PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23835587-8 2013 DMBA/TPA application resulted in significant increases in c-jun and p50, which were reversed by a number of different treatments. Tetradecanoylphorbol Acetate 5-8 jun proto-oncogene Mus musculus 58-63 33144667-4 2020 Tetracycline-inducible BACH2 expression resulted in suppression of phorbol 12-myristate 13-acetate (PMA)/ionomycin-driven activation of a luciferase reporter containing BACH2/AP-1 target sequences from the mouse Ifng + 18k enhancer. Tetradecanoylphorbol Acetate 67-98 jun proto-oncogene Mus musculus 175-179 33144667-4 2020 Tetracycline-inducible BACH2 expression resulted in suppression of phorbol 12-myristate 13-acetate (PMA)/ionomycin-driven activation of a luciferase reporter containing BACH2/AP-1 target sequences from the mouse Ifng + 18k enhancer. Tetradecanoylphorbol Acetate 100-103 jun proto-oncogene Mus musculus 175-179 26100520-4 2015 The combination of ursolic acid + resveratrol inhibited TPA-induced signaling pathways, including EGFR, STAT3, Src, Akt, Cox-2, Fas, NF-kappaB, p38 MAPK, c-Jun, and JNK1/2 while increasing levels of tumor suppressors, such as p21 and PDCD4, to a greater extent compared with the groups treated with the individual compounds. Tetradecanoylphorbol Acetate 56-59 jun proto-oncogene Mus musculus 154-159 26100520-7 2015 Furthermore, NF-kappaB, Egr-1, and AP-1 DNA binding activities after TPA treatment were dramatically decreased by the combination of ursolic acid + resveratrol. Tetradecanoylphorbol Acetate 69-72 jun proto-oncogene Mus musculus 35-39 25374129-10 2014 In addition, piceatannol decreased TPA-induced expression of c-Fos and the DNA binding of AP-1. Tetradecanoylphorbol Acetate 35-38 jun proto-oncogene Mus musculus 90-94 25374129-11 2014 CONCLUSION: Piceatannol inhibits TPA-induced COX-2 and iNOS expression by blocking the activation of NF-kappaB and AP-1 via suppression of the IKKbeta activity and phosphorylation of MAP kinases, which provides a mechanistic basis of its anti-inflammatory effects in mouse skin. Tetradecanoylphorbol Acetate 33-36 jun proto-oncogene Mus musculus 115-119 23852815-9 2014 All tested compounds decreased TPA-induced c-jun mRNA levels in skin. Tetradecanoylphorbol Acetate 31-34 jun proto-oncogene Mus musculus 43-48 24380573-0 2014 Naturally occurring phenolic acids modulate TPA-induced activation of EGFR, AP-1, and STATs in mouse epidermis. Tetradecanoylphorbol Acetate 44-47 jun proto-oncogene Mus musculus 76-80 24380573-2 2014 In this study we investigated the possible interference of naturally occurring phenolic acids with EGFR, activator protein-1 (AP-1), and signal transducers and activators of transcription (STATs) pathways activated by topical application of tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) in Balb/c mice epidermis. Tetradecanoylphorbol Acetate 256-292 jun proto-oncogene Mus musculus 105-124 23708096-2 2013 Topical application of LicE (0.5-2 mg) effectively inhibited TPA-induced (1) ear edema formation; (2) phosphorylation of stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK), c-Jun, and extracellular signal regulated kinase 1/2; and (3) expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 proteins in mouse skin. Tetradecanoylphorbol Acetate 61-64 jun proto-oncogene Mus musculus 153-158 23429041-6 2013 DHA also remarkably reduced PMA-induced p65, C/EBPbeta, c-jun and CREB nuclear translocation. Tetradecanoylphorbol Acetate 28-31 jun proto-oncogene Mus musculus 56-61 23708096-2 2013 Topical application of LicE (0.5-2 mg) effectively inhibited TPA-induced (1) ear edema formation; (2) phosphorylation of stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK), c-Jun, and extracellular signal regulated kinase 1/2; and (3) expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 proteins in mouse skin. Tetradecanoylphorbol Acetate 61-64 jun proto-oncogene Mus musculus 189-194 23105093-6 2012 Both supershift and ChIP assays revealed the presence of the AP-1 component c-JUN at the PED/PEA-15 promoter upon 12-O-tetradecanoylphorbol-13-acetate stimulation of the cells. Tetradecanoylphorbol Acetate 114-150 jun proto-oncogene Mus musculus 76-81 23002036-7 2013 Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. Tetradecanoylphorbol Acetate 61-97 jun proto-oncogene Mus musculus 147-152 23002036-7 2013 Chromatin immunoprecipitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (TRE-III) responsible for c-Jun-mediated transcriptional activation of Gipr. Tetradecanoylphorbol Acetate 99-102 jun proto-oncogene Mus musculus 147-152 22842666-5 2012 Moreover, pterostilbene markedly suppressed TPA-induced activation of extracellular signal-regulated kinase (ERK)1/2, p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK)1/2, phosphatidylinositol 3-kinase (PI3K) and Akt, which are upstream of NFkappaB and activator protein 1 (AP-1). Tetradecanoylphorbol Acetate 44-47 jun proto-oncogene Mus musculus 278-297 22842666-5 2012 Moreover, pterostilbene markedly suppressed TPA-induced activation of extracellular signal-regulated kinase (ERK)1/2, p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK)1/2, phosphatidylinositol 3-kinase (PI3K) and Akt, which are upstream of NFkappaB and activator protein 1 (AP-1). Tetradecanoylphorbol Acetate 44-47 jun proto-oncogene Mus musculus 299-303 22542552-6 2012 In addition, piperine inhibited PMA-induced NF-kappaB, C/EBP and c-Jun nuclear translocation. Tetradecanoylphorbol Acetate 32-35 jun proto-oncogene Mus musculus 65-70 22001392-5 2011 We first demonstrate that AP-1 activation by 12-O-tetradecanoylphorbol-13-acetate induces PTPROt expression with concurrent recruitment of c-fos and c-jun to its promoter. Tetradecanoylphorbol Acetate 45-81 jun proto-oncogene Mus musculus 26-30 22542552-0 2012 Piperine inhibits PMA-induced cyclooxygenase-2 expression through downregulating NF-kappaB, C/EBP and AP-1 signaling pathways in murine macrophages. Tetradecanoylphorbol Acetate 18-21 jun proto-oncogene Mus musculus 102-106 22210038-2 2011 Heat-inactivated LP (heated at 60 C for 30 min) potently inhibited the expression of TNF-alpha and IL-4 as well as the activation of their transcription factors, NF-kappaB and c-jun, in phorbol 12"-myristate 13"-acetate-stimulated RBL-2H3 cells. Tetradecanoylphorbol Acetate 186-219 jun proto-oncogene Mus musculus 176-181 22001392-5 2011 We first demonstrate that AP-1 activation by 12-O-tetradecanoylphorbol-13-acetate induces PTPROt expression with concurrent recruitment of c-fos and c-jun to its promoter. Tetradecanoylphorbol Acetate 45-81 jun proto-oncogene Mus musculus 149-154 20179211-4 2010 DATS significantly attenuated the DNA binding of activator protein-1 (AP-1), one of the transcription factors that regulate COX-2 expression, in TPA-stimulated mouse skin. Tetradecanoylphorbol Acetate 145-148 jun proto-oncogene Mus musculus 49-68 21480506-8 2011 Moreover, significant increases in the protein levels analyzed by ELISA of c-Jun, p65, and p53 were observed in the skin of DMBA/TPA treated mice, whereas mice treated with 2 and DMBA/TPA had a similar expression of these transcription factors than the control mice. Tetradecanoylphorbol Acetate 129-132 jun proto-oncogene Mus musculus 75-80 21480506-8 2011 Moreover, significant increases in the protein levels analyzed by ELISA of c-Jun, p65, and p53 were observed in the skin of DMBA/TPA treated mice, whereas mice treated with 2 and DMBA/TPA had a similar expression of these transcription factors than the control mice. Tetradecanoylphorbol Acetate 184-187 jun proto-oncogene Mus musculus 75-80 20469933-10 2010 MEK1/2, c-Jun, and STAT3 knockdown also reduced basal as well as PMA-induced Tspo mRNA levels in NIH-3T3 cells. Tetradecanoylphorbol Acetate 65-68 jun proto-oncogene Mus musculus 8-13 21400615-4 2011 Western blot analysis revealed that 5"-NIO inhibited activities of Raf-1 (S338), MEK1/2, ERK1/2, JNK, and c-Jun induced by EGF or TPA, respectively, whereas it did not affect autophosphorylation of epidermal growth factor receptor (EGFR) induced by EGF or TPA. Tetradecanoylphorbol Acetate 130-133 jun proto-oncogene Mus musculus 106-111 21400615-5 2011 In addition, 5"-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Tetradecanoylphorbol Acetate 69-72 jun proto-oncogene Mus musculus 90-95 21400615-5 2011 In addition, 5"-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Tetradecanoylphorbol Acetate 69-72 jun proto-oncogene Mus musculus 159-178 21400615-5 2011 In addition, 5"-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Tetradecanoylphorbol Acetate 69-72 jun proto-oncogene Mus musculus 180-184 21400615-5 2011 In addition, 5"-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Tetradecanoylphorbol Acetate 229-232 jun proto-oncogene Mus musculus 159-178 21400615-5 2011 In addition, 5"-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Tetradecanoylphorbol Acetate 229-232 jun proto-oncogene Mus musculus 180-184 21542454-9 2011 Tumors obtained in DMBA/TPA group were associated with enhanced expression of NF-kappaB and AP-1 when compared to the control counterparts. Tetradecanoylphorbol Acetate 24-27 jun proto-oncogene Mus musculus 92-96 20232358-1 2010 Dietary energy restriction (DER, 40% calorie reduction from fat and carbohydrate) inhibited mouse skin carcinogenesis and decreased 12-O-tetradecanoyl-13-phorbol acetate (TPA)-induced activator protein-1 (AP-1):DNA binding previously. Tetradecanoylphorbol Acetate 171-174 jun proto-oncogene Mus musculus 205-209 20232358-3 2010 TPA significantly increased c-jun, jun B, c-fos, fra-1, and fra-2 and decreased jun D within 3-6 h after treatment. