 0-13 tumor necrosis factor Homo sapiens 108-135 9022083-3 1997 To determine modes of retinoid action in the modulation of inflammatory responses, we explored effects of all-trans-retinoic acid (t-RA) on the TNFalpha-induced expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin in cultured human dermal microvascular endothelial cells. Tretinoin 109-129 tumor necrosis factor Homo sapiens 144-152 9040946-4 1997 The maximal induction of MMP-13 mRNAs by TNF-alpha was noted after a 6-h incubation, whereas with TGF-beta, the maximal stimulation was observed after 24 h. The up-regulation of MMP-13 mRNA abundance by TNF-alpha and TGF-beta was dependent on protein synthesis and was prevented partially by dexamethasone and retinoic acid. Tretinoin 310-323 tumor necrosis factor Homo sapiens 203-212 9022083-4 1997 Pretreatment with t-RA specifically prevented TNFalpha-induced VCAM-1 expression, but not ICAM-1 and E-selectin induction. Tretinoin 18-22 tumor necrosis factor Homo sapiens 46-54 8900181-6 1996 Electrophoretic mobility shift assays with nuclear extracts of A3 cells showed that stimulation with ATRA and TNF-alpha for more than 16 h resulted in enhanced NF-kappaB binding compared to that induced by TNF-alpha alone. Tretinoin 101-105 tumor necrosis factor Homo sapiens 206-215 9022083-7 1997 In transcriptional activation studies, the TNFalpha-mediated activation of the human VCAM-1 promoter was inhibited after t-RA treatment, while the ICAM-1 promoter activation was unaffected, indicating that the selective inhibition of CAM expression is regulated in part at the level of gene transcription. Tretinoin 121-125 tumor necrosis factor Homo sapiens 43-51 8900181-7 1996 The simultaneous treatment with ATRA and TNF-alpha also resulted in changes in the composition of NF-kappaB complexes bound to the IL-8 NF-kappaB site, preventing the formation of two TNF-alpha-inducible binding activities. Tretinoin 32-36 tumor necrosis factor Homo sapiens 184-193 8702454-5 1996 Serum levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF alpha), and IL-1 beta normalized within 7 days after the first administration of tretinoin, transiently increased at the time of radiotherapy, increased again after withdrawal of the tretinoin, and decreased again after its reintroduction. Tretinoin 152-161 tumor necrosis factor Homo sapiens 38-65 8702454-7 1996 This study documents in vivo the ability of all-trans-retinoic acid to down-regulate the release of IL-6, IL-1 beta, and TNF alpha, and illustrates its potential as a therapeutic agent in conditions associated with chronic overproduction of proinflammatory cytokines. Tretinoin 44-67 tumor necrosis factor Homo sapiens 121-130 8702454-5 1996 Serum levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF alpha), and IL-1 beta normalized within 7 days after the first administration of tretinoin, transiently increased at the time of radiotherapy, increased again after withdrawal of the tretinoin, and decreased again after its reintroduction. Tretinoin 152-161 tumor necrosis factor Homo sapiens 67-76 8752654-5 1996 As a consequence, RA derivatives also reduced the production of tumor necrosis factor alpha by these cells by 70%. Tretinoin 18-20 tumor necrosis factor Homo sapiens 64-91 8752654-8 1996 Therefore, RA derivatives downregulate tumor necrosis factor-alpha release and the NO-transduction pathway through the inhibition of inducible NO synthase transcription. Tretinoin 11-13 tumor necrosis factor Homo sapiens 39-66 7818524-6 1995 We present evidence that both the cis- and trans- forms of RA and to a lesser extent, the RA precursor beta-carotene, can inhibit recombinant human TNF cytolytic activity in mouse L-929 cells. Tretinoin 59-61 tumor necrosis factor Homo sapiens 148-151 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 tumor necrosis factor Homo sapiens 252-279 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 25-38 tumor necrosis factor Homo sapiens 281-290 