PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18583263-7 2008 RSG inhibited protein synthesis enhancement and increased (3)H-leucine incorporation induced by ET-1 and PMA, and antagonized the effects of ET-1 and PMA in promoting PKC activity and c-fos protein expression in the myocytes. Tetradecanoylphorbol Acetate 150-153 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 184-189 19225867-6 2009 Activation of protein kinase C (PKC) with phorbol myristate acetate increased c-Fos and c-Jun mRNA, whereas inhibition of PKC with bisindolylmaleimide as well as inhibition of extracellular signal-regulated kinases (ERK) 1/2 with PD98059 abolished the NE-induced increase in c-Fos and c-Jun gene expression. Tetradecanoylphorbol Acetate 42-67 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 78-83 18197392-0 2008 hnRNP-R regulates the PMA-induced c-fos expression in retinal cells. Tetradecanoylphorbol Acetate 22-25 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 34-39 11333365-6 2001 Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. Tetradecanoylphorbol Acetate 53-84 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 99-104 15086447-4 2004 RESULTS: Stimulation with fetal bovine serum (FBS), phorbol 12-myristate 13-acetate (PMA) and ET-1 caused about a doubling of c-fos mRNA. Tetradecanoylphorbol Acetate 52-83 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 126-131 15086447-4 2004 RESULTS: Stimulation with fetal bovine serum (FBS), phorbol 12-myristate 13-acetate (PMA) and ET-1 caused about a doubling of c-fos mRNA. Tetradecanoylphorbol Acetate 85-88 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 126-131 12787062-8 2003 Stimulation of TH gene promoter activity, which was observed in control cell lines treated with either 50 mm KCl or TPA was also dramatically inhibited in the c-Fos-deficient cells. Tetradecanoylphorbol Acetate 116-119 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 159-164 15804434-4 2005 PMA increased c-fos gene expression in neuronal cultures of Wistar rat brain and the PMA-induced c-fos gene expression was inhibited by the PKC inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7). Tetradecanoylphorbol Acetate 0-3 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 14-19 15804434-4 2005 PMA increased c-fos gene expression in neuronal cultures of Wistar rat brain and the PMA-induced c-fos gene expression was inhibited by the PKC inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7). Tetradecanoylphorbol Acetate 0-3 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 97-102 15804434-7 2005 In SHR brain neuronal cultures, the PMA-induced c-fos gene expression was enhanced as compared with that of Wistar Kyoto rats (WKY), while basal c-fos gene expression was almost the same in both neuronal cultures. Tetradecanoylphorbol Acetate 36-39 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 48-53 12041912-10 2002 The addition of phorbol 12-myristate 13-acetate increased mRNA expression for both c-fos and 24-hydroxylase in 1,25(OH)2D3-treated UMR-106 cells. Tetradecanoylphorbol Acetate 16-47 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 83-88 11561718-1 2001 The effects of forskolin (FSK) and phobol 12-myristate-13-acetate (PMA) on c-fos and c-jun mRNA expressions in rat C6 glioma cells were studied. Tetradecanoylphorbol Acetate 67-70 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 75-80 11561718-6 2001 Cycloheximide (CHX) caused a superinduction of the FSK- or PMA-induced c-fos mRNA level. Tetradecanoylphorbol Acetate 59-62 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 71-76 11333365-6 2001 Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. Tetradecanoylphorbol Acetate 86-89 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 99-104 10908728-0 2000 Annexin-I inhibits PMA-induced c-fos SRE activation by suppressing cytosolic phospholipase A2 signal. Tetradecanoylphorbol Acetate 19-22 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 31-36 11272178-4 2001 The general applicability of the approach is exemplified by doxycyclin-(Tet-On) and phorbol 12-myristate 13-acetate-induced (c-fos) promoter activation, with green fluorescent protein (GFP) and red fluorescent protein (DsRed) as semiquantitative and immediate reporters, of transcription activation. Tetradecanoylphorbol Acetate 84-115 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 125-130 10908728-6 2000 The stimulation of Rat2 fibroblast cells with phorbol 12-myristate 13-acetate (PMA) induced the c-fos serum response element (SRE). Tetradecanoylphorbol Acetate 46-77 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 96-101 10908728-6 2000 The stimulation of Rat2 fibroblast cells with phorbol 12-myristate 13-acetate (PMA) induced the c-fos serum response element (SRE). Tetradecanoylphorbol