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 28-33 20232358-4 2010 AP-1:DNA binding reached a maximum 2.5-fold induction over controls 4 h after TPA treatment and antibodies to jun B, jun D, and fra-2 in the EMSA binding reaction resulted in supershifts in both acetone- and TPA-treated mice 1-6 h after treatment. Tetradecanoylphorbol Acetate 78-81 jun proto-oncogene Mus musculus 0-4 20232358-4 2010 AP-1:DNA binding reached a maximum 2.5-fold induction over controls 4 h after TPA treatment and antibodies to jun B, jun D, and fra-2 in the EMSA binding reaction resulted in supershifts in both acetone- and TPA-treated mice 1-6 h after treatment. Tetradecanoylphorbol Acetate 208-211 jun proto-oncogene Mus musculus 0-4 20232358-8 2010 While sham animals treated with either acetone or TPA contained jun B, jun D, and fra-2 proteins in the AP-1:DNA complex by supershift analysis, fra-2 was no longer seen in adx DER animals. Tetradecanoylphorbol Acetate 50-53 jun proto-oncogene Mus musculus 104-108 20179211-4 2010 DATS significantly attenuated the DNA binding of activator protein-1 (AP-1), one of the transcription factors that regulate COX-2 expression, in TPA-stimulated mouse skin. Tetradecanoylphorbol Acetate 145-148 jun proto-oncogene Mus musculus 70-74 20179211-5 2010 DATS also diminished TPA-induced expression of c-Jun and c-Fos, the principal components of AP-1, and blunted the activation of c-Jun NH(2)-terminal kinase (JNK) and Akt. Tetradecanoylphorbol Acetate 21-24 jun proto-oncogene Mus musculus 47-52 20179211-5 2010 DATS also diminished TPA-induced expression of c-Jun and c-Fos, the principal components of AP-1, and blunted the activation of c-Jun NH(2)-terminal kinase (JNK) and Akt. Tetradecanoylphorbol Acetate 21-24 jun proto-oncogene Mus musculus 92-96 20179211-7 2010 The JNK or Akt kinase assay, taking c-Jun fusion protein as a substrate, revealed that TPA induced JNK- or Akt-mediated c-Jun phosphorylation in mouse skin, which was significantly attenuated by DATS or respective pharmacologic inhibitors. Tetradecanoylphorbol Acetate 87-90 jun proto-oncogene Mus musculus 36-41 20179211-7 2010 The JNK or Akt kinase assay, taking c-Jun fusion protein as a substrate, revealed that TPA induced JNK- or Akt-mediated c-Jun phosphorylation in mouse skin, which was significantly attenuated by DATS or respective pharmacologic inhibitors. Tetradecanoylphorbol Acetate 87-90 jun proto-oncogene Mus musculus 120-125 20179211-9 2010 Taken together, the inhibitory effects of DATS on TPA-induced AP-1 activation and COX-2 expression through modulation of JNK or Akt signaling may partly account for its antitumor-promoting effect on mouse skin carcinogenesis. Tetradecanoylphorbol Acetate 50-53 jun proto-oncogene Mus musculus 62-66 17234724-8 2007 Activation of AP-1 in skin was detected as early as 2 weeks following Cum-OOH or TPA exposure. Tetradecanoylphorbol Acetate 81-84 jun proto-oncogene Mus musculus 14-18 19139002-6 2008 The activation of activator protein-1 and nuclear factor-kappaB induced by TPA was dose dependently inhibited by delphinidin treatment. Tetradecanoylphorbol Acetate 75-78 jun proto-oncogene Mus musculus 18-37 18400024-6 2008 Most PBP fractions decreased TPA-induced cell proliferation by decreasing activation of signalling kinases (c-Jun N-terminal protein kinase, extracellular signal-regulated protein kinase, p38 protein kinase and Akt), transcription factors (activator protein-1 and nuclear factor kappa B) and inflammatory protein (cyclooxygenase 2). Tetradecanoylphorbol Acetate 29-32 jun proto-oncogene Mus musculus 240-286 18234971-0 2008 A JNK1/AP-1-dependent, COX-2 induction is implicated in 12-O-tetradecanoylphorbol-13-acetate-induced cell transformation through regulating cell cycle progression. Tetradecanoylphorbol Acetate 56-92 jun proto-oncogene Mus musculus 7-11 18425423-7 2008 Significant increase in the protein levels of c-jun, p65, and p53 by ELISA were observed in DMBA/TPA treated mice tumors whereas less expression was observed in LA and LAM treated tumors. Tetradecanoylphorbol Acetate 97-100 jun proto-oncogene Mus musculus 46-51 17846172-3 2007 After AP-1 inactivation, epidermal proliferation induced by 7,12-dimethylbenz(a)-anthracene/12-O-tetradecanoylphorbol-13-acetate at the early stage of carcinogenesis was substantially inhibited. Tetradecanoylphorbol Acetate 92-128 jun proto-oncogene Mus musculus 6-10 17440073-0 2007 SAG/ROC2/Rbx2 is a novel activator protein-1 target that promotes c-Jun degradation and inhibits 12-O-tetradecanoylphorbol-13-acetate-induced neoplastic transformation. Tetradecanoylphorbol Acetate 97-133 jun proto-oncogene Mus musculus 25-44 17372274-5 2007 Humulone also diminished TPA-induced DNA binding of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 25-28 jun proto-oncogene Mus musculus 90-109 17372274-5 2007 Humulone also diminished TPA-induced DNA binding of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 25-28 jun proto-oncogene Mus musculus 111-115 17372274-11 2007 The present study revealed that topical application of SP600125, a pharmacological inhibitor of c-Jun-N-terminal kinase (JNK), abrogated the activation of AP-1 and the expression of COX-2 in TPA-treated mouse skin. Tetradecanoylphorbol Acetate 191-194 jun proto-oncogene Mus musculus 155-159 17372274-12 2007 Taken together, humulone suppressed TPA-induced activation of NF-kappaB and AP-1 and subsequent expression of COX-2 by blocking upstream kinases IKK and JNK, respectively, which may account for its antitumor-promoting effects on mouse skin carcinogenesis. Tetradecanoylphorbol Acetate 36-39 jun proto-oncogene Mus musculus 76-80 17440073-0 2007 SAG/ROC2/Rbx2 is a novel activator protein-1 target that promotes c-Jun degradation and inhibits 12-O-tetradecanoylphorbol-13-acetate-induced neoplastic transformation. Tetradecanoylphorbol Acetate 97-133 jun proto-oncogene Mus musculus 66-71 17440073-7 2007 TPA-mediated SAG induction was significantly reduced in JB6-Cl.41 cells overexpressing a dominant-negative c-Jun, indicating a requirement of c-Jun/AP-1. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 107-112 17440073-7 2007 TPA-mediated SAG induction was significantly reduced in JB6-Cl.41 cells overexpressing a dominant-negative c-Jun, indicating a requirement of c-Jun/AP-1. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 142-147 17440073-7 2007 TPA-mediated SAG induction was significantly reduced in JB6-Cl.41 cells overexpressing a dominant-negative c-Jun, indicating a requirement of c-Jun/AP-1. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 148-152 17440073-9 2007 When overexpressed, SAG remarkably reduced both basal and TPA-induced c-Jun levels, whereas SAG small interfering RNA (siRNA) silencing increased substantially the levels of both basal and TPA-induced c-Jun. Tetradecanoylphorbol Acetate 58-61 jun proto-oncogene Mus musculus 70-75 17440073-9 2007 When overexpressed, SAG remarkably reduced both basal and TPA-induced c-Jun levels, whereas SAG small interfering RNA (siRNA) silencing increased substantially the levels of both basal and TPA-induced c-Jun. Tetradecanoylphorbol Acetate 189-192 jun proto-oncogene Mus musculus 201-206 17143503-7 2007 Finally, TPA stimulated the activation of CREB and AP-1, but 6-MITC did not block TPA-induced COX-2 expression. Tetradecanoylphorbol Acetate 9-12 jun proto-oncogene Mus musculus 51-55 16910781-4 2006 12-O-Tetradecanoylphorbol 13-acetate (TPA), an activator of protein kinase C and an inducer of NFkappaB and AP-1, protected the cells. Tetradecanoylphorbol Acetate 0-36 jun proto-oncogene Mus musculus 108-112 16999939-6 2006 Besides NF-kappaB, the p38 MAP kinase-mediated activation of activator protein-1 (AP-1) has also been attributed to TPA-induced COX-2 expression in mouse skin. Tetradecanoylphorbol Acetate 116-119 jun proto-oncogene Mus musculus 61-80 16999939-6 2006 Besides NF-kappaB, the p38 MAP kinase-mediated activation of activator protein-1 (AP-1) has also been attributed to TPA-induced COX-2 expression in mouse skin. Tetradecanoylphorbol Acetate 116-119 jun proto-oncogene Mus musculus 82-86 16999939-7 2006 Among the MAP kinases, extracellular signal-regulated protein kinase (ERK) and p38 MAP kinase have been shown to regulate TPA-induced NF-kappaB activation, while p38 MAP kinase and c-Jun-N-terminal kinase are preferentially involved in TPA-induced activation of AP-1 in mouse skin in vivo. Tetradecanoylphorbol Acetate 122-125 jun proto-oncogene Mus musculus 262-266 16910781-4 2006 12-O-Tetradecanoylphorbol 13-acetate (TPA), an activator of protein kinase C and an inducer of NFkappaB and AP-1, protected the cells. Tetradecanoylphorbol Acetate 38-41 jun proto-oncogene Mus musculus 108-112 16365389-4 2006 Furthermore, tissue-specific junB knockout mice respond to 12-O-tetradecanoyl-phorbol-13-acetate, a potent AP-1 activator, with markedly increased and sustained epidermal RAE-1epsilon expression. Tetradecanoylphorbol Acetate 59-96 jun proto-oncogene Mus musculus 107-111 16478713-3 2006 Under improved selection conditions using a TPA-responsive element (TRE) as a bait DNA, known interactors c-fos and c-jun were simultaneously enriched about 100-fold from a model library (a 1:1:20 000 mixture of c-fos, c-jun and gst genes) after one round of selection. Tetradecanoylphorbol Acetate 44-47 jun proto-oncogene Mus musculus 116-121 16740738-6 2006 Importantly, knockdown of paxillin inhibited EGF- or TPA-induced c-Jun phosphorylation at Ser(63) and Ser(73). Tetradecanoylphorbol Acetate 53-56 jun proto-oncogene Mus musculus 65-70 16277019-9 2005 Binding of activator protein-1 (AP-1) to the 12-tetradecanoylphorbol-13-acetate-responsive element (TRE) sequence in LPS-stimulated cells was inhibited by bis-FA at 1 microM and dehydrodiisoeugenol at 0.1 microM, but not by the parent monomers isoeugenol and ferulic acid. Tetradecanoylphorbol Acetate 45-79 jun proto-oncogene Mus musculus 11-30 16277019-9 2005 Binding of activator protein-1 (AP-1) to the 12-tetradecanoylphorbol-13-acetate-responsive element (TRE) sequence in LPS-stimulated cells was inhibited by bis-FA at 1 microM and dehydrodiisoeugenol at 0.1 microM, but not by the parent monomers isoeugenol and ferulic acid. Tetradecanoylphorbol Acetate 45-79 jun proto-oncogene Mus musculus 32-36 15972968-5 2005 Moreover, dexamethasone, which is a potent inhibitor of AP-1-mediated transactivation that exhibits anti-inflammatory and anti-tumor promoting activities, inhibited TPA-induced expression of Rab11a. Tetradecanoylphorbol Acetate 165-168 jun proto-oncogene Mus musculus 56-60 15972968-6 2005 Within the Rab11a gene promoter, we identified a functional AP-1 binding element that exhibited elevated c-Fos binding activity after TPA treatment