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 tumor necrosis factor Homo sapiens 252-279 21552804-2 1995 We report that all-trans retinoic acid (tRA) synergizes with LPS to enhance the production of granulocyte colony-stimulating factor (G-CSF) in PMA-treated cells, whereas the production of granulocyte-macrophage CSF, interleukin 1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha) is minimally affected by tRA. Tretinoin 40-43 tumor necrosis factor Homo sapiens 281-290 7780141-1 1995 Because retinoids are known to modulate the growth and differentiation effects of tumor necrosis factor (TNF), we investigated the effect of all-trans-retinoic acid (RA) on the cell surface expression of TNF receptors in human histiocytic lymphoma U-937 cells. Tretinoin 141-164 tumor necrosis factor Homo sapiens 204-207 7780141-1 1995 Because retinoids are known to modulate the growth and differentiation effects of tumor necrosis factor (TNF), we investigated the effect of all-trans-retinoic acid (RA) on the cell surface expression of TNF receptors in human histiocytic lymphoma U-937 cells. Tretinoin 166-168 tumor necrosis factor Homo sapiens 204-207 7780141-2 1995 RA decreased the specific binding of 125I-labeled TNF to these cells in a dose- and time-dependent manner. Tretinoin 0-2 tumor necrosis factor Homo sapiens 50-53 7780141-8 1995 RA treatment also decreased TNF receptors on acute monocytic leukemia cell line THP-1. Tretinoin 0-2 tumor necrosis factor Homo sapiens 28-31 7780141-11 1995 The downregulation of TNF receptors by RA correlated with the downmodulation of the antiproliferative effects of TNF against U-937 cells. Tretinoin 39-41 tumor necrosis factor Homo sapiens 22-25 7780141-11 1995 The downregulation of TNF receptors by RA correlated with the downmodulation of the antiproliferative effects of TNF against U-937 cells. Tretinoin 39-41 tumor necrosis factor Homo sapiens 113-116 7780141-12 1995 Overall, our results indicate that RA downmodulates both the p60 and p80 form of the TNF receptor on cells of myeloid origin, which correlates with the cellular response. Tretinoin 35-37 tumor necrosis factor Homo sapiens 85-88 7739519-2 1995 We report here on the effects of exogenous TNF-alpha on SK-N-MC human neuroblastoma cells differentiated to a neuronal phenotype with retinoic acid, TNF-alpha caused a dose-dependent loss of viability and a corresponding increase in apoptosis in differentiated SK-N-MC cells but not in undifferentiated cultures. Tretinoin 134-147 tumor necrosis factor Homo sapiens 43-52 7739519-2 1995 We report here on the effects of exogenous TNF-alpha on SK-N-MC human neuroblastoma cells differentiated to a neuronal phenotype with retinoic acid, TNF-alpha caused a dose-dependent loss of viability and a corresponding increase in apoptosis in differentiated SK-N-MC cells but not in undifferentiated cultures. Tretinoin 134-147 tumor necrosis factor Homo sapiens 149-158 7818524-6 1995 We present evidence that both the cis- and trans- forms of RA and to a lesser extent, the RA precursor beta-carotene, can inhibit recombinant human TNF cytolytic activity in mouse L-929 cells. Tretinoin 90-92 tumor necrosis factor Homo sapiens 148-151 8269032-0 1993 Involvement of transforming growth factor-alpha and its receptor in the growth response of cultured human epidermal cells to retinoic acid. Tretinoin 125-138 tumor necrosis factor Homo sapiens 15-47 8025957-0 1994 Upregulation of tumor necrosis factor-alpha production by retrovirally transduced human tumor-infiltrating lymphocytes using trans-retinoic acid. Tretinoin 125-144 tumor necrosis factor Homo sapiens 16-43 8025957-1 1994 The ability of retinoic acid (RA) to upregulate gene expression in human tumor-infiltrating lymphocytes (TIL) transduced with a Moloney murine leukemia virus containing the cDNA encoding tumor necrosis factor (TNF) has been studied. Tretinoin 15-28 tumor necrosis factor Homo sapiens 210-213 7943653-8 1994 RA also induced