PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27357360-7 2016 After RA treatment, NLRR2 expression was increased and correlated with the upregulation of c-Jun, a member of the activator protein-1 (AP-1) family in NB cells. Tretinoin 6-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 27357360-7 2016 After RA treatment, NLRR2 expression was increased and correlated with the upregulation of c-Jun, a member of the activator protein-1 (AP-1) family in NB cells. Tretinoin 6-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-133 27357360-7 2016 After RA treatment, NLRR2 expression was increased and correlated with the upregulation of c-Jun, a member of the activator protein-1 (AP-1) family in NB cells. Tretinoin 6-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 135-139 22110742-10 2011 Mechanistically, RA sensitization by MLN4924 was mediated via enhanced apoptosis, likely through accumulation of pro-apoptotic proteins NOXA and c-JUN, two well-known substrates of SAG-SCF E3 ligase. Tretinoin 17-19 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-150 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 179-184 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 222-227 18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-85 19299558-2 2009 Here, we report that, while the nuclear receptor corepressor (NCoR) and silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) corepressors establish repression checkpoints on broad sets of inflammatory response genes in macrophages and are required for nearly all of the transrepression activities of liver X receptors (LXRs), they can be selectively recruited via c-Jun or the Ets repressor Tel, respectively, establishing NCoR-specific, SMRT-specific, and NCoR/SMRT-dependent promoters. Tretinoin 94-107 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 383-388 18443043-1 2008 Retinoic acid (RA) inhibits matrix metalloproteinase 9 (MMP-9) expression due to AP-1 inhibition resulting from retinoic acid receptors (RARs) competing for limiting amounts of coactivator proteins. Tretinoin 15-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-85 15218018-2 2004 We have previously reported that the activation of c-Jun amino-terminal kinase (JNK) is required for the retinoic acid-induced neural differentiation of P19 cells. Tretinoin 105-118 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-56 16959971-5 2006 Furthermore, the expression of COX-2, Cx-43, CRABPI, the transcription factor c-Jun and the retinoic acid receptor RARbeta altered in response to different concentrations of ATRA, suggesting that the differential expression of cellular retinoid-binding proteins may lead to different levels of retinoic acid being delivered to its nuclear targets, leading to the differential expression of specific target genes within the myometrium during pregnancy. Tretinoin 174-178 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-83 16052510-5 2005 The decrease in N-terminal phosphorylation of c-Jun does not appear to be modulated by JNK or ERK, since their protein expression patterns and kinase activity do not correlate with the repression of AP-1 activity following treatment with atRA. Tretinoin 238-242 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-51 15219855-4 2004 In this study, we report that Sp1, Sp3, and c-Jun increase transactivation of the L-RARE during RA treatment. Tretinoin 84-86 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-49 15219855-9 2004 Our data suggest that Sp1, Sp3, and c-Jun play an important role in gene expression through the L-RARE during RA treatment. Tretinoin 98-100 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41 12052888-1 2002 Up-regulation of the c-jun gene is a critical event in the retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 59-72 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 14581379-10 2003 All-trans-retinoic acid, a prototypic AP-1 antagonist, blocked bryostatin-mediated induction of COX-2. Tretinoin 0-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-42 12186877-2 2002 All-trans-retinoic acid (t-RA) inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis by inhibiting the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway. Tretinoin 0-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-154 12186877-2 2002 All-trans-retinoic acid (t-RA) inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis by inhibiting the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway. Tretinoin 25-29 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-154 12052888-1 2002 Up-regulation of the c-jun gene is a critical event in the retinoic acid (RA)-mediated differentiation of embryonal carcinoma F9 cells. Tretinoin 74-76 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 11980644-6 2002 Treatment with RA stimulated an interaction between RA receptor-alpha and CBP/p300; a corresponding decrease in the interaction between CBP/p300 and c-Jun was observed. Tretinoin 15-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 149-154 12052888-4 2002 Moreover, chromatin immunoprecipitation assays showed that the JDP2/HDAC3 complex, which binds to the differentiation response element within the c-jun promoter in undifferentiated F9 cells, was replaced by the p300 complex in response to RA, with an accompanying change in the histone acetylation status of the chromatin, the initiation of transcription of the c-jun gene, and the subsequent differentiation of F9 cells. Tretinoin 239-241 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-151 11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 15-28 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 164-183 12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-18 11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 15-28 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 185-189 11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 30-32 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 164-183 11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tretinoin 