of keratinocytes. Tetradecanoylphorbol Acetate 134-137 jun proto-oncogene Mus musculus 60-64 15639337-9 2005 While TPA-induced activation of nuclear factor-(kappa)B remained unaffected by both extracts, they inhibited TPA-induced activation of activator protein-1 (AP-1) and attenuated the expression of its key component c-Fos. Tetradecanoylphorbol Acetate 6-9 jun proto-oncogene Mus musculus 135-154 15826073-5 2005 Pretreatment of JB6 P+ mouse epidermal cells with lingonberry extracts produced a dose-dependent inhibition on the activation of activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) induced by either 12-O-tetradecanoylphorbol-13-acetate (TPA) or ultraviolet-B (UVB). Tetradecanoylphorbol Acetate 212-248 jun proto-oncogene Mus musculus 129-148 15826073-5 2005 Pretreatment of JB6 P+ mouse epidermal cells with lingonberry extracts produced a dose-dependent inhibition on the activation of activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) induced by either 12-O-tetradecanoylphorbol-13-acetate (TPA) or ultraviolet-B (UVB). Tetradecanoylphorbol Acetate 212-248 jun proto-oncogene Mus musculus 150-154 15826073-5 2005 Pretreatment of JB6 P+ mouse epidermal cells with lingonberry extracts produced a dose-dependent inhibition on the activation of activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) induced by either 12-O-tetradecanoylphorbol-13-acetate (TPA) or ultraviolet-B (UVB). Tetradecanoylphorbol Acetate 250-253 jun proto-oncogene Mus musculus 129-148 15826073-5 2005 Pretreatment of JB6 P+ mouse epidermal cells with lingonberry extracts produced a dose-dependent inhibition on the activation of activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) induced by either 12-O-tetradecanoylphorbol-13-acetate (TPA) or ultraviolet-B (UVB). Tetradecanoylphorbol Acetate 250-253 jun proto-oncogene Mus musculus 150-154 15639337-9 2005 While TPA-induced activation of nuclear factor-(kappa)B remained unaffected by both extracts, they inhibited TPA-induced activation of activator protein-1 (AP-1) and attenuated the expression of its key component c-Fos. Tetradecanoylphorbol Acetate 6-9 jun proto-oncogene Mus musculus 156-160 15639337-9 2005 While TPA-induced activation of nuclear factor-(kappa)B remained unaffected by both extracts, they inhibited TPA-induced activation of activator protein-1 (AP-1) and attenuated the expression of its key component c-Fos. Tetradecanoylphorbol Acetate 109-112 jun proto-oncogene Mus musculus 135-154 15639337-9 2005 While TPA-induced activation of nuclear factor-(kappa)B remained unaffected by both extracts, they inhibited TPA-induced activation of activator protein-1 (AP-1) and attenuated the expression of its key component c-Fos. Tetradecanoylphorbol Acetate 109-112 jun proto-oncogene Mus musculus 156-160 15520189-6 2004 Expression levels of activator protein-1 family members (c-jun, junB, junD, and c-fos) and transforming growth factor (TGF)-alpha were significantly lower in TPA-treated Smad3(-/-) skin, cultured keratinocytes, and papillomas, as compared with Smad3(+/+) controls. Tetradecanoylphorbol Acetate 158-161 jun proto-oncogene Mus musculus 57-62 14729583-4 2004 In another study, celecoxib attenuated the DNA binding activity of activator protein 1 (AP-1) through suppression of c-Jun and c-Fos expression in TPA-treated mouse skin. Tetradecanoylphorbol Acetate 147-150 jun proto-oncogene Mus musculus 67-86 14729583-6 2004 In the same animal model, TPA treatment resulted in rapid activation via phosphorylation of extracellular signal-regulated protein kinase (ERK)1/2 and p38 MAP kinase, which are upstream of AP-1 in mouse skin. Tetradecanoylphorbol Acetate 26-29 jun proto-oncogene Mus musculus 189-193 15064752-4 2004 Previous studies have established that expression of a dominant-negative c-Jun (TAM67) inhibits phorbol 12-tetradecanoyl-13-acetate (TPA)-induced AP-1 transactivation as well as transformation in mouse epidermal JB6/P+ cells and tumor promotion in mouse skin carcinogenesis. Tetradecanoylphorbol Acetate 133-136 jun proto-oncogene Mus musculus 73-78 14729583-4 2004 In another study, celecoxib attenuated the DNA binding activity of activator protein 1 (AP-1) through suppression of c-Jun and c-Fos expression in TPA-treated mouse skin. Tetradecanoylphorbol Acetate 147-150 jun proto-oncogene Mus musculus 88-92 14729583-7 2004 In order to clarify the roles of p38 and ERK in TPA-induced AP-1 activation, we utilized the pharmacologic inhibitors of these enzymes. Tetradecanoylphorbol Acetate 48-51 jun proto-oncogene Mus musculus 60-64 14729583-8 2004 The p38 inhibitor SB203580 blocked TPA-mediated AP-1 activation, while the MEK1/2 inhibitor U0126 was not inhibitory despite suppression of c-Fos expression in mouse skin. Tetradecanoylphorbol Acetate 35-38 jun proto-oncogene Mus musculus 48-52 14729583-4 2004 In another study, celecoxib attenuated the DNA binding activity of activator protein 1 (AP-1) through suppression of c-Jun and c-Fos expression in TPA-treated mouse skin. Tetradecanoylphorbol Acetate 147-150 jun proto-oncogene Mus musculus 117-122 15063796-6 2004 TPA stimulated ERK-dependent increases in c-Fos protein and the c-Fos content of AP-1 complexes. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 81-85 15063796-7 2004 MMP-13 promoter studies indicated that TPA requires AP-1, but not Runx, to induce MMP-13 gene expression. Tetradecanoylphorbol Acetate 39-42 jun proto-oncogene Mus musculus 52-56 14661063-6 2004 TPA-induced c-Jun expression was transient in TNFR1-/- and TNFR2-/- compared to wt epidermis and this was reflected by reduced induction of the AP-1-responsive genes granulocyte/macrophage-colony stimulating factor, matrix metalloproteinase-9 and matrix metalloproteinase-3. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 12-17 15630167-7 2004 In addition, resveratrol prevented TPA-induced DNA binding of activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 35-38 jun proto-oncogene Mus musculus 62-81 15630167-7 2004 In addition, resveratrol prevented TPA-induced DNA binding of activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 35-38 jun proto-oncogene Mus musculus 83-87 12204819-6 2002 A concentration of > 0.2 nM TPA or 0.12 ng/mL (0.02 nM) EGF produced a significant increase in transformation response as well as in extracellular signal-regulated protein kinase (ERK), SRE, or AP-1 activation. Tetradecanoylphorbol Acetate 31-34 jun proto-oncogene Mus musculus 197-201 12632075-0 2003 Rhein inhibits TPA-induced activator protein-1 activation and cell transformation by blocking the JNK-dependent pathway. Tetradecanoylphorbol Acetate 15-18 jun proto-oncogene Mus musculus 27-46 12433932-4 2003 However, in the present study we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2 selective inhibitor, effectively suppressed the activation of transcription factor activator protein 1 (AP-1) induced by ultraviolet B (UVB) or 12-O-tetradecanoylphorbol-13-acetate in mouse epidermal JB6 cells. Tetradecanoylphorbol Acetate 249-285 jun proto-oncogene Mus musculus 188-207 12433932-4 2003 However, in the present study we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2 selective inhibitor, effectively suppressed the activation of transcription factor activator protein 1 (AP-1) induced by ultraviolet B (UVB) or 12-O-tetradecanoylphorbol-13-acetate in mouse epidermal JB6 cells. Tetradecanoylphorbol Acetate 249-285 jun proto-oncogene Mus musculus 209-213 12527890-0 2003 Differential requirement of EGF receptor and its tyrosine kinase for AP-1 transactivation induced by EGF and TPA. Tetradecanoylphorbol Acetate 109-112 jun proto-oncogene Mus musculus 69-73 12527890-2 2003 It is thought that the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 activity is because of the activation of the PKC/MAPK/AP-1 pathway, although the detailed molecular mechanism has not been fully characterized. Tetradecanoylphorbol Acetate 23-59 jun proto-oncogene Mus musculus 74-78 12527890-2 2003 It is thought that the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 activity is because of the activation of the PKC/MAPK/AP-1 pathway, although the detailed molecular mechanism has not been fully characterized. Tetradecanoylphorbol Acetate 23-59 jun proto-oncogene Mus musculus 133-137 12527890-2 2003 It is thought that the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 activity is because of the activation of the PKC/MAPK/AP-1 pathway, although the detailed molecular mechanism has not been fully characterized. Tetradecanoylphorbol Acetate 61-64 jun proto-oncogene Mus musculus 74-78 12527890-2 2003 It is thought that the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 activity is because of the activation of the PKC/MAPK/AP-1 pathway, although the detailed molecular mechanism has not been fully characterized. Tetradecanoylphorbol Acetate 61-64 jun proto-oncogene Mus musculus 133-137 12527890-4 2003 Currently, little is known about whether EGFR or its tyrosine kinase is necessary for TPA-induced AP-1 activation. Tetradecanoylphorbol Acetate 86-89 jun proto-oncogene Mus musculus 98-102 12527890-6 2003 We demonstrated that the TPA or epidermal growth factor (EGF) induced AP-1 activation in the B82L cells that express wild-type EGFR, but not in the B82 cell, whereas autophosphorylation at tyrosine(1173) of EGFR in B82L cells was only induced by EGF, but not TPA. Tetradecanoylphorbol Acetate 25-28 jun proto-oncogene Mus musculus 70-74 12527890-7 2003 The expression of tyrosine kinase-deficient EGFR (mutation at Lys-721) (B82M721) resulted in deficiency of AP-1 induction in cellular response to EGF, while TPA treatment led to fully AP-1 activation. Tetradecanoylphorbol Acetate 157-160 jun proto-oncogene Mus musculus 184-188 12527890-9 2003 Based on these results, we conclude that TPA-induced AP-1 activation requires the basal level-EGFR protein, but not EGFR tyrosine kinase and EGFR autophosphorylation at tyrosine(1173), whereas both EGFR tyrosine kinase and EGFR autophosphorylation at Y(1173) play a critical role in EGF-induced AP-1 activation. Tetradecanoylphorbol Acetate 41-44 jun proto-oncogene Mus musculus 53-57 12527890-9 2003 Based on these results, we conclude that TPA-induced AP-1 activation requires the basal level-EGFR protein, but not EGFR tyrosine kinase and EGFR autophosphorylation at tyrosine(1173), whereas both EGFR tyrosine kinase and EGFR autophosphorylation at Y(1173) play a critical role in EGF-induced AP-1 activation. Tetradecanoylphorbol Acetate 41-44 jun proto-oncogene Mus musculus 295-299 12616721-3 2003 The DNA binding activity of AP-1 proteins to a concensus DNA regulatory binding element known as TRE (TPA Responsive Element) is used as an in vitro assay for AP-1 activity in the nucleus of skin cells. Tetradecanoylphorbol Acetate 102-105 jun proto-oncogene Mus musculus 28-32 12616721-3 2003 The DNA binding activity of AP-1 proteins to a concensus DNA regulatory binding element known as TRE (TPA Responsive Element) is used as an in vitro assay for AP-1 activity in the nucleus of skin cells. Tetradecanoylphorbol Acetate 102-105 jun proto-oncogene Mus musculus 159-163 12209884-3 2002 TPA-induced mitogen activated protein kinases (MAPK) phosphorylation, ornithine decarboxylase (ODC), c-Jun, and cyclooxygenase 2 (COX-2) protein expressions in a time-dependent manner, and the maximal inductive time point is at 1 h for MAPK phosphorylation and 6 h for others. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 101-106 12209884-4 2002 Flavanone, 2"-OH flavanone, 4"-OH flavanone, 6-OH flavanone showed the dose-dependent inhibition on TPA-stimulated MAPK phosphorylation, COX-2, ODC, c-Jun protein expressions. Tetradecanoylphorbol Acetate 100-103 jun proto-oncogene Mus musculus 149-154 12209884-7 2002 And, PD98059, a specific inhibitor of ERKs, inhibited TPA-induced MAPK phosphorylation, accompanied by decreasing COX-2, c-Jun, and ODC protein expression, and showed dose-dependent inhibition on TPA-induced proliferation in cells. Tetradecanoylphorbol Acetate 54-57 jun proto-oncogene Mus musculus 121-126 12209884-8 2002 These results demonstrated that PGE(2) is an important mediator in TPA-induced proliferation, and MAPK phosphorylation was located at the upstream of COX-2, c-Jun, and ODC gene expressions in TPA-induced responses. Tetradecanoylphorbol Acetate 192-195 jun proto-oncogene Mus musculus 157-162 12209884-9 2002 Furthermore, flavanone, 2"-OH flavanone, 4"-OH flavanone, 6-OH flavanone (100 microM) suppressed TPA-induced colony formation associated with blocking MAPK phosphorylation, ODC, c-Jun, and COX-2 proteins expression. Tetradecanoylphorbol Acetate 97-100 jun proto-oncogene Mus musculus 178-183 12204819-9 2002 These findings suggest that the signaling pathway leading to the activation of ERK, TCF, and AP-1 proteins constitutes a major factor determining the risk of tumor promotion by TPA or EGF. Tetradecanoylphorbol Acetate 177-180 jun proto-oncogene Mus musculus 93-97 12115530-7 2002 Moreover, DA-9601 abrogated the TPA-mediated activation of NF-kappa B/Rel and AP-1 in mouse epidermis. Tetradecanoylphorbol Acetate 32-35 jun proto-oncogene Mus musculus 78-82 12101411-6 2002 A marked delay in TPA-induced intracellular translocation and downregulation of PKC alpha was observed in TNF-alpha(-/-) epidermis, which correlated with the deregulated TPA-induced AP-1 activation and c-Jun expression. Tetradecanoylphorbol Acetate 18-21 jun proto-oncogene Mus musculus 202-207 12112313-3 2002 Expression of dominant-negative c-jun (TAM67) in the mouse skin protects mice from 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced papillomagenesis without blocking mitogen-induced hyperproliferation. Tetradecanoylphorbol Acetate 121-157 jun proto-oncogene Mus musculus 32-37 12112313-3 2002 Expression of dominant-negative c-jun (TAM67) in the mouse skin protects mice from 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced papillomagenesis without blocking mitogen-induced hyperproliferation. Tetradecanoylphorbol Acetate 159-162 jun proto-oncogene Mus musculus 32-37 10754199-5 2000 In mouse fibroblast cells, momordin I suppressed the AP-1 activity induced by phorbol 12-myristate 13-acetate (PMA), as well as blocked the de novo synthesis of AP-1 protein. Tetradecanoylphorbol Acetate 78-109 jun proto-oncogene Mus musculus 53-57 11532864-1 2001 The aim of this study was to determine the effects of 40% dietary energy restriction (DER) relative to ad libitum feeding on AP-1-DNA binding and expression of c-Jun protein and c-jun mRNA in SENCAR mouse skin treated with acetone or 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 234-270 jun proto-oncogene Mus musculus 160-165 11532864-1 2001 The aim of this study was to determine the effects of 40% dietary energy restriction (DER) relative to ad libitum feeding on AP-1-DNA binding and expression of c-Jun protein and c-jun mRNA in SENCAR mouse skin treated with acetone or 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 272-275 jun proto-oncogene Mus musculus 160-165 11532864-3 2001 AP-1-DNA binding, measured by electrophoretic mobility shift assay, showed that TPA treatment for 4 h increased AP-1-DNA binding by 2-fold over acetone controls (P < 0.05) and that DER reduced basal and TPA-induced AP-1-DNA binding in comparison with ad libitum fed groups in sham-operated mice (P < 0.05). Tetradecanoylphorbol Acetate 80-83 jun proto-oncogene Mus musculus 0-4 11532864-3 2001 AP-1-DNA binding, measured by electrophoretic mobility shift assay, showed that TPA treatment for 4 h increased AP-1-DNA binding by 2-fold over acetone controls (P < 0.05) and that DER reduced basal and TPA-induced AP-1-DNA binding in comparison with ad libitum fed groups in sham-operated mice (P < 0.05). Tetradecanoylphorbol Acetate 80-83 jun proto-oncogene Mus musculus 112-116 11532864-3 2001 AP-1-DNA binding, measured by electrophoretic mobility shift assay, showed that TPA treatment for 4 h increased AP-1-DNA binding by 2-fold over acetone controls (P < 0.05) and that DER reduced basal and TPA-induced AP-1-DNA binding in comparison with ad libitum fed groups in sham-operated mice (P < 0.05). Tetradecanoylphorbol Acetate 80-83 jun proto-oncogene Mus musculus 112-116 11532864-3 2001 AP-1-DNA binding, measured by electrophoretic mobility shift assay, showed that TPA treatment for 4 h increased AP-1-DNA binding by 2-fold over acetone controls (P < 0.05) and that DER reduced basal and TPA-induced AP-1-DNA binding in comparison with ad libitum fed groups in sham-operated mice (P < 0.05). Tetradecanoylphorbol Acetate 206-209 jun proto-oncogene Mus musculus 0-4 11532864-4 2001 TPA treatment increased c-Jun protein levels in control fed mice (4-fold) and in DER mice (2-fold) over basal levels 4 h post-treatment (P < 0.05). Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 24-29 11532864-6 2001 TPA induction of c-jun mRNA was also reduced by DER compared with ad libitum fed mice (P < 0.05). Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 17-22 11358830-0 2001 Organ-specific activation of activator protein-1 in transgenic mice by 12-o-tetradecanoylphorbol-13-acetate with different administration methods. Tetradecanoylphorbol Acetate 71-107 jun proto-oncogene Mus musculus 29-48 11358830-5 2001 injection), we analyzed TPA-stimulated activator protein-1 (AP-1) activity in various organs (liver, kidney, brain, lung, spleen, heart, stomach, colon, esophagus, and skin) from transgenic mice expressing the AP-1 luciferase reporter gene. Tetradecanoylphorbol Acetate 24-27 jun proto-oncogene Mus musculus 39-58 11358830-5 2001 injection), we analyzed TPA-stimulated activator protein-1 (AP-1) activity in various organs (liver, kidney, brain, lung, spleen, heart, stomach, colon, esophagus, and skin) from transgenic mice expressing the AP-1 luciferase reporter gene. Tetradecanoylphorbol Acetate 24-27 jun proto-oncogene Mus musculus 60-64 11358830-6 2001 Topical application of TPA by painting the skin on the back of mice raised AP-1 activity 122.6-fold, and the highest peak of AP-1 activity was at 12 h after administration of TPA. Tetradecanoylphorbol Acetate 23-26 jun proto-oncogene Mus musculus 75-79 11358830-6 2001 Topical application of TPA by painting the skin on the back of mice raised AP-1 activity 122.6-fold, and the highest peak of AP-1 activity was at 12 h after administration of TPA. Tetradecanoylphorbol Acetate 23-26 jun proto-oncogene Mus musculus 125-129 11358830-6 2001 Topical application of TPA by painting the skin on the back of mice raised AP-1 activity 122.6-fold, and the highest peak of AP-1 activity was at 12 h after administration of TPA. Tetradecanoylphorbol Acetate 175-178 jun proto-oncogene Mus musculus 125-129 11358830-7 2001 Drinking water containing TPA caused a 25.8-fold induction of AP-1 activity in the skin, whereas gavage feeding with TPA caused a 34.2-fold induction of AP-1 in the skin. Tetradecanoylphorbol Acetate 26-29 jun proto-oncogene Mus musculus 62-66 11358830-7 2001 Drinking water containing TPA caused a 25.8-fold induction of AP-1 activity in the skin, whereas gavage feeding with TPA caused a 34.2-fold induction of AP-1 in the skin. Tetradecanoylphorbol Acetate 117-120 jun proto-oncogene Mus musculus 153-157 11358830-9 2001 injection of TPA induced a 49.56-fold or 20.4-fold increase in AP-1 activity in the skin, respectively. Tetradecanoylphorbol Acetate 13-16 jun proto-oncogene Mus musculus 63-67 11358830-10 2001 The highest peaks of AP-1 activity in the skin were at 12 h after drinking, feeding, or injection of TPA. Tetradecanoylphorbol Acetate 101-104 jun proto-oncogene Mus musculus 21-25 11358830-12 2001 injection of TPA raised AP-1 activity 13.9-fold, drinking TPA raised AP-1 activity 8.4-fold, and painting with TPA caused a 2.4-fold induction of AP-1 activity. Tetradecanoylphorbol Acetate 13-16 jun proto-oncogene Mus musculus 24-28 11358830-12 2001 injection of TPA raised AP-1 activity 13.9-fold, drinking TPA raised AP-1 activity 8.4-fold, and painting with TPA caused a 2.4-fold induction of AP-1 activity. Tetradecanoylphorbol Acetate 58-61 jun proto-oncogene Mus musculus 69-73 11358830-12 2001 injection of TPA raised AP-1 activity 13.9-fold, drinking TPA raised AP-1 activity 8.4-fold, and painting with TPA caused a 2.4-fold induction of AP-1 activity. Tetradecanoylphorbol Acetate 58-61 jun proto-oncogene Mus musculus 