a moderate increase in M theta tumor necrosis factor-alpha (TNF alpha) production, which was down-regulated by ethanol both at the level of secreted and cell-associated TNF alpha. Tretinoin 0-2 tumor necrosis factor Homo sapiens 76-85 7943653-8 1994 RA also induced a moderate increase in M theta tumor necrosis factor-alpha (TNF alpha) production, which was down-regulated by ethanol both at the level of secreted and cell-associated TNF alpha. Tretinoin 0-2 tumor necrosis factor Homo sapiens 185-194 7521152-7 1994 In the presence of ATRA, GM-CSF potentiated production and secretion of tumor necrosis factor-alpha (TNF) in response to lipopolysaccharide, as well as interferon-gamma which is a potent inducer of monocytic differentiation in APL cells. Tretinoin 19-23 tumor necrosis factor Homo sapiens 72-99 7521152-7 1994 In the presence of ATRA, GM-CSF potentiated production and secretion of tumor necrosis factor-alpha (TNF) in response to lipopolysaccharide, as well as interferon-gamma which is a potent inducer of monocytic differentiation in APL cells. Tretinoin 19-23 tumor necrosis factor Homo sapiens 101-104 7521152-8 1994 On the other hand, production of TNF in ATRA-treated cells was not affected by G-CSF which significantly enhanced granulocytic differentiation. Tretinoin 40-44 tumor necrosis factor Homo sapiens 33-36 1316917-1 1992 Expression of the two known receptors for TNF was studied in the promyelocytic leukemia cell line HL-60 before and after differentiation of the cells along the granulocyte lineage (induced by incubation with retinoic acid), or along the macrophage lineage (induced by incubation with the phorbol diester, PMA). Tretinoin 208-221 tumor necrosis factor Homo sapiens 42-45 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 tumor necrosis factor Homo sapiens 84-116 8445950-6 1993 The results also demonstrate that ATRA-induced c-fms expression is potentiated by exposure to tumor necrosis factor alpha (TNF alpha) or dibutyryl cyclic adenosine monophosphate (cAMP). Tretinoin 34-38 tumor necrosis factor Homo sapiens 94-121 8445950-6 1993 The results also demonstrate that ATRA-induced c-fms expression is potentiated by exposure to tumor necrosis factor alpha (TNF alpha) or dibutyryl cyclic adenosine monophosphate (cAMP). Tretinoin 34-38 tumor necrosis factor Homo sapiens 123-132 1330076-3 1992 The approximate 50% downregulation of TM antigen and cofactor activity induced by TNF-alpha (10 U/mL for 24 hours) was completely prevented when the cells were coincubated with both TNF-alpha and 10 mumol/L RA. Tretinoin 207-209 tumor necrosis factor Homo sapiens 82-91 1330076-4 1992 In accordance with changes in cell surface TM antigen levels, the 70% decrease in TM messenger RNA (mRNA) induced by TNF-alpha was also prevented by 10 mumol/L RA. Tretinoin 160-162 tumor necrosis factor Homo sapiens 117-126 1330076-7 1992 The effects of RA on the regulation of TM and TF expression in the cells exposed to TNF-alpha was dose-dependent from 0.01 to 10 mumol/L RA. Tretinoin 15-17 tumor necrosis factor Homo sapiens 84-93 1330076-7 1992 The effects of RA on the regulation of TM and TF expression in the cells exposed to TNF-alpha was dose-dependent from 0.01 to 10 mumol/L RA. Tretinoin 137-139 tumor necrosis factor Homo sapiens 84-93 1330076-8 1992 The present results suggest that RA may affect on the mRNA level to alter TM and TF expression, effectively counteracting expression of prothrombotic properties of endothelial cells induced by inflammatory cytokines such as TNF-alpha. Tretinoin 33-35 tumor necrosis factor Homo sapiens 224-233 1717193-5 1991 ATRA inhibited both IL-1 beta- and TNF alpha-induced secretion of prostaglandin-E2 (PGE2), a potent feedback inhibitor of cytokine-stimulated HSN proliferation. Tretinoin 0-4 tumor necrosis factor Homo sapiens 35-44 2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 14-27 tumor necrosis factor Homo sapiens 69-90 2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 