30-32 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 185-189 12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-189 12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-189 12183893-10 2002 Mutagenesis in AP1 sites belonging to the HPV promoter region (LCR) completely abolished the HPV promoter activity in different cell lines; these results and biochemistry assays on this AP1 transcription factor, that includes protein-protein interactions between AP1 and another factors as E7 from HPV, and YY-1; the post-translattional modification and, the retinoic acid interaction; suggest a role for this AP1 factor in tissue-specific transcription of the human papillomavirus. Tretinoin 359-372 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-189 12053118-6 2002 RA dramatically inhibits this process via suppression of c-fos/c-jun expression and inhibition of the c-Jun N-terminal kinase activation. Tretinoin 0-2 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 63-68 12053118-6 2002 RA dramatically inhibits this process via suppression of c-fos/c-jun expression and inhibition of the c-Jun N-terminal kinase activation. Tretinoin 0-2 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 102-107 12386300-2 2002 In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1). Tretinoin 34-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 140-159 12386300-2 2002 In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1). Tretinoin 34-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 161-165 12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-115 12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 212-225 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 260-265 12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-115 12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 227-229 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 260-265 12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-115 12903123-2 2002 We show here that a repressor of AP-1, JDP2 (Jun dimerization protein 2), inhibits the transactivation of the c-jun gene by ATF-2 and p300, by recruitment of a histone deacetylase complex, thereby repressing the retinoic acid (RA)-induced transcription of the c-jun gene and inhibiting the RA-mediated differentiation of F9 cells. Tretinoin 290-292 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 260-265 10974019-0 2000 c-Jun-dependent inhibition of cutaneous procollagen transcription following ultraviolet irradiation is reversed by all-trans retinoic acid. Tretinoin 125-138 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 11776129-0 2000 Mechanism of inhibition on activator protein-1 activity by all-trans retinoic acid in gastric cancer cells. Tretinoin 69-82 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-46 11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-49 11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-55 11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 9-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-150 11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 69-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-49 11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 69-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-55 11776129-4 2000 RESULTS: ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). Tretinoin 69-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-150 11776129-5 2000 ATRA can also inhibit the expression of cJun and cFos. Tretinoin 0-4 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-44 11776129-6 2000 One of the mechanisms for ATRA to inhibit the growth of gastric cancer cells may be through its inhibitory effect on the AP-1 activity and its influence on up-regulation of RAR alpha expression. Tretinoin 26-30 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 121-125 11776129-8 2000 CONCLUSIONS: ATRA inhibits the growth of gastric cancer cells through the regulation of AP-1 activity. Tretinoin 13-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 88-92 11513861-2 2001 Concomitant with this RA-induced neural differentiation, we observed an activation of the c-Jun amino-terminal kinase (JNK). Tretinoin 22-24 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-95 10974019-6 2000 Pretreatment of human skin in vivo with all-trans retinoic acid inhibits UV induction of c-Jun and protects skin against loss of procollagen synthesis. Tretinoin 50-63 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 89-94 10508860-8 1999 PS1 suppressed c-jun-associated apoptosis by retinoic acid in F9 embryonic carcinoma cells, whereas this suppression of apoptosis is attenuated by mutation in PS1. Tretinoin 45-58 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-20 10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 177-181 10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 221-226 10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tretinoin 45-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 240-244 10866321-6 2000 However, RARbeta showed a strong RA-independent inhibition of AP-1 activity, whereas inhibition of AP-1 activity by RARalpha and RARgamma was RA dependent. Tretinoin 9-11 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 62-66 10475063-1 1999 We have characterized an element (differentiation response element, DRE) in the promoter region of the c-jun gene that is both necessary and sufficient for retinoic acid (RA) and adenovirus early region (E1A) mediated up-regulation of c-jun gene expression during the differentiation of F9 cells. Tretinoin 156-169 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108 10400643-12 1999 The anti-apoptotic action of t-RA was ascribed, at least in part, to dual suppression of the cell death pathway mediated by JNK and AP-1. Tretinoin 29-33 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-136 10475063-1 1999 We have characterized an element (differentiation response element, DRE) in the promoter region of the c-jun gene that is both necessary and sufficient