Acetate 79-82 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 96-101 9874176-6 1998 Phorbol myristate acetate was also able to increase c-fos mRNA expression. Tetradecanoylphorbol Acetate 0-25 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 52-57 10693946-3 2000 Significant increases in the levels of c-fos, c-jun, and egr-1 but not NGFIB mRNA were observed in PC12 cells exposed to lead or phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 129-160 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 39-44 10460009-7 1999 Furthermore, this c-fos expression is not inhibited by cycloheximide, but is completely abolished by pretreatment with TPA, so that the c-fos gene is a direct target of TGF-beta1 signalling and PKC is involved in this c-fos induction. Tetradecanoylphorbol Acetate 119-122 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 18-23 10460009-7 1999 Furthermore, this c-fos expression is not inhibited by cycloheximide, but is completely abolished by pretreatment with TPA, so that the c-fos gene is a direct target of TGF-beta1 signalling and PKC is involved in this c-fos induction. Tetradecanoylphorbol Acetate 119-122 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 136-141 10460009-7 1999 Furthermore, this c-fos expression is not inhibited by cycloheximide, but is completely abolished by pretreatment with TPA, so that the c-fos gene is a direct target of TGF-beta1 signalling and PKC is involved in this c-fos induction. Tetradecanoylphorbol Acetate 119-122 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 136-141 9879660-4 1998 Treatment of PC12 cells with a combination of agents (NGF, forskolin, and tetradecanoylphorbol acetate [TPA]) increased c-fos expression over that detected with NGF alone. Tetradecanoylphorbol Acetate 74-102 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 120-125 9879660-4 1998 Treatment of PC12 cells with a combination of agents (NGF, forskolin, and tetradecanoylphorbol acetate [TPA]) increased c-fos expression over that detected with NGF alone. Tetradecanoylphorbol Acetate 104-107 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 120-125 9710591-1 1998 The proto-oncogenes jun and fos are members of the AP-1 family of transcription factors, which activate transcription of target genes via the tetradecanoyl phorbol acetate response element (TRE). Tetradecanoylphorbol Acetate 142-171 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 28-31 9242432-1 1997 Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), increase c-fos and c-jun mRNA levels and AP-1 DNA binding activity in rat pleural mesothelial (RPM) cells, a target cell of asbestos-induced mesotheliomas (N. H. Heintz et al., Proc. Tetradecanoylphorbol Acetate 47-83 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 100-105 9515031-3 1998 In the transient transfection assay, TGF-beta1 potentiated NE- or 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated c-fos promoter/enhancer, but not forskolin-activated c-fos promoter/enhancer. Tetradecanoylphorbol Acetate 66-102 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 119-124 9515031-3 1998 In the transient transfection assay, TGF-beta1 potentiated NE- or 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated c-fos promoter/enhancer, but not forskolin-activated c-fos promoter/enhancer. Tetradecanoylphorbol Acetate 104-107 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 119-124 9515031-3 1998 In the transient transfection assay, TGF-beta1 potentiated NE- or 12-O-tetradecanoylphorbol-13-acetate (TPA)-activated c-fos promoter/enhancer, but not forskolin-activated c-fos promoter/enhancer. Tetradecanoylphorbol Acetate 104-107 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 172-177 9515031-4 1998 The c-fos serum response element (SRE) and the TPA response element (TRE) were responsible for TGF-beta1-induced potentiation of the NE or TPA action. Tetradecanoylphorbol Acetate 139-142 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 4-9 9515031-5 1998 Although TGF-beta1 activated not only the wild-type c-fos SRE, but also the mutated c-fos SRE, which contains an intact binding site for the serum response factor (SRF) but lacks the ternary complex factor (TCF) binding site, TPA activated the wild-type c-fos SRE but not the mutated c-fos SRE. Tetradecanoylphorbol Acetate 226-229 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 84-89 9515031-5 1998 Although TGF-beta1 activated not only the wild-type c-fos SRE, but also the mutated c-fos SRE, which contains an intact binding site for the serum response factor (SRF) but lacks the ternary complex factor (TCF) binding site, TPA activated the wild-type c-fos SRE but not the mutated c-fos SRE. Tetradecanoylphorbol Acetate 226-229 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 84-89 9515031-5 