14-27 tumor necrosis factor Homo sapiens 92-95 2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 29-31 tumor necrosis factor Homo sapiens 69-90 2230595-1 1990 The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. Tretinoin 29-31 tumor necrosis factor Homo sapiens 92-95 2230595-5 1990 Addition of RA (0.5 microM) to DLS restored LPS-induced TNF release by HPBM, and supplementation with ROH (1.0 microM) resulted in release of TNF-like activity, but only after 3 days of in vitro culture. Tretinoin 12-14 tumor necrosis factor Homo sapiens 56-59 2230595-6 1990 The maintenance of TNF release by the addition of exogenous RA after 3 days of in vitro culture suggested that depletion of endogenous RA was partially responsible for loss of TNF-like activity. Tretinoin 60-62 tumor necrosis factor Homo sapiens 19-22 2230595-6 1990 The maintenance of TNF release by the addition of exogenous RA after 3 days of in vitro culture suggested that depletion of endogenous RA was partially responsible for loss of TNF-like activity. Tretinoin 135-137 tumor necrosis factor Homo sapiens 19-22 2199088-2 1990 The strongest differentiation inducing activity on promyelocytic HL60 cells and histiocytic U937 cells was obtained by combining recombinant tumor necrosis factor (rTNF), interferon-gamma (IFN-gamma), retinoic acid (RA), and 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3). Tretinoin 216-218 tumor necrosis factor Homo sapiens 141-162 2613750-0 1989 Modulation of transforming growth factor alpha-dependent expression of epidermal growth factor receptor gene by transforming growth factor beta, triiodothyronine, and retinoic acid. Tretinoin 167-180 tumor necrosis factor Homo sapiens 14-46 35173714-6 2022 However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1beta, IL-6, IL-8 and TNF-alpha. Tretinoin 9-13 tumor necrosis factor Homo sapiens 152-161 2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 89-102 tumor necrosis factor Homo sapiens 173-182 2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 89-102 tumor necrosis factor Homo sapiens 275-284 2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 200-213 tumor necrosis factor Homo sapiens 173-182 2742744-4 1989 Messenger RNA for ALP was clearly demonstrated when the cells were treated with 1 microM retinoic acid for 24 h. Recombinant human tumour necrosis factor-alpha (recombinant TNF-alpha) interacted with retinoic acid to potentiate the rise in ALP activity, although recombinant TNF-alpha alone had no effect. Tretinoin 200-213 tumor necrosis factor Homo sapiens 275-284 2742744-6 1989 By observing the rate of decay of mRNA for actin and ALP, we were able to demonstrate that the interaction between retinoic acid and recombinant TNF-alpha modulated the steady state of ALP mRNA. Tretinoin 115-128 tumor necrosis factor Homo sapiens 145-154 3103717-1 1987 In this study, we analyzed the effect of tumor necrosis factor (TNF) on retinoic acid (RA)-induced myeloid differentiation of the promyelocytic HL-60 leukemia cell line. Tretinoin 72-85 tumor necrosis factor Homo sapiens 41-62 2823943-3 1987 With the promyelocytic HL-60 cells, TNF alpha (greater than or equal to 2.5 U/mL) in combination with RA synergistically inhibited clonal growth; TNF alpha at lower concentrations (less than or equal to 1 U/mL) plus RA (10(-9) mol/L) were antagonistic in their inhibition of growth. Tretinoin 216-218 tumor necrosis factor Homo sapiens 36-45 2823943-5 1987 In addition, RA (10(-9) to 10(-7) mol/L) increased the number of TNF alpha receptors on HL-60 cells 1.3- to 1.7-fold without changing the affinity for the TNF alpha receptor. Tretinoin 13-15 tumor necrosis factor Homo sapiens 65-74 2823943-6 1987 With the more immature KG-1 myeloblasts, concentrations of TNF alpha greater than 10 U/mL synergistically interacted with RA to inhibit clonal growth; at lower concentrations of TNF alpha (less than 10 U/mL), RA appeared to inhibit the expected effect of