for retinoic acid (RA) and adenovirus early region (E1A) mediated up-regulation of c-jun gene expression during the differentiation of F9 cells. Tretinoin 171-173 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108 9649304-4 1998 Point mutations that reduced transactivation by atRA also reduced atRA-induced transrepression of AP1 transcription, correlating ligand-induced activation and repression. Tretinoin 48-52 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-101 9973257-5 1999 Using a mammalian two-hybrid system, we report here that human RARalpha (hRARalpha) can disrupt in a RA-dependent manner the homo- and heterodimerization properties of c-Jun and c-Fos. Tretinoin 63-65 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 168-173 9973257-6 1999 This inhibition of dimerization is cell specific, occurring only in those cells that exhibit RA-induced repression of AP-1 transcriptional activity. Tretinoin 93-95 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-122 10780480-3 1999 In wild type F9 cells, induction of c-jun gene was observed at 18 h after treatment with RA. Tretinoin 89-91 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41 10780480-4 1999 Interestingly, RA-dependent expression of c-jun gene was not induced in cells expressing the p300-directed ribozyme. Tretinoin 15-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-47 9732061-10 1998 All-trans retinoic acid acts to inhibit induction of c-Jun protein by ultraviolet irradiation, thereby preventing increased matrix metalloproteinases and ensuing dermal damage. Tretinoin 10-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-58 9864179-6 1999 C-Jun amino-terminal kinase (JNK) was not tyrosine-phosphorylated by any cytokine despite the existence of JNK proteins in human neutrophils, whereas it was tyrosine-phosphorylated by TNF in undifferentiated and all-trans retinoic acid-differentiated HL-60 cells. Tretinoin 222-235 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 9649304-4 1998 Point mutations that reduced transactivation by atRA also reduced atRA-induced transrepression of AP1 transcription, correlating ligand-induced activation and repression. Tretinoin 66-70 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-101 9502786-0 1998 Retinoic acid inhibits induction of c-Jun protein by ultraviolet radiation that occurs subsequent to activation of mitogen-activated protein kinase pathways in human skin in vivo. Tretinoin 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41 7977784-8 1994 RA repressed serum-stimulated induction of the immediate early genes c-fos and c-jun, whose protein products dimerize to form AP-1. Tretinoin 0-2 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-84 9436983-0 1998 p300 and ATF-2 are components of the DRF complex, which regulates retinoic acid- and E1A-mediated transcription of the c-jun gene in F9 cells. Tretinoin 66-79 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 119-124 9377582-4 1997 The c-jun-transfected MCF7 cells had increased basal AP-1 transactivation activity and increased expression of AP-1-regulated genes but were resistant to the antiproliferative effects of atRA. Tretinoin 187-191 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 9377582-5 1997 However, MCF7 cells transfected with a deletion mutant of c-jun, TAM-67, which lacks most of the amino-terminal transactivation domain of cJun and is unable to activate AP-1-dependent gene expression, were sensitive to the growth-inhibitory effects of atRA. Tretinoin 252-256 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-63 9377582-9 1997 However, retinoic acid responsive element DNA binding activity was intact in c-jun-transfected cells. Tretinoin 9-22 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-82 8959344-10 1996 Stimulation of AP1 activity by phorbol ester was suppressed by retinoic acid, and cotransfection with a c-jun expression vector reversed the retinoic acid response. Tretinoin 63-76 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-18 8959344-10 1996 Stimulation of AP1 activity by phorbol ester was suppressed by retinoic acid, and cotransfection with a c-jun expression vector reversed the retinoic acid response. Tretinoin 141-154 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-18 8959344-10 1996 Stimulation of AP1 activity by phorbol ester was suppressed by retinoic acid, and cotransfection with a c-jun expression vector reversed the retinoic acid response. Tretinoin 141-154 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-109 8959344-11 1996 Based on these data, we suggest that suppression of involucrin promoter activity by retinoic acid may be mediated through interaction with the AP1 transcriptional complex. Tretinoin 84-97 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 143-146 7489817-0 1995 Differential regulation of AP1 activity by retinoic acid in hormone-dependent and -independent breast cancer cells. Tretinoin 43-56 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-30 7489817-5 1995 AP1 overexpression abrogated RA repression in MCF7 cells. Tretinoin 29-31 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-3 1590797-0 1992 Activin synergistically increased c-jun mRNA in P19 embryonal carcinoma cells in the presence of retinoic acid. Tretinoin 97-110 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 34-39 7521841-1 1994 Induction of differentiation of F9 teratocarcinoma stem cells by retinoic acid and cAMP has been shown to involve the activation of the transcription factor AP-1 (a heterodimer of the proto-oncogene products c-Fos and c-Jun); moreover, stable expression of either Fos or Jun drives F9 cells into differentiation. Tretinoin 65-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 157-161 7521841-1 1994 Induction of differentiation of F9 teratocarcinoma stem cells by retinoic acid and cAMP has been shown to involve the activation of the transcription factor AP-1 (a heterodimer of the proto-oncogene products c-Fos and c-Jun); moreover, stable expression of either