1998 Although TGF-beta1 activated not only the wild-type c-fos SRE, but also the mutated c-fos SRE, which contains an intact binding site for the serum response factor (SRF) but lacks the ternary complex factor (TCF) binding site, TPA activated the wild-type c-fos SRE but not the mutated c-fos SRE. Tetradecanoylphorbol Acetate 226-229 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 84-89 9242432-1 1997 Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), increase c-fos and c-jun mRNA levels and AP-1 DNA binding activity in rat pleural mesothelial (RPM) cells, a target cell of asbestos-induced mesotheliomas (N. H. Heintz et al., Proc. Tetradecanoylphorbol Acetate 85-88 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 100-105 8864900-8 1996 A 24 h pretreatment with PMA at 10(-7) M inhibited the mitogenic response, tyrosine phosphorylation of MAPK, and induction of c-fos mRNA subsequent to the addition of PMA, but not bFGF. Tetradecanoylphorbol Acetate 25-28 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 126-131 9067632-5 1997 Depletion of protein kinase C by PMA pre-treatment resulted in substantial inhibition of the c-fos signal. Tetradecanoylphorbol Acetate 33-36 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 93-98 9192514-4 1997 Phorbol myristate acetate (PMA) elicits a similar increase in c-fos and c-jun mRNAs, but is unable to stimulate transcription of collagenase in these cells. Tetradecanoylphorbol Acetate 0-25 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 62-67 9192514-4 1997 Phorbol myristate acetate (PMA) elicits a similar increase in c-fos and c-jun mRNAs, but is unable to stimulate transcription of collagenase in these cells. Tetradecanoylphorbol Acetate 27-30 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 62-67 8903410-8 1996 HGF, phorbol myristate acetate (PMA) and a DG analog, oleylacetylglycerol (OAG), activated the expression of c-jun and c-fos messenger RNAs (mRNAs). Tetradecanoylphorbol Acetate 5-30 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 119-124 8903410-8 1996 HGF, phorbol myristate acetate (PMA) and a DG analog, oleylacetylglycerol (OAG), activated the expression of c-jun and c-fos messenger RNAs (mRNAs). Tetradecanoylphorbol Acetate 32-35 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 119-124 8864900-8 1996 A 24 h pretreatment with PMA at 10(-7) M inhibited the mitogenic response, tyrosine phosphorylation of MAPK, and induction of c-fos mRNA subsequent to the addition of PMA, but not bFGF. Tetradecanoylphorbol Acetate 167-170 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 126-131 7864828-4 1995 Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells. Tetradecanoylphorbol Acetate 118-121 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 32-35 8837013-4 1996 A transient induction of both c-fos and c-jun mRNAs by TPA was observed in both cell populations, together with an associated suppression of BSP mRNA in the fetal rat calvarial cells. Tetradecanoylphorbol Acetate 55-58 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 30-35 8654580-3 1996 The Fos and Jun components of AP1 were induced rapidly and transiently in PC12 cells following the addition of phorbol ester (phorbol 12-myristate 13-acetate, PMA). Tetradecanoylphorbol Acetate 126-157 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 4-7 8654580-3 1996 The Fos and Jun components of AP1 were induced rapidly and transiently in PC12 cells following the addition of phorbol ester (phorbol 12-myristate 13-acetate, PMA). Tetradecanoylphorbol Acetate 159-162 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 4-7 8838143-3 1996 Treatment of cells with TPA increased c-fos mRNA 20-fold with only a 2-fold increase in c-jun mRNA levels. Tetradecanoylphorbol Acetate 24-27 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 38-43 7657802-4 1995 During cardiocyte hypertrophy evoked by endothelin-1, Phenylephrine, or PMA, the steady state level of BNP mRNA increased as rapidly as the "immediate-early" induction of the c-fos gene expression, and reached a maximal level within 1 h. Actinomycin D, a transcriptional inhibitor, completely diminished the response, while the translational blocked with cycloheximide did not inhibit it. Tetradecanoylphorbol Acetate 72-75 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 175-180 7589783-6 1995 Under identical conditions, TPA and serum rapidly induce c-fos transcription in RENE1 cells, indicating that the lack of inducibility by estradiol is not due to a general inhibitor of transcription of these genes. Tetradecanoylphorbol Acetate 28-31 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 57-62 7656159-7 1995 Immunocytochemical investigation also confirmed that heparin could inhibit the expression of nuclear oncogene c-fos and c-jun in the MsC stimulated