69-73 11358830-12 2001 injection of TPA raised AP-1 activity 13.9-fold, drinking TPA raised AP-1 activity 8.4-fold, and painting with TPA caused a 2.4-fold induction of AP-1 activity. Tetradecanoylphorbol Acetate 58-61 jun proto-oncogene Mus musculus 69-73 11358830-12 2001 injection of TPA raised AP-1 activity 13.9-fold, drinking TPA raised AP-1 activity 8.4-fold, and painting with TPA caused a 2.4-fold induction of AP-1 activity. Tetradecanoylphorbol Acetate 58-61 jun proto-oncogene Mus musculus 69-73 11358830-14 2001 injection of TPA raised AP-1 activity 3.9-fold, drinking TPA induced a 1.2-fold increase in AP-1 activity, but painting with TPA had no effect. Tetradecanoylphorbol Acetate 13-16 jun proto-oncogene Mus musculus 24-28 11358830-14 2001 injection of TPA raised AP-1 activity 3.9-fold, drinking TPA induced a 1.2-fold increase in AP-1 activity, but painting with TPA had no effect. Tetradecanoylphorbol Acetate 57-60 jun proto-oncogene Mus musculus 92-96 11358830-14 2001 injection of TPA raised AP-1 activity 3.9-fold, drinking TPA induced a 1.2-fold increase in AP-1 activity, but painting with TPA had no effect. Tetradecanoylphorbol Acetate 57-60 jun proto-oncogene Mus musculus 92-96 11358830-20 2001 These results indicate that the skin is the most sensitive organ to TPA induction of AP-1 activity. Tetradecanoylphorbol Acetate 68-71 jun proto-oncogene Mus musculus 85-89 11358830-21 2001 The data suggest that the organ-specific, tumor-promoting effect of TPA may be through AP-1 activation and phosphorylation of ERKs and p38 kinase. Tetradecanoylphorbol Acetate 68-71 jun proto-oncogene Mus musculus 87-91 12032821-3 2002 In the present study, we report that reduction of MnSOD by heterozygous knockout of the MnSOD gene (Sod2 -/+, MnSOD KO) increased the levels of oxidative damage proteins and the activity of AP-1 following TPA treatment. Tetradecanoylphorbol Acetate 205-208 jun proto-oncogene Mus musculus 190-194 12032821-12 2002 Taken together, these results suggest that: (1) MnSOD deficiency enhanced TPA-induced oxidative stress and AP-1 and p53 levels, consistent with the increase in both proliferation and apoptosis events in the MnSOD KO mice, and (2) increased apoptosis may negate increased proliferation in the MnSOD deficient mice during an early stage of tumor development. Tetradecanoylphorbol Acetate 74-77 jun proto-oncogene Mus musculus 107-111 12058867-6 2002 1alpha25(OH)2D3 interfered with RA inhibition of the TPA-response element binding activity of AP-1 in the cytokine-treated cells. Tetradecanoylphorbol Acetate 53-56 jun proto-oncogene Mus musculus 94-98 11507057-6 2001 TPA increased activator protein-1 (AP-1) binding activity within 6 h in nontransgenic mice, but increased AP-1 binding activity was delayed in the transgenic mice. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 14-33 11507057-6 2001 TPA increased activator protein-1 (AP-1) binding activity within 6 h in nontransgenic mice, but increased AP-1 binding activity was delayed in the transgenic mice. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 35-39 11285196-1 2001 Ongoing studies in our laboratory have demonstrated that dietary energy restriction (DER) inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 transcription factor binding to DNA in the epidermis of SENCAR mice. Tetradecanoylphorbol Acetate 100-136 jun proto-oncogene Mus musculus 151-155 11285196-1 2001 Ongoing studies in our laboratory have demonstrated that dietary energy restriction (DER) inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 transcription factor binding to DNA in the epidermis of SENCAR mice. Tetradecanoylphorbol Acetate 138-141 jun proto-oncogene Mus musculus 151-155 11285196-12 2001 Taken together, our results indicated for the first time that DER blocked the TPA stimulation of ERK activity and suggested that the inhibition of TPA-induced AP-1 activity by DER is likely through inhibition of ERK but not JNK or p38 kinase pathway. Tetradecanoylphorbol Acetate 78-81 jun proto-oncogene Mus musculus 159-163 11285196-12 2001 Taken together, our results indicated for the first time that DER blocked the TPA stimulation of ERK activity and suggested that the inhibition of TPA-induced AP-1 activity by DER is likely through inhibition of ERK but not JNK or p38 kinase pathway. Tetradecanoylphorbol Acetate 147-150 jun proto-oncogene Mus musculus 159-163 11231886-4 2001 Topical application of curcumin was reported to inhibit TPA-induced c-fos, c-jun and c-myc gene expression in mouse skin. Tetradecanoylphorbol Acetate 56-59 jun proto-oncogene Mus musculus 75-80 11231886-8 2001 CONCLUSIONS: Whereas earlier work demonstrated that topical application of curcumin to mouse skin inhibited TPA-induced expression of c-fos, c-jun and c-myc oncogenes, our results are the first to show that orally consumed curcumin significantly inhibited DMBA- and TPA-induced ras and fos gene expression in mouse skin. Tetradecanoylphorbol Acetate 108-111 jun proto-oncogene Mus musculus 141-146 10842315-1 2000 The tumor promoter phorbol 13-myristate 12-acetate (PMA), the best characterized protein kinase C agonist, frequently regulates gene expression via activation of Fos/Jun (AP-1) complexes. Tetradecanoylphorbol Acetate 52-55 jun proto-oncogene Mus musculus 171-175 10754199-5 2000 In mouse fibroblast cells, momordin I suppressed the AP-1 activity induced by phorbol 12-myristate 13-acetate (PMA), as well as blocked the de novo synthesis of AP-1 protein. Tetradecanoylphorbol Acetate 111-114 jun proto-oncogene Mus musculus 53-57 10737590-2 2000 Treatment of NG108-15 cells with TPA (100 nM) for 48 h increased delta-opioid receptor mRNA levels, whereas different concentrations of forskolin induced a transient down-regulation of mRNA 5 h after treatment, followed by increased mRNA levels after 48 h. Reporter gene assays in transiently transfected NG108-15 cells in combination with electrophoretic mobility shift assays indicate that the increase of delta-opioid receptor mRNA after stimulation with TPA is mediated by transcription factor AP-1, which binds 355 bp upstream of the start codon within the gene promoter. Tetradecanoylphorbol Acetate 33-36 jun proto-oncogene Mus musculus 498-502 10662601-4 2000 Electrophoretic mobility shift assay (EMSA) revealed that VT modulated AP-1 binding activity in a concentration- and time-dependent manner when using a synchronous model in which VT was added concurrently with phorbol 12-myristate 13-acetate (PMA) and ionomycin (ION) to EL-4 cells. Tetradecanoylphorbol Acetate 210-241 jun proto-oncogene Mus musculus 71-75 10662601-4 2000 Electrophoretic mobility shift assay (EMSA) revealed that VT modulated AP-1 binding activity in a concentration- and time-dependent manner when using a synchronous model in which VT was added concurrently with phorbol 12-myristate 13-acetate (PMA) and ionomycin (ION) to EL-4 cells. Tetradecanoylphorbol Acetate 243-246 jun proto-oncogene Mus musculus 71-75 10200990-4 1999 METHODS: We measured type I collagen synthesis in murine mesangial cells exposed to estradiol, phorbol 12-myristate 13-acetate (an activator of AP-1), or curcumin (an inhibitor of AP-1). Tetradecanoylphorbol Acetate 95-126 jun proto-oncogene Mus musculus 144-148 11216470-6 2000 In the present study, we found that topical application of TPA onto dorsal skin of female ICR mice resulted in marked activation of epidermal NF-kappaB and AP-1. Tetradecanoylphorbol Acetate 59-62 jun proto-oncogene Mus musculus 156-160 10563991-7 1999 We also analyzed the AP-1 binding activity by electrophoretic mobility shift assay and c-Jun gene expression by northern blot and western blot, the results showed that TF-3 is the most potent inhibitor on TPA-induced AP-1 binding activity and c-Jun gene expression among these five tea polyphenols. Tetradecanoylphorbol Acetate 205-208 jun proto-oncogene Mus musculus 87-92 10563991-7 1999 We also analyzed the AP-1 binding activity by electrophoretic mobility shift assay and c-Jun gene expression by northern blot and western blot, the results showed that TF-3 is the most potent inhibitor on TPA-induced AP-1 binding activity and c-Jun gene expression among these five tea polyphenols. Tetradecanoylphorbol Acetate 205-208 jun proto-oncogene Mus musculus 217-221 10563991-7 1999 We also analyzed the AP-1 binding activity by electrophoretic mobility shift assay and c-Jun gene expression by northern blot and western blot, the results showed that TF-3 is the most potent inhibitor on TPA-induced AP-1 binding activity and c-Jun gene expression among these five tea polyphenols. Tetradecanoylphorbol Acetate 205-208 jun proto-oncogene Mus musculus 243-248 10535756-1 1999 The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) can induce expression of many immediate-early genes, such as c-fos and c-jun. Tetradecanoylphorbol Acetate 19-55 jun proto-oncogene Mus musculus 133-138 10535756-1 1999 The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) can induce expression of many immediate-early genes, such as c-fos and c-jun. Tetradecanoylphorbol Acetate 57-60 jun proto-oncogene Mus musculus 133-138 10523861-1 1999 Activator protein 1 (AP-1) transactivation and ornithine decarboxylase (ODC) activity have been established as essential downstream effectors of mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 175-211 jun proto-oncogene Mus musculus 0-19 10523861-1 1999 Activator protein 1 (AP-1) transactivation and ornithine decarboxylase (ODC) activity have been established as essential downstream effectors of mouse skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 175-211 jun proto-oncogene Mus musculus 21-25 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 25-61 jun proto-oncogene Mus musculus 123-127 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 25-61 jun proto-oncogene Mus musculus 152-156 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 25-61 jun proto-oncogene Mus musculus 152-156 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 63-66 jun proto-oncogene Mus musculus 123-127 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 63-66 jun proto-oncogene Mus musculus 152-156 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 