TNF alpha. Tretinoin 122-124 tumor necrosis factor Homo sapiens 59-68 2823943-6 1987 With the more immature KG-1 myeloblasts, concentrations of TNF alpha greater than 10 U/mL synergistically interacted with RA to inhibit clonal growth; at lower concentrations of TNF alpha (less than 10 U/mL), RA appeared to inhibit the expected effect of TNF alpha. Tretinoin 209-211 tumor necrosis factor Homo sapiens 59-68 3103717-1 1987 In this study, we analyzed the effect of tumor necrosis factor (TNF) on retinoic acid (RA)-induced myeloid differentiation of the promyelocytic HL-60 leukemia cell line. Tretinoin 72-85 tumor necrosis factor Homo sapiens 64-67 33301441-0 2020 Retinoic acid improves baseline barrier function and attenuates TNF-alpha-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o. Tretinoin 0-13 tumor necrosis factor Homo sapiens 64-73 6607753-6 1984 An activity, co-chromatographing with DIF, acts synergistically with retinoic acid to induce maturation not only of HL-60, but also of the monoblast-like cell line U-937 (measured as percentage of cells reducing NBT). Tretinoin 69-82 tumor necrosis factor Homo sapiens 38-41 33301441-5 2020 RA was also effective in alleviating TNF-alpha-induced 16HBE barrier leak, attenuating 60% of the TNF-alpha-induced leak to 14C-mannitol and 80% of the leak to 14C-inulin. Tretinoin 0-2 tumor necrosis factor Homo sapiens 37-46 33301441-2 2020 This paper thus sought to determine whether RA could improve baseline barrier function and attenuate TNF-alpha-induced barrier leak in the human bronchial epithelial cell culture model, 16HBE14o- (16HBE). Tretinoin 44-46 tumor necrosis factor Homo sapiens 101-110 33301441-5 2020 RA was also effective in alleviating TNF-alpha-induced 16HBE barrier leak, attenuating 60% of the TNF-alpha-induced leak to 14C-mannitol and 80% of the leak to 14C-inulin. Tretinoin 0-2 tumor necrosis factor Homo sapiens 98-107 33301441-8 2020 The presence of RA partially reversed TNF-alpha"s effects on these select TJ proteins. Tretinoin 16-18 tumor necrosis factor Homo sapiens 38-47 33301441-9 2020 Lastly, RA completely abrogated the TNF-alpha-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. Tretinoin 8-10 tumor necrosis factor Homo sapiens 36-45 33301441-9 2020 Lastly, RA completely abrogated the TNF-alpha-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. Tretinoin 8-10 tumor necrosis factor Homo sapiens 36-39 31801802-11 2020 In conclusion, these results have demonstrated the therapeutic potential of retinoic acid on RA FLS provided TNF could be counterbalanced, either with high ATRA doses or with TNF inhibitors. Tretinoin 76-89 tumor necrosis factor Homo sapiens 109-112 32168763-5 2020 The amount of secreted TNF-alpha in the supernatant of NB4 TG2 knockout cells was close to 50 times lower than in ATRA-treated differentiated wild-type NB4 cells. Tretinoin 114-118 tumor necrosis factor Homo sapiens 23-32 32168763-6 2020 The irreversible inhibitor of TG2 NC9 not only decreased reactive oxygen species production 28-fold, but decreased the concentration of MCP-1, IL-1beta and TNF-alpha 8-, 15- and 61-fold, respectively in the combined ATRA + ATO-treated wild-type NB4 cell culture. Tretinoin 216-220 tumor necrosis factor Homo sapiens 156-165 32361568-9 2020 DMSO-HL and ATRA-HL cells both produced TNF-alpha and IL-8 after lipopolysaccharide (LPS) or PM treatment, whereas non-differentiated HL-60 cells did not. Tretinoin 12-16 tumor necrosis factor Homo sapiens 40-49 32448273-9 2020 In vivo studies suggested the topical application of TRA and BT dual-loaded liposomal gel had the best ability to reduce the thickness of epidermal and the level of cytokines (TNF-alpha and IL-6), largely alleviating the symptoms of psoriasis. Tretinoin 53-56 tumor necrosis factor Homo sapiens 176-185 31801802-11 2020 In conclusion, these results have demonstrated the therapeutic potential of retinoic acid on RA FLS provided TNF could be counterbalanced, either