by PMA. Tetradecanoylphorbol Acetate 151-154 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 110-115 7585834-10 1995 Phorbol 12-myristate 13-acetate also decreased [Ca2+]i transients, caused c-fos induction, and provoked hypertrophy in myocytes. Tetradecanoylphorbol Acetate 0-31 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 74-79 7585834-14 1995 Phorbol 12-myristate 13-acetate did not affect [Ca2+]i or cellular growth in nonmyocytes but did cause c-fos induction. Tetradecanoylphorbol Acetate 0-31 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 103-108 7864828-4 1995 Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells. Tetradecanoylphorbol Acetate 123-126 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 32-35 7864828-4 1995 Gel-retardation assay indicates Fos as a component of the complex formed between the consensus oligonucleotide of the TPA (PMA, phorbol 12-myristate 13-acetate) response element (TRE) and nuclear extract prepared from butyrate-treated cells. Tetradecanoylphorbol Acetate 128-159 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 32-35 7533872-2 1995 In isolated rat hepatocytes angiotensin II and phorbol 12-myristate 13-acetate (PMA) induce the expression of c-fos. Tetradecanoylphorbol Acetate 47-78 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 110-115 7533872-2 1995 In isolated rat hepatocytes angiotensin II and phorbol 12-myristate 13-acetate (PMA) induce the expression of c-fos. Tetradecanoylphorbol Acetate 80-83 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 110-115 7796933-6 1995 Consistently, ionomycin plus low doses of TPA solely reproduced the potent effect of TRH on c-fos transcripts. Tetradecanoylphorbol Acetate 42-45 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-97 7796933-7 1995 Data collected from TRH and TPA down-regulated cells indicated that TRH probably recruits TPA-dependent PKC isoforms for stimulating c-fos but not jun B transcripts. Tetradecanoylphorbol Acetate 28-31 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 133-138 7796933-7 1995 Data collected from TRH and TPA down-regulated cells indicated that TRH probably recruits TPA-dependent PKC isoforms for stimulating c-fos but not jun B transcripts. Tetradecanoylphorbol Acetate 90-93 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 133-138 7988435-13 1994 a convergence of TPA, FSH, and cAMP mediated signals in prepubertal Sertoli cells may occur with the induction of specific AP-1 site binding complex(es) containing jun and fos proteins. Tetradecanoylphorbol Acetate 17-20 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 172-175 8013086-5 1994 The protein kinase C activators (12-O-tetradecanoylphorbol 13-acetate [TPA], phorbol 12,13-dibutyrate, and 1-oleyl-2-acetyl-rac-glycerol) induced c-fos mRNA expression, which was also potentiated by TGF-beta 1. Tetradecanoylphorbol Acetate 33-69 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 146-151 8035171-6 1994 An analysis of the effects of IL-1 and TPA on immediate early gene expression indicated that IL-1 preferentially induced c-jun gene expression, whereas TPA greatly increased c-fos and zif/268 gene expression. Tetradecanoylphorbol Acetate 152-155 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 174-179 8455942-5 1993 In addition, transformation of rat embryo cells induced by an activated ras gene in the presence of the tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA) or by ras plus SV40 large T antigen is also inhibited by this dominant-negative mutant, suggesting that a member of the jun or fos family is involved in the pathways leading to transformation in these systems as well. Tetradecanoylphorbol Acetate 119-156 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 290-293 8455942-5 1993 In addition, transformation of rat embryo cells induced by an activated ras gene in the presence of the tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA) or by ras plus SV40 large T antigen is also inhibited by this dominant-negative mutant, suggesting that a member of the jun or fos family is involved in the pathways leading to transformation in these systems as well. Tetradecanoylphorbol Acetate 158-161 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 290-293 1338729-10 1992 Analogous effects were observed with TPA which minimally stimulated c-fos and c-jun mRNAs on day 0, but markedly increased these messages on day 2. Tetradecanoylphorbol Acetate 37-40 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 68-73 1383560-0 1992 AP-1 complex and c-fos transcription are involved in TPA provoked and trans-synaptic inductions of the tyrosine hydroxylase gene: insights into long-term regulatory mechanisms. Tetradecanoylphorbol Acetate 53-56 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 17-22 1330491-10 1992 