63-66 jun proto-oncogene Mus musculus 152-156 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 68-104 jun proto-oncogene Mus musculus 123-127 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 68-104 jun proto-oncogene Mus musculus 152-156 10449779-6 1999 TAM67 expression blocked 12-O-tetradecanoylphorbol 13-acetate (TPA, phorbol 12-tetradecanoate 13-acetate) induction of the AP-1-regulated luciferase in AP-1 luciferase/TAM67 mice, but did not inhibit induction of candidate AP-1 target genes, collagenase-1 or stromelysin-3. Tetradecanoylphorbol Acetate 68-104 jun proto-oncogene Mus musculus 152-156 10064335-6 1999 Induction of AP-1 by the phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is essential to tumor promotion. Tetradecanoylphorbol Acetate 54-90 jun proto-oncogene Mus musculus 13-17 10064335-6 1999 Induction of AP-1 by the phorbol ester tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is essential to tumor promotion. Tetradecanoylphorbol Acetate 92-95 jun proto-oncogene Mus musculus 13-17 10064335-12 1999 We propose that this results in attenuation in the induction of the AP-1 transcription factor by TPA. Tetradecanoylphorbol Acetate 97-100 jun proto-oncogene Mus musculus 68-72 10064335-13 1999 Because AP-1 induction by TPA is obligatory for mouse skin promotion, we propose this as an essential component of the mechanism of DER prevention of mouse skin carcinogenesis. Tetradecanoylphorbol Acetate 26-29 jun proto-oncogene Mus musculus 8-12 9891065-10 1999 Furthermore, TPA treatment of serum-starved NIH 3T3 cells led to phosphorylation of SEK1, and constitutively active mutants of PKC-alpha and PKC-epsilon activated the transactivation domain of c-Jun, a major substrate of JNK. Tetradecanoylphorbol Acetate 13-16 jun proto-oncogene Mus musculus 193-198 9873060-1 1999 Previously, we reported that in papilloma-producing 308 mouse keratinocytes, the tumor promoter okadaic acid, a serine-threonine phosphatase inhibitor, increased binding of activator protein 1 (AP-1) to a consensus 12-O-tetradecanoylphorbol-13-acetate-responsive element (Rosenberger, S. F., and Bowden, G. T. (1996) Oncogene 12, 2301-2308). Tetradecanoylphorbol Acetate 215-251 jun proto-oncogene Mus musculus 173-192 9873060-1 1999 Previously, we reported that in papilloma-producing 308 mouse keratinocytes, the tumor promoter okadaic acid, a serine-threonine phosphatase inhibitor, increased binding of activator protein 1 (AP-1) to a consensus 12-O-tetradecanoylphorbol-13-acetate-responsive element (Rosenberger, S. F., and Bowden, G. T. (1996) Oncogene 12, 2301-2308). Tetradecanoylphorbol Acetate 215-251 jun proto-oncogene Mus musculus 194-198 10381133-3 1998 TPA treatment also elevates the expression of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), c-myc, c-fos, c-jun, transforming growth factor-beta1 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha). Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 112-117 10370867-9 1999 As judged by the reverse transcriptase-polymerase chain reaction, resveratrol selectively inhibited TPA-induced expression of c-fos and transforming growth factor-beta 1 (TGF-beta 1), but did not affect other TPA-induced gene products including COX-1, COX-2, c-myc, c-jun, and tumor necrosis factor-alpha. Tetradecanoylphorbol Acetate 100-103 jun proto-oncogene Mus musculus 266-271 9886845-2 1999 A luciferase reporter gene was constructed downstream from either a promoter for the mouse vas deferens protein, or a trimerized 12-O-tetradecanoyl phorbol-13-acetate-response element site whose transcriptions are activated by androgen and 12-O-tetradecanoyl phorbol-13-acetate, a potent AP-1 activator. Tetradecanoylphorbol Acetate 129-166 jun proto-oncogene Mus musculus 288-292 9315102-2 1997 Here, we have analysed AP-1 transcriptional activity in mouse keratinocytes treated with calcium and 12-O-tetradecanoyl phorbol-13-acetate (TPA), two agents that induce terminal differentiation of keratinocytes with different phenotypic consequences. Tetradecanoylphorbol Acetate 101-138 jun proto-oncogene Mus musculus 23-27 9703914-5 1998 In fact, in the high metastatic BL6 cells the long-term treatment for 24 hours with TPA, with no c-PKC activation or the inhibition with Go6976 as well as with BIM, induced an increased NF-kB and AP1 DNA-binding activity. Tetradecanoylphorbol Acetate 84-87 jun proto-oncogene Mus musculus 196-199 9703914-6 1998 In contrast, in the low metastatic B16F1 cells the short-term treatment with TPA, induced the activation of c-PKCs isoforms, and enhanced NF-kB and AP1 DNA-binding activity. Tetradecanoylphorbol Acetate 77-80 jun proto-oncogene Mus musculus 148-151 9315102-2 1997 Here, we have analysed AP-1 transcriptional activity in mouse keratinocytes treated with calcium and 12-O-tetradecanoyl phorbol-13-acetate (TPA), two agents that induce terminal differentiation of keratinocytes with different phenotypic consequences. Tetradecanoylphorbol Acetate 140-143 jun proto-oncogene Mus musculus 23-27 9315102-5 1997 In contrast, AP-1 reporter activity was increased in keratinocytes treated with TPA. Tetradecanoylphorbol Acetate 80-83 jun proto-oncogene Mus musculus 13-17 9315102-7 1997 Analysis of AP-1 protein expression in calcium- and TPA-treated keratinocytes demonstrated that only TPA increased the expression of c-Jun, while Jun B and Jun D were induced by both of these agents. Tetradecanoylphorbol Acetate 101-104 jun proto-oncogene Mus musculus 133-138 9270030-8 1997 Supershift electrophoresis mobility shift assay revealed that Jun B and c-Jun were absent from the AP-1/DNA complex following TNF-alpha but present following TPA treatment. Tetradecanoylphorbol Acetate 158-161 jun proto-oncogene Mus musculus 72-77 9254887-4 1997 Cotransfection of K14TAM67 with luciferase plasmid reporter DNAs produced inhibition of basal and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 and NF kappa B activity but had no effect on p53-dependent transcriptional activity. Tetradecanoylphorbol Acetate 98-134 jun proto-oncogene Mus musculus 149-153 9254887-4 1997 Cotransfection of K14TAM67 with luciferase plasmid reporter DNAs produced inhibition of basal and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 and NF kappa B activity but had no effect on p53-dependent transcriptional activity. Tetradecanoylphorbol Acetate 136-139 jun proto-oncogene Mus musculus 149-153 9159159-5 1997 The results showed that the SR11302, an AP-1 inhibition-specific retinoid, and other AP-1 inhibitors such as trans-retinoic acid and fluocinolone acetonide, markedly inhibit both 12-O-tetradecanoylphorbol-13-acetate-induced papilloma formation and AP-1 activation in 7,12-dimethyl benz(a)anthracene-initiated mouse skin (P < 0.05). Tetradecanoylphorbol Acetate 179-215 jun proto-oncogene Mus musculus 40-44 9159159-5 1997 The results showed that the SR11302, an AP-1 inhibition-specific retinoid, and other AP-1 inhibitors such as trans-retinoic acid and fluocinolone acetonide, markedly inhibit both 12-O-tetradecanoylphorbol-13-acetate-induced papilloma formation and AP-1 activation in 7,12-dimethyl benz(a)anthracene-initiated mouse skin (P < 0.05). Tetradecanoylphorbol Acetate 179-215 jun proto-oncogene Mus musculus 85-89 9159159-5 1997 The results showed that the SR11302, an AP-1 inhibition-specific retinoid, and other AP-1 inhibitors such as trans-retinoic acid and fluocinolone acetonide, markedly inhibit both 12-O-tetradecanoylphorbol-13-acetate-induced papilloma formation and AP-1 activation in 7,12-dimethyl benz(a)anthracene-initiated mouse skin (P < 0.05). Tetradecanoylphorbol Acetate 179-215 jun proto-oncogene Mus musculus 85-89 9254887-6 1997 This suggests that blocking TPA-induced AP-1- or NF kappa B-regulated gene expression by TAM67 inhibits TPA-induced progression. Tetradecanoylphorbol Acetate 28-31 jun proto-oncogene Mus musculus 40-44 9254887-6 1997 This suggests that blocking TPA-induced AP-1- or NF kappa B-regulated gene expression by TAM67 inhibits TPA-induced progression. Tetradecanoylphorbol Acetate 104-107 jun proto-oncogene Mus musculus 40-44 9254887-10 1997 These results suggest that the action of the dominant negative jun mutant on AP-1 and NF kappa B gene regulation results in complex alterations in the levels of downstream effector genes, such as the metalloproteinases, that effect TPA-induced cellular invasion. Tetradecanoylphorbol Acetate 232-235 jun proto-oncogene Mus musculus 77-81 9591190-4 1997 It also reduces 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced increases in skin inflammation, epidermal DNA synthesis, ornithine decarboxylase (ODC) mRNA level, ODC activity, hyperplasia, formation of c-Fos, and c-Jun proteins, hydrogen peroxide, and the oxidized DNA base 5-hydroxymethyl-2"-deoxyuridine (HmdU). Tetradecanoylphorbol Acetate 16-52 jun proto-oncogene Mus musculus 217-222 9591190-4 1997 It also reduces 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced increases in skin inflammation, epidermal DNA synthesis, ornithine decarboxylase (ODC) mRNA level, ODC activity, hyperplasia, formation of c-Fos, and c-Jun proteins, hydrogen peroxide, and the oxidized DNA base 5-hydroxymethyl-2"-deoxyuridine (HmdU). Tetradecanoylphorbol Acetate 54-57 jun proto-oncogene Mus musculus 217-222 9022811-3 1997 AP-1 DNA binding to the jun 12-O-tetradecanoylphorbol-13-acetate-response element (TGACATCA) as determined by gel shift analysis was strongly induced by OA (100 ng/mL) at 6 and 12 h. Preincubation of nuclear extracts with anti-c-jun antibody demonstrated that c-jun was a major component of the DNA-bound AP-1 complex induced by OA in 308 cells. Tetradecanoylphorbol Acetate 28-64 jun proto-oncogene Mus musculus 0-4 9022811-3 1997 AP-1 DNA binding to the jun 12-O-tetradecanoylphorbol-13-acetate-response element (TGACATCA) as determined by gel shift analysis was strongly induced by OA (100 ng/mL) at 6 and 12 h. Preincubation of nuclear extracts with anti-c-jun antibody demonstrated that c-jun was a major component of the DNA-bound AP-1 complex induced by OA in 308 cells. Tetradecanoylphorbol Acetate 28-64 jun proto-oncogene Mus musculus 227-232 9022811-3 1997 AP-1 DNA binding to the jun 