with high ATRA doses or with TNF inhibitors. Tretinoin 76-89 tumor necrosis factor Homo sapiens 175-178 32863302-9 2020 In short, ATRA inhibited TNF-alpha induced synovitis by the regulation of inflammatory cytokines and inhibiting NF-kappaB signal transduction and potentially promoting autophagy, apoptosis and angiogenesis, displaying its role in alleviating synovial inflammation in patients with RA. Tretinoin 10-14 tumor necrosis factor Homo sapiens 25-34 31950055-4 2019 Similarly, ATRA enhanced the expression and production of TNF-alpha and IL-1beta in THP-1 cells upon flagellin challenge. Tretinoin 11-15 tumor necrosis factor Homo sapiens 58-67 30986261-13 2019 In addition, ATRA treatment decreased the levels of IL4, IL6 and TNFalpha in A549 cells, whereas it increased IL4 and TNFalpha levels in PTGDR-transfected cells. Tretinoin 13-17 tumor necrosis factor Homo sapiens 65-73 31950055-8 2019 Anti-CD14 antibody treatment prior to ATRA and flagellin treatments completely abolished ATRA-enhanced TNF-alpha and IL-1beta production. Tretinoin 89-93 tumor necrosis factor Homo sapiens 103-112 31263060-3 2019 TNF-alpha treatment has been investigated as part of a combined therapy for acute myeloid leukemia due to its modifying effects on all-trans retinoic acid (ATRA) mediated differentiation into granulocytes. Tretinoin 141-154 tumor necrosis factor Homo sapiens 0-9 31263060-3 2019 TNF-alpha treatment has been investigated as part of a combined therapy for acute myeloid leukemia due to its modifying effects on all-trans retinoic acid (ATRA) mediated differentiation into granulocytes. Tretinoin 156-160 tumor necrosis factor Homo sapiens 0-9 30986261-13 2019 In addition, ATRA treatment decreased the levels of IL4, IL6 and TNFalpha in A549 cells, whereas it increased IL4 and TNFalpha levels in PTGDR-transfected cells. Tretinoin 13-17 tumor necrosis factor Homo sapiens 118-126 30059166-8 2018 ATRA inhibited physiologically induced (RANKL) osteoclast formation of human peripheral blood monocytes and mouse BMM as well as human monocytes stimulated with the pro-inflammatory compounds, TNF-alpha and LPS. Tretinoin 0-4 tumor necrosis factor Homo sapiens 193-202 30237268-7 2019 This study demonstrates that transglutaminase 2 expression induced by all-trans retinoic acid treatment reprograms inflammatory signaling networks governed by nuclear factor kappa-light-chain-enhancer of activated B-cell activation, resulting in overexpression of TNF-alpha and IL-1beta in differentiating APL cells, suggesting that atypically expressed transglutaminase 2 is a promising target for leukemia treatment. Tretinoin 80-93 tumor necrosis factor Homo sapiens 264-273 28408791-0 2017 All-Trans Retinoic Acid Modulates TLR4/NF-kappaB Signaling Pathway Targeting TNF-alpha and Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer. Tretinoin 10-23 tumor necrosis factor Homo sapiens 77-86 29055789-5 2017 The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-alpha) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. Tretinoin 106-108 tumor necrosis factor Homo sapiens 133-160 29055789-5 2017 The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-alpha) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. Tretinoin 106-108 tumor necrosis factor Homo sapiens 162-171 29055789-7 2017 Importantly, addition of rTM to this co-culture system inhibited the RA-induced phosphorylation of p38 and VE-cadherin and decreased ICAM1 and vascular permeability in EA.hy926 cells, without a decrease inthe levels of TNF-alpha. Tretinoin 69-71 tumor necrosis factor Homo sapiens 219-228 28404891-3 2017 HMGB1 and the pro-inflammatory cytokines IL-1beta and TNF-alpha were gradually released from NB4 and HL-60 cells treated with ATRA and/or ATO. Tretinoin 126-130 tumor necrosis factor Homo sapiens 54-63 28408791-9 2017 Collectively, our study indicates that AtRA modulates in situ LPS/TLR4/NF-kappaB signaling pathway targeting NOS2 and TNF-alpha expression. Tretinoin 