c-fos mRNA was induced by treatment with 50 ng/ml tetradecanoyl phorbol acetate or by 40 ng/ml forskolin, while induction of Egr-1 mRNA was stimulated by treatment with tetradecanoyl phorbol acetate, but not forskolin. Tetradecanoylphorbol Acetate 50-79 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-5 1480173-9 1992 8-Bromo-cAMP and phorbol 12-myristate 13-acetate (PMA) caused increases in the abundance of c-fos and c-jun transcripts. Tetradecanoylphorbol Acetate 17-48 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-97 1480173-9 1992 8-Bromo-cAMP and phorbol 12-myristate 13-acetate (PMA) caused increases in the abundance of c-fos and c-jun transcripts. Tetradecanoylphorbol Acetate 50-53 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-97 1375896-4 1992 Uterine levels of c-fos mRNA observed after treatment with the phorbol ester phorbol 12-myristate 13-acetate are not decreased by a 3-h pretreatment with progesterone. Tetradecanoylphorbol Acetate 77-108 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 18-23 1374838-7 1992 The effect of the DHPs was stereospecific; (+)Bay K 8644, a Ca2+ antagonist, inhibited PMA-induced increases in c-fos and NGFI-A mRNAs. Tetradecanoylphorbol Acetate 87-90 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 112-117 1577756-5 1992 In the present study, the phorbol ester, phorbol 12-myristate 13-acetate (PMA), stimulated c-fos transcription in a rapid and dose-dependent manner with an 800% increase in transcription following 15-30 min of addition. Tetradecanoylphorbol Acetate 41-72 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 91-96 1577756-5 1992 In the present study, the phorbol ester, phorbol 12-myristate 13-acetate (PMA), stimulated c-fos transcription in a rapid and dose-dependent manner with an 800% increase in transcription following 15-30 min of addition. Tetradecanoylphorbol Acetate 74-77 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 91-96 1577756-9 1992 When H4 cells were pretreated with PMA for 24 h, there was a decrease of 20-45% in both cytosolic and membrane PKC activity and a complete loss of PMA"s induction of c-fos transcription. Tetradecanoylphorbol Acetate 35-38 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 166-171 1577756-11 1992 When cells were pretreated with PMA for 24 h, the insulin-induced increase in transcription of c-fos was reduced by 50%. Tetradecanoylphorbol Acetate 32-35 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 95-100 1309563-5 1992 The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated c-fos expression but did not trigger cell proliferation. Tetradecanoylphorbol Acetate 51-54 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 67-72 1371276-2 1992 Previous experiments have shown that heparin inhibits induction of c-fos and c-myc protooncogene mRNA in rat VSMC stimulated by phorbol 12-myristate 13-acetate (PMA) but not when stimulated by epidermal growth factor (EGF) (Pukac, L. A., Castellot, J. J., Wright, T. C., Caleb, B. L., and Karnovsky, M. J. Tetradecanoylphorbol Acetate 128-159 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 67-72 1309563-5 1992 The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated c-fos expression but did not trigger cell proliferation. Tetradecanoylphorbol Acetate 18-49 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 67-72 1521461-5 1992 12-O-Tetradecanoylphorbol-13-acetate (TPA)-responsive element-like sequences have been identified in upstream regions of the GST-P gene, and oncogene products c-jun and c-fos are suggested to activate the gene. Tetradecanoylphorbol Acetate 0-36 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 169-174 1543678-8 1992 In vivo treatment with the phorbol ester TPA rapidly elevates uterine levels of fos, jun, and myc transcripts, indicating that expression of these protooncogenes is under non-estrogenic as well as estrogenic regulation in this target tissue. Tetradecanoylphorbol Acetate 41-44 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 80-83 1312200-5 1992 Treatment of the C6 cells with phorbol 12-myristate 13-acetate caused a 13-fold increase in c-fos expression 0.5 h after administration and a decrease in proenkephalin mRNA. Tetradecanoylphorbol Acetate 31-62 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-97 1521461-5 1992 12-O-Tetradecanoylphorbol-13-acetate (TPA)-responsive element-like sequences have been identified in upstream regions of the GST-P gene, and oncogene products c-jun and c-fos are suggested to activate the gene. Tetradecanoylphorbol Acetate 38-41 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 169-174 1782669-7 1991 Induction of c-fos and c-myc occurred at both temperatures after the stimulation with FBS, TPA or A23187. Tetradecanoylphorbol Acetate 91-94 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 