12-O-tetradecanoylphorbol-13-acetate-response element (TGACATCA) as determined by gel shift analysis was strongly induced by OA (100 ng/mL) at 6 and 12 h. Preincubation of nuclear extracts with anti-c-jun antibody demonstrated that c-jun was a major component of the DNA-bound AP-1 complex induced by OA in 308 cells. Tetradecanoylphorbol Acetate 28-64 jun proto-oncogene Mus musculus 260-265 9022811-3 1997 AP-1 DNA binding to the jun 12-O-tetradecanoylphorbol-13-acetate-response element (TGACATCA) as determined by gel shift analysis was strongly induced by OA (100 ng/mL) at 6 and 12 h. Preincubation of nuclear extracts with anti-c-jun antibody demonstrated that c-jun was a major component of the DNA-bound AP-1 complex induced by OA in 308 cells. Tetradecanoylphorbol Acetate 28-64 jun proto-oncogene Mus musculus 305-309 9290125-6 1997 In addition to PKC activation, active oxygen species production, and c-jun induction, our data suggest that TPA treatment induces cellular transformation by other unknown routes, because some tested compounds have an inhibitory effect on TPA-induced transformation but have no or a slight inhibitory effect on PKC activation, active oxygen species production, and c-jun induction. Tetradecanoylphorbol Acetate 108-111 jun proto-oncogene Mus musculus 69-74 9290125-6 1997 In addition to PKC activation, active oxygen species production, and c-jun induction, our data suggest that TPA treatment induces cellular transformation by other unknown routes, because some tested compounds have an inhibitory effect on TPA-induced transformation but have no or a slight inhibitory effect on PKC activation, active oxygen species production, and c-jun induction. Tetradecanoylphorbol Acetate 108-111 jun proto-oncogene Mus musculus 364-369 8989917-6 1996 Suppression of TPA (100 ng/mL)-induced c-jun and c-fos gene expression was also observed in the mouse fibroblast cells pretreated with crocetin (30, 60, and 120 microM). Tetradecanoylphorbol Acetate 15-18 jun proto-oncogene Mus musculus 39-44 21594328-1 1996 The effects of genistein, a soybean isoflavone, on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced expression of c-fos and c-jun in CD-1 mouse skin have been investigated. Tetradecanoylphorbol Acetate 51-88 jun proto-oncogene Mus musculus 127-132 8969886-8 1996 PMA, on the other hand, induces equally well c-fos, c-jun and c-myc. Tetradecanoylphorbol Acetate 0-3 jun proto-oncogene Mus musculus 52-57 8625496-2 1996 Although numerous works have extensively investigated the induction mechanisms of c-jun by UV, hydrogen peroxide or 12-O-tetradecanoylphorbol-13-acetate, the mechanism induced by alkylating agents has received little attention. Tetradecanoylphorbol Acetate 116-152 jun proto-oncogene Mus musculus 82-87 8695223-6 1996 Treatment of NIH 3T3 cells with 100 ng/ml TPA and 10, 50 and 100 microM apigenin resulted in 50, 80 and 100% suppression of TPA-induced C-JUN expression, respectively. Tetradecanoylphorbol Acetate 42-45 jun proto-oncogene Mus musculus 136-141 8695223-6 1996 Treatment of NIH 3T3 cells with 100 ng/ml TPA and 10, 50 and 100 microM apigenin resulted in 50, 80 and 100% suppression of TPA-induced C-JUN expression, respectively. Tetradecanoylphorbol Acetate 124-127 jun proto-oncogene Mus musculus 136-141 8649769-2 1996 Okadaic acid increased AP-1 binding to a consensus TPA responsive element (TRE) within 2 h; maximum stimulation was observed at 6 h followed by a gradual decrease to basal levels within 24 h. Jun B, Jun D and Fos B proteins were identified as the major components of the AP-1 complex binding to the TRE element at 6 h. Inhibition of transcription with actinomycin D and inhibition of protein synthesis with cycloheximide abrogated the okadaic acid effect on AP-1 DNA binding, indicating that transcription and translation are required for okadaic acid increased TRE binding activity. Tetradecanoylphorbol Acetate 51-54 jun proto-oncogene Mus musculus 23-27 8622882-7 1996 Gel shift assays demonstrated the mobility pattern of TPA-responsive element (TRE) binding complex with AP-1 derived from H-ras transfectants migrated faster than those from Balb-Neo1, v-myc and H-ras/v-myc. Tetradecanoylphorbol Acetate 54-57 jun proto-oncogene Mus musculus 104-108 21594328-1 1996 The effects of genistein, a soybean isoflavone, on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced expression of c-fos and c-jun in CD-1 mouse skin have been investigated. Tetradecanoylphorbol Acetate 90-93 jun proto-oncogene Mus musculus 127-132 21594328-2 1996 A promoting dose (8.5 mu mol) of TPA significantly increases transcript levels of c-fos, and 2.7 and 3.2 kb c-jun mRNA in mouse skin by 7.0-, 3.2-, and 1.7-fold, respectively. Tetradecanoylphorbol Acetate 33-36 jun proto-oncogene Mus musculus 108-113 21594328-5 1996 Genistein exhibited only a weak suppressive effect on TPA-induced c-jun mRNA expression. Tetradecanoylphorbol Acetate 54-57 jun proto-oncogene Mus musculus 66-71 7579389-5 1995 Downregulation of protein kinase C (PKC) by chronic exposure of stromal cells to the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 400 nmol/L) did not effect c-jun expression induced by arachidonate. Tetradecanoylphorbol Acetate 138-141 jun proto-oncogene Mus musculus 170-175 7579389-6 1995 Moreover, pretreatment of cells with the PKC inhibitor, calphostin C (1 mumol/L), caused a marked decrease of c-jun expression induced by TPA, but had no influence on c-jun expression induced by arachidonate. Tetradecanoylphorbol Acetate 138-141 jun proto-oncogene Mus musculus 110-115 21552848-5 1995 Enhancement of AP-1 activity by TPA increased the formation of anchorage independent colonies by tumorigenic RT101 cells. Tetradecanoylphorbol Acetate 32-35 jun proto-oncogene Mus musculus 15-19 7553596-2 1995 The c-Fos protein is inducible by TPA and thus is associated with c-Jun to result in an increased AP-1 activity in mouse fibroblast cells. Tetradecanoylphorbol Acetate 34-37 jun proto-oncogene Mus musculus 66-71 8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tetradecanoylphorbol Acetate 57-93 jun proto-oncogene Mus musculus 26-45 7602115-8 1995 Curcumin markedly inhibited AP-1 binding activity to 12-tetradecanoyl phorbol-13-acetate-responsive element (TRE) in the cytokine-treated cells. Tetradecanoylphorbol Acetate 53-88 jun proto-oncogene Mus musculus 28-32 7954373-0 1994 Curcumin inhibits TPA induced expression of c-fos, c-jun and c-myc proto-oncogenes messenger RNAs in mouse skin. Tetradecanoylphorbol Acetate 18-21 jun proto-oncogene Mus musculus 51-56 7954373-7 1994 In the present studies, we investigated the effect of curcumin on the expression of c-fos, c-jun and c-myc oncogenes in TPA-treated mouse skin in CD-1 mice. Tetradecanoylphorbol Acetate 120-123 jun proto-oncogene Mus musculus 91-96 7954373-8 1994 A 30-nmol dose of TPA increased the levels of mRNAs for c-fos, c-jun and c-myc oncogenes by 2-3-fold compared with control. Tetradecanoylphorbol Acetate 18-21 jun proto-oncogene Mus musculus 63-68 7954373-11 1994 A dose of 10 mumol of curcumin was found to inhibit 90% TPA-induced expression of c-fos and c-jun, and 60% of c-myc. Tetradecanoylphorbol Acetate 56-59 jun proto-oncogene Mus musculus 92-97 7869421-3 1994 The exposure to MC and/or PMA caused a rapid increase in c-fos mRNA content, which was immediately followed by an increase in c-jun mRNA, prior to NGF mRNA elevation. Tetradecanoylphorbol Acetate 26-29 jun proto-oncogene Mus musculus 126-131 7955078-9 1994 Topical application of 5 nmol TPA to the backs of CD-1 mice once a day for 5 days caused epidermal hyperplasia and the levels of c-Jun were increased in the suprabasal layer of the epidermis and in the muscle layer of the dermis. Tetradecanoylphorbol Acetate 30-33 jun proto-oncogene Mus musculus 129-134 7766308-1 1995 Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) induce neoplastic transformation, elevated c-jun protein expression, and activator protein-1 (AP-1)-dependent gene expression in JB6 mouse epidermal cells sensitive to tumor promoters (clone 415a P+ cells). Tetradecanoylphorbol Acetate 24-60 jun proto-oncogene Mus musculus 144-149 7766308-1 1995 Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) induce neoplastic transformation, elevated c-jun protein expression, and activator protein-1 (AP-1)-dependent gene expression in JB6 mouse epidermal cells sensitive to tumor promoters (clone 415a P+ cells). Tetradecanoylphorbol Acetate 24-60 jun proto-oncogene Mus musculus 174-193 7766308-1 1995 Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) induce neoplastic transformation, elevated c-jun protein expression, and activator protein-1 (AP-1)-dependent gene expression in JB6 mouse epidermal cells sensitive to tumor promoters (clone 415a P+ cells). Tetradecanoylphorbol Acetate 24-60 jun proto-oncogene Mus musculus 195-199 7766308-1 1995 Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) induce neoplastic transformation, elevated c-jun protein expression, and activator protein-1 (AP-1)-dependent gene expression in JB6 mouse epidermal cells sensitive to tumor promoters (clone 415a P+ cells). Tetradecanoylphorbol Acetate 62-65 jun proto-oncogene Mus musculus 144-149 7766308-1 1995 Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) induce neoplastic transformation, elevated c-jun protein expression, and activator protein-1 (AP-1)-dependent gene expression in JB6 mouse epidermal cells sensitive to tumor promoters (clone 415a P+ cells). Tetradecanoylphorbol Acetate 62-65 jun proto-oncogene Mus musculus 174-193 7766308-1 1995 Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) induce neoplastic transformation, elevated c-jun protein expression, and activator protein-1 (AP-1)-dependent gene expression in JB6 mouse epidermal cells sensitive to tumor promoters (clone 415a P+ cells). Tetradecanoylphorbol Acetate 62-65 jun proto-oncogene Mus musculus 195-199 7829270-4 1995 Both DNFB and TPA caused marked induction of ODC, c-fos and c-jun mRNA. Tetradecanoylphorbol Acetate 14-17 jun proto-oncogene Mus musculus 60-65 7835696-5 1995 Electrophoretic mobility shift assays and mutational analyses suggest that the promoter site is bound by nuclear protein