39-43 tumor necrosis factor Homo sapiens 118-127 26256243-6 2015 ATRA could reverse the inhibition expression of ADAMTS13 by TNF-alpha. Tretinoin 0-4 tumor necrosis factor Homo sapiens 60-69 26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 140-159 tumor necrosis factor Homo sapiens 34-61 26617752-13 2015 ATRA decreased anti-oxygen protein Nrf2 and HO-1, and increases inflammatory factors NF-kappaB and TNF-alpha. Tretinoin 0-4 tumor necrosis factor Homo sapiens 99-108 26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 140-159 tumor necrosis factor Homo sapiens 63-72 26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 161-165 tumor necrosis factor Homo sapiens 34-61 26146052-1 2015 OBJECTIVE: To study the effect of tumor necrosis factor alpha (TNF-alpha) on apoptosis of human promyelocytic leukemia cells induced by all-trans retinoic acid (ATRA). Tretinoin 161-165 tumor necrosis factor Homo sapiens 63-72 26146052-6 2015 CONCLUSION: TNF-alpha may have potential for strengthening the differentiation and apoptosis of acute promyelocytic leukemia cells induced by ATRA. Tretinoin 142-146 tumor necrosis factor Homo sapiens 12-21 25725371-4 2015 Here, we demonstrate that human skin MCs display substantial susceptibility to RA by which they are instructed to increase pro-inflammatory mediators (IL-1beta, IL-8, TNF-alpha) but not histamine release. Tretinoin 79-81 tumor necrosis factor Homo sapiens 167-176 23834309-5 2014 The in vitro effect of ATRA on lipopolysaccharide (LPS)-induced TNF-alpha production by human peripheral blood mononuclear cells (PBMC) was assessed by ELISA and RT-PCR. Tretinoin 23-27 tumor necrosis factor Homo sapiens 64-73 25403801-7 2015 In addition, the high levels of tumor necrosis factor-alpha, interleukin-1beta, and receptor activator of nuclear factor-kappa B ligand (RANKL) expression induced by LPS were inhibited after treatment with atRA. Tretinoin 206-210 tumor necrosis factor Homo sapiens 32-59 26124839-8 2015 ATRA-pretreated MSCs significantly decreased not only the vital pathogenic cytokine in AS, tumor necrosis factor-alpha (TNF-alpha), but also AS-boosting factors interleukin-17 (IL-17A) and interferon-gamma (IFN-gamma). Tretinoin 0-4 tumor necrosis factor Homo sapiens 91-118 26124839-8 2015 ATRA-pretreated MSCs significantly decreased not only the vital pathogenic cytokine in AS, tumor necrosis factor-alpha (TNF-alpha), but also AS-boosting factors interleukin-17 (IL-17A) and interferon-gamma (IFN-gamma). Tretinoin 0-4 tumor necrosis factor Homo sapiens 120-129 23834309-9 2014 In vitro, ATRA pretreatment decreased the overproduction of TNF-alpha by LPS-stimulated PBMC of ALD patients. Tretinoin 10-14 tumor necrosis factor Homo sapiens 60-69 23861398-0 2013 beta-Transducin repeat-containing protein 1 (beta-TrCP1)-mediated silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) protein degradation promotes tumor necrosis factor alpha (TNFalpha)-induced inflammatory gene expression. Tretinoin 88-101 tumor necrosis factor Homo sapiens 167-194 23861398-0 2013 beta-Transducin repeat-containing protein 1 (beta-TrCP1)-mediated silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) protein degradation promotes tumor necrosis factor alpha (TNFalpha)-induced inflammatory gene expression. Tretinoin 88-101 tumor necrosis factor Homo sapiens 196-204 21237205-4 2011 Furthermore, when stimulated with flagellin, ATRA-induced THP-1 cells expressed multiple cytokines, including TNF-alpha, IL-1beta, and IL-12p40, and several co-stimulatory molecules, such as CD40, CD80, CD86, and MHC class I and II. Tretinoin 45-49 tumor necrosis factor Homo sapiens 110-119 22666666-8 2009 Conditioned media from SCF, NGF or RA-treated HMC-1 cells, and SCF, NGF, DMSO or RA-treated THP-1 cells enhanced immune complex transport via enhancing the expression of the CD23 in HT29 cells and the release of inflammatory mediator TNF-alpha. Tretinoin 81-83 tumor necrosis factor Homo sapiens 234-243