13-18 1659543-8 1991 However, tetradecanoyl-13-phorbol acetate (TPA, 200 nM) was able to induce c-fos mRNA expression. Tetradecanoylphorbol Acetate 43-46 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 75-80 1659543-9 1991 The protein kinase C (PKC) inhibitors H-7 (0.3-30 microM) and staurosporine (0.75 micrograms/ml) blocked FSH-induced c-fos mRNA expression in cultured granulosa cells while HA 1004, an inhibitor of cGMP- and cAMP-dependent protein kinases at 30 microM had no effect on TPA-induced c-fos expression, and only minimally inhibited FSH-induced c-fos expression. Tetradecanoylphorbol Acetate 269-272 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 117-122 2054934-6 1991 ET-1, TPA, and ionomycin similarly induced the expression of c-fos after 30 minutes, which returned to an undetectable level after 6 hours. Tetradecanoylphorbol Acetate 6-9 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 61-66 1716733-4 1991 It has been found that in E1Aad5 + cHa-ras-transformed cells the expression of c-fos promoter has a constitutive, non-inducible character while in REF cells and cells immortalized by E1Aad5 the fos-promoter can be regulated by serum growth factors, EGF, and TPA. Tetradecanoylphorbol Acetate 258-261 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 79-84 1828153-7 1991 Ang II (10(9) - 10(-8) M) and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA, 10(-8) M) rapidly induced c-fos as well as c-Jun and Jun-B mRNA expression in RASM cells. Tetradecanoylphorbol Acetate 60-91 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 124-129 1828153-7 1991 Ang II (10(9) - 10(-8) M) and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA, 10(-8) M) rapidly induced c-fos as well as c-Jun and Jun-B mRNA expression in RASM cells. Tetradecanoylphorbol Acetate 93-96 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 124-129 1899867-4 1991 Stimulation with arginine vasopressin, epidermal growth factor, or phorbol myristate acetate increased [3H]thymidine incorporation and mRNA levels of the immediate-early response genes c-fos and Egr-1. Tetradecanoylphorbol Acetate 67-92 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 185-190 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 173-198 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 16-21 2099192-5 1990 The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC. Tetradecanoylphorbol Acetate 128-159 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 25-30 2099192-5 1990 The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC. Tetradecanoylphorbol Acetate 128-159 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 104-109 2099192-5 1990 The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC. Tetradecanoylphorbol Acetate 161-164 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 25-30 2099192-5 1990 The effect of heparin on c-fos mRNA induction was selective for specific mitogens, as heparin inhibited c-fos mRNA induction in phorbol 12-myristate 13-acetate (TPA) stimulated but not epidermal growth factor (EGF) stimulated VSMC. Tetradecanoylphorbol Acetate 161-164 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 104-109 2166202-2 1990 Marked induction of c-fos mRNA in astrocytes was observed after treatment with epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), dibutyryl cyclic AMP (db-cAMP), and phorbol diester (TPA; 12-O-tetra-decanoylphorbol 13-acetate), which are known to induce the proliferation or differentiation of astrocytes. Tetradecanoylphorbol Acetate 202-205 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 20-25 2166202-3 1990 Increase of c-fos protein immunoreactivity (IR) was obtained after treatment with fetal calf serum, EGF, bFGF, db-cAMP and TPA. Tetradecanoylphorbol Acetate 123-126 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 12-17 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 200-203 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 111-116 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 173-198 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 111-116 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 173-198 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 111-116 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 173-198 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 111-116 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 200-203 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 16-21 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 200-203 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 111-116 1690514-3 1990 Peak effects on c-fos mRNA occurred between 15 and 30 min and were completely gone after 2 h. The elevation in c-fos mRNA was, in part, dependent on protein kinase C, since phorbol myristate acetate (PMA) also elevated