Fos or Jun drives F9 cells into differentiation. Tretinoin 65-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 218-223 8163572-4 1994 We show that inhibition of expression of the cartilage phenotype by retinoic acid in epiphyseal chondrocytes is associated with positive regulation of AP-1 responsive metalloprotease genes, as well as induction of gene expression for the two components of the transcription factor AP-1, c-fos and c-jun. Tretinoin 68-81 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 297-302 8152301-8 1994 Treatment of KHOS cells with retinoic acid and dexamethasone, which are known to suppress c-fos/c-jun and AP-1, suppressed the production of the MPs. Tretinoin 29-42 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 96-101 8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 145-158 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 285-289 8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 175-177 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 285-289 8415704-1 1993 We report here that the fusion of PML, a nuclear protein defined by the t(15;17) chromosomal translocation in acute promyelocytic leukemia, with retinoic acid receptor alpha (RAR alpha) changes the RAR alpha from a retinoic acid (RA)-dependent inhibitor to a RA-dependent activator of AP-1 transcriptional activity. Tretinoin 198-200 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 285-289 8415704-6 1993 In view of the association between AP-1 activity and hemopoietic differentiation, we suggest that these properties of PML-RAR alpha could contribute to the leukemic phenotype and its response to RA. Tretinoin 122-124 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 35-39 8375477-6 1993 Although c-jun expression was induced with RA, rapid and predominant induction of junB expression was specifically observed with NaB, which is regulated by both transcriptional and post-transcriptional mechanisms. Tretinoin 43-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-14 7854354-4 1994 Using a RA-responsive element and reporter gene construct transfected into a T cell, we found: 1) T cell activation and PKC activators enhance transactivation by RA, 2) down-regulation of PKC protein has little effect on RA transactivation but abolishes superinduction by phorbol ester, which is restored by cotransfection of a PKC alpha-expression vector, and 3) cotransfection of dominant-negative c-jun does not prevent superinduction by phorbol ester. Tretinoin 8-10 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 400-405 1331926-1 1992 Retinoic acid inhibits the enzyme collagenase by forming an inactive complex between the liganded nuclear retinoic acid receptors and c-Jun, a protein that is itself an activator of the collagenase gene. Tretinoin 0-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 134-139 1590797-3 1992 Activin (lng/ml) was sufficient to induce the synergistic increase of c-jun mRNA in P19 EC cells with all-trans-retinoic acid. Tretinoin 102-125 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-75 1371335-5 1992 Release of the differentiation block in the ras-transformed 32DC13(G) cells by co-treatment with retinoic acid and G-CSF partially restored the normal c-fos and c-jun mRNA induction pattern, suggesting that the proper activation of these genes may be important for myeloid differentiation. Tretinoin 97-110 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 161-166 1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 36-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88 2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tretinoin 128-141 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-231 1648728-1 1991 We present evidence that retinoic acid can down-regulate transcriptional activation by the nuclear protooncogene c-jun. Tretinoin 25-38 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-118 1648728-6 1991 These data suggest that the RAR alpha may form a nonproductive complex with c-Jun and provides a simple mechanisms by which retinoic acid may limit cell growth and possibly malignant progression. Tretinoin 124-137 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 76-81 1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 36-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-119 1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 51-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88 1963081-2 1990 The induction of differentiation by retinoic acid (RA) leads to an accumulation of c-jun mRNA caused by increased c-jun transcription. Tretinoin 51-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-119 1963081-3 1990 This induction is an indirect response to RA and requires a functional AP1 binding site within the c-jun promoter. Tretinoin 42-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-74 1963081-3 1990 This induction is an indirect response to RA and requires a functional AP1 binding site within the c-jun promoter. Tretinoin 42-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-104 1963081-13 1990 Thus, the induction of c-jun transcription by RA, although indirect, can have an important role in the differentiation process. Tretinoin 46-48 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 23-28 30709899-0 2019 Repression of hepatocyte nuclear factor 4 alpha by AP-1 underlies dyslipidemia associated with retinoic acid. Tretinoin 95-108 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-55 34179313-8 2021 Compared with ATRA group, inhibition of miR-200a-3p, 200c-3p, and 141-3p significantly strengthened the expression of Fra1/Jun (AP1), Ets1/PEA3, Brn3, and Zeb1/AREB6 at varying degrees. Tretinoin 14-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 128-131 30709899-11 2019 Collectively, these results indicate that atRA activates JNK and ERK pathways and the downstream target AP-1 represses HNF4alpha transactivation of the CYP7A1 promoter, potentially responsible for hypercholesterolemia. Tretinoin 42-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-108