c-fos mRNA and further increased c-fos mRNA expression by endothelin, but the effects were not additive. Tetradecanoylphorbol Acetate 200-203 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 111-116 2769792-3 1989 In contrast, EGF, FGF, and TPA were equally effective in inducing accumulation of TIS8 and TIS28/c-fos mRNAs. Tetradecanoylphorbol Acetate 27-30 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 97-102 2404011-1 1990 12-O-Tetradecanoylphorbol-13-acetate (TPA) activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene in the wild type PC-12 cells but not in the variant PC-12 cells that originated from the wild type cells. Tetradecanoylphorbol Acetate 0-36 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 57-62 2404011-1 1990 12-O-Tetradecanoylphorbol-13-acetate (TPA) activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene in the wild type PC-12 cells but not in the variant PC-12 cells that originated from the wild type cells. Tetradecanoylphorbol Acetate 38-41 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 57-62 2514685-2 1989 Activators of protein kinase C, such as TPA, mellitin and phospholipase C and the calcium ionophore, A23187, induced c-fos mRNA in the presence or absence of cyclosporin A. Tetradecanoylphorbol Acetate 40-43 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 117-122 2507902-5 1989 Transforming ras protein activated an intracellular signal pathway, which led to the induction of 12-O-tetradecanoyl phorbol-13-acetate-responsive elements; activation was enhanced by coexpression of the proto-oncogene jun (encoding AP-1) and was further augmented by fos. Tetradecanoylphorbol Acetate 98-135 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 268-271 2501508-2 1989 Induction of c-fos by epidermal growth factor, A23187, dBcAMP, or TPA in the same cells is not affected. Tetradecanoylphorbol Acetate 66-69 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 13-18 3301843-7 1987 The phorbol ester phorbol 12-myristate 13-acetate (PMA) also induces c-myc and c-fos mRNAs without inducing DNA synthesis. Tetradecanoylphorbol Acetate 18-49 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 79-84 2856403-2 1987 In these basal conditions, the individual addition of TSH, insulin, insulin-like growth factor-I (IGF-I), phorbol 12-myristate 13-acetate (TPA), alpha 1-adrenergic agents, or A23187, increase c-myc and/or c-fos proto-oncogene expression. Tetradecanoylphorbol Acetate 106-137 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 205-210 3329719-2 1987 c-fos and c-myc oncogenes expression was measured in these cells after addition of their specific growth factor TSH and after treatment with either forskolin, an activator of adenylate cyclase or with a tumor promoter, TPA. Tetradecanoylphorbol Acetate 219-222 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 0-5 2837462-4 1988 In rat thymic lymphocytes, the increase in the level of c-fos RNA induced by the combination of 12-O-tetradecanoylphorbol 13-acetate and ionomycin was unaffected by inhibition of the antiport with 5-(N-ethyl-N-propyl)amiloride. Tetradecanoylphorbol Acetate 96-132 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 56-61 2827679-3 1988 Moreover, protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate and Ca2+-ionophore A23187 increased the c-fos mRNA level in an additive manner. Tetradecanoylphorbol Acetate 38-74 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 115-120 3301843-7 1987 The phorbol ester phorbol 12-myristate 13-acetate (PMA) also induces c-myc and c-fos mRNAs without inducing DNA synthesis. Tetradecanoylphorbol Acetate 51-54 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 79-84 3301843-8 1987 However, the mechanism of this induction appears to be different from the insulin-induced induction since pretreatment of cells with PMA blocks only the PMA-mediated, not the insulin-mediated, induction of c-myc and c-fos. Tetradecanoylphorbol Acetate 133-136 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 216-221 2997786-4 1985 cAMP, epidermal growth factor, the phorbol ester phorbol 12-myristate 13-acetate, and K+ depolarization also induce the fos gene. Tetradecanoylphorbol Acetate 49-80 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 120-123 28842814-11 2017 Activation of PKCgamma by PMA aggravated allodynia and increased the expression of CGRP and c-Fos. Tetradecanoylphorbol Acetate 26-29 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-97 32505192-9 2020 Subsequently, PMA induced MMP-9 expression via PKCdelta-mediated reactive oxygen species (ROS) generation, extracellular signal-regulated kinase 1/2 (ERK1/2) activation, and then induced c-Fos/AP-1 signaling pathway. Tetradecanoylphorbol Acetate 14-17 Fos proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 187-192