complexes containing cAMP-independent members of the ATF/CREB family of proteins and c-Jun, and are functionally distinct from the AP1-related TPA-response element (TRE) binding activity. Tetradecanoylphorbol Acetate 264-267 jun proto-oncogene Mus musculus 206-211 8063765-10 1994 Furthermore, RA inhibited activator protein-1 binding to 12-O-tetradecanoylphorbol 13-acetate-response element (TRE) in the cells treated with TNF-alpha, suggesting that RA acts as a potent negative regulator for activator protein-1 binding activity to TRE in the osteoblastic cells. Tetradecanoylphorbol Acetate 57-93 jun proto-oncogene Mus musculus 213-232 8150544-2 1994 The response of c-jun was elicited by the protein kinase-C activators TPA and A23187 in ESb but not in Eb cells. Tetradecanoylphorbol Acetate 70-73 jun proto-oncogene Mus musculus 16-21 8027056-8 1994 In addition, both TPA and IL-1 alpha caused increases not only in the phosphorylation of c-Jun and c-Fos protein but also in the transactivating activity of AP-1 nuclear transcription factor. Tetradecanoylphorbol Acetate 18-21 jun proto-oncogene Mus musculus 89-94 1543537-3 1992 The nuclear proto-oncogenes c-fos and c-jun are referred to as early response genes because the classical tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces their expression to maximal levels within 2 h after treatment. Tetradecanoylphorbol Acetate 121-157 jun proto-oncogene Mus musculus 38-43 8142009-4 1994 In nuclear protein extracts of 308, AP-1 sequence-specific binding to an oligonucleotide containing a single high-affinity AP-1 binding site was induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, as determined by gel shift analysis. Tetradecanoylphorbol Acetate 175-211 jun proto-oncogene Mus musculus 36-40 8142009-4 1994 In nuclear protein extracts of 308, AP-1 sequence-specific binding to an oligonucleotide containing a single high-affinity AP-1 binding site was induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, as determined by gel shift analysis. Tetradecanoylphorbol Acetate 175-211 jun proto-oncogene Mus musculus 123-127 8392062-2 1993 J774 cells responded to either phorbol 12-myristate 13-acetate (PMA) or LPS by the transient increase in the expression levels of c-jun and junB mRNA, but not of junD mRNA. Tetradecanoylphorbol Acetate 31-62 jun proto-oncogene Mus musculus 130-135 8392062-2 1993 J774 cells responded to either phorbol 12-myristate 13-acetate (PMA) or LPS by the transient increase in the expression levels of c-jun and junB mRNA, but not of junD mRNA. Tetradecanoylphorbol Acetate 64-67 jun proto-oncogene Mus musculus 130-135 1594601-5 1992 Cotransfection experiments showed that the increase in c-jun expression resulted from elevated activity of the transcription factor AP-1 and was mediated through the phorbol 12-tetradecanoate 13-acetate response element in the c-jun promoter. Tetradecanoylphorbol Acetate 166-202 jun proto-oncogene Mus musculus 55-60 1594601-5 1992 Cotransfection experiments showed that the increase in c-jun expression resulted from elevated activity of the transcription factor AP-1 and was mediated through the phorbol 12-tetradecanoate 13-acetate response element in the c-jun promoter. Tetradecanoylphorbol Acetate 166-202 jun proto-oncogene Mus musculus 132-136 1594601-5 1992 Cotransfection experiments showed that the increase in c-jun expression resulted from elevated activity of the transcription factor AP-1 and was mediated through the phorbol 12-tetradecanoate 13-acetate response element in the c-jun promoter. Tetradecanoylphorbol Acetate 166-202 jun proto-oncogene Mus musculus 227-232 1731339-2 1992 We now find that this EpRE is composed of two adjacent 9-base-pair motifs related in sequence to the AP-1 binding site, a transcriptional enhancer originally identified as the phorbol 12-myristate 13-acetate (PMA) response element and known to be regulated by the binding of protein products of c-jun and c-fos genes. Tetradecanoylphorbol Acetate 176-207 jun proto-oncogene Mus musculus 295-300 1731339-2 1992 We now find that this EpRE is composed of two adjacent 9-base-pair motifs related in sequence to the AP-1 binding site, a transcriptional enhancer originally identified as the phorbol 12-myristate 13-acetate (PMA) response element and known to be regulated by the binding of protein products of c-jun and c-fos genes. Tetradecanoylphorbol Acetate 209-212 jun proto-oncogene Mus musculus 295-300 8313375-6 1994 Of interest was the finding that 12-O-tetradecanoylphorbol-13-acetate induction of other cellular genes known to be regulated by AP-1 was not inhibited in the benign tumor cells expressing v-jun. Tetradecanoylphorbol Acetate 33-69 jun proto-oncogene Mus musculus 129-133 8344255-1 1993 The trans-acting factor AP-1 is a heterodimeric complex composed of c-Jun and c-Fos family proteins which bind and regulate genes containing a TPA responsive enhancer element. Tetradecanoylphorbol Acetate 143-146 jun proto-oncogene Mus musculus 24-28 8344255-1 1993 The trans-acting factor AP-1 is a heterodimeric complex composed of c-Jun and c-Fos family proteins which bind and regulate genes containing a TPA responsive enhancer element. Tetradecanoylphorbol Acetate 143-146 jun proto-oncogene Mus musculus 68-73 8397795-9 1993 c-fos and c-jun proteins synthesized in vitro could bind to the DNA fragment containing this sequence, but the binding was weaker than to the TPA-responsive element (TGACTCA). Tetradecanoylphorbol Acetate 142-145 jun proto-oncogene Mus musculus 10-15 1281302-4 1992 Transcriptional activation of the c-jun, junB and c-fos genes following TPA/serum induction was unaffected and efficient transactivation of AP-1 reporter constructs was demonstrated in these cells. Tetradecanoylphorbol Acetate 72-75 jun proto-oncogene Mus musculus 34-39 1400499-0 1992 Distal AP-1 binding sites mediate basal level enhancement and TPA induction of the mouse heme oxygenase-1 gene. Tetradecanoylphorbol Acetate 62-65 jun proto-oncogene Mus musculus 7-11 1400499-7 1992 These functions are mediated by the AP-1 binding sites as multiple copies of the region A motif also confer TPA induction and c-Jun/c-Fos transactivation upon a heterologous promoter. Tetradecanoylphorbol Acetate 108-111 jun proto-oncogene Mus musculus 36-40 1331038-6 1992 Treatment of quiescent C2 cells with a tumor promoter, 12-O-tetradecanoylphorbol 13-acetate, transiently induced c-jun and c-fos mRNAs, and temporarily deinduced myoD and myogenin mRNAs just after the expression of the protooncogenes. Tetradecanoylphorbol Acetate 55-91 jun proto-oncogene Mus musculus 113-118 1634770-2 1992 To illuminate mechanisms that may couple these events, we examined the expression and function of tetradecanoyl phorbol acetate-response element (TRE)-binding proteins (i.e., activator protein 1, (AP-1)) in the murine B lymphoma cell line BAL-17.7.1 (BAL-17), which models primary B lymphocyte responses in a number of respects. Tetradecanoylphorbol Acetate 98-127 jun proto-oncogene Mus musculus 175-194 1313769-0 1992 Serum-, TPA-, and Ras-induced expression from Ap-1/Ets-driven promoters requires Raf-1 kinase. Tetradecanoylphorbol Acetate 8-11 jun proto-oncogene Mus musculus 46-50 1543537-3 1992 The nuclear proto-oncogenes c-fos and c-jun are referred to as early response genes because the classical tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) induces their expression to maximal levels within 2 h after treatment. Tetradecanoylphorbol Acetate 159-162 jun proto-oncogene Mus musculus 38-43 1774959-4 1991 On the other hand, the protein kinase C agonist, TPA, strongly activated c-jun expression but poorly promoted expression (transcription) of c-myc in FDC-P1. Tetradecanoylphorbol Acetate 49-52 jun proto-oncogene Mus musculus 73-78 1722214-7 1991 Two different sequences involved in mediating TPA-induced transcription of the urokinase plasminogen activator and of the c-jun gene, respectively, competed for proteins with affinity toward the VLX binding site. Tetradecanoylphorbol Acetate 46-49 jun proto-oncogene Mus musculus 122-127 1774959-9 1991 In addition, TPA mediated expression of the transfected c-myc gene in FDMT myc.A1 was accompanied by augmented transcription of c-jun and c-fos in response to TPA. Tetradecanoylphorbol Acetate 13-16 jun proto-oncogene Mus musculus 128-133 1774959-9 1991 In addition, TPA mediated expression of the transfected c-myc gene in FDMT myc.A1 was accompanied by augmented transcription of c-jun and c-fos in response to TPA. Tetradecanoylphorbol Acetate 159-162 jun proto-oncogene Mus musculus 128-133 2062642-1 1991 cyr61 is an immediate early gene that is transcriptionally activated in 3T3 fibroblasts by serum, platelet-derived growth factor, fibroblast growth factor, and the tumor promoter TPA with kinetics similar to the induction of c-fos. Tetradecanoylphorbol Acetate 179-182 jun proto-oncogene Mus musculus 12-27 1905019-2 1991 Functional activation of transcriptional factor c-Jun/AP-1 is believed to play an important role in signal transduction of phorbol 12-myristate 13-acetate-induced tumor promotion. Tetradecanoylphorbol Acetate 123-154 jun proto-oncogene Mus musculus 48-53 1905019-2 1991 Functional activation of transcriptional factor c-Jun/AP-1 is believed to play an important role in signal transduction of phorbol 12-myristate 13-acetate-induced tumor promotion. Tetradecanoylphorbol Acetate 123-154 jun proto-oncogene Mus musculus 54-58 1714585-5 1991 Furthermore, thapsigargin could synergize with the tumor promoter phorbol 12-myristate 13-acetate to induce c-fos but not c-jun. Tetradecanoylphorbol Acetate 66-97 jun proto-oncogene Mus musculus 122-127 1700789-12 1990 Phorbol myristate acetate also stimulated hexose transport as well as expression of the GLUT-1 gene and several immediate-early genes in quiescent 3T3-L1 cells. Tetradecanoylphorbol Acetate 0-25 jun proto-oncogene Mus musculus 112-127 2138707-0 1990 mXBP/CRE-BP2 and c-Jun form a complex which binds to the cyclic AMP, but not to the 12-O-tetradecanoylphorbol-13-acetate, response element. Tetradecanoylphorbol Acetate 84-120 jun proto-oncogene Mus musculus 17-22 2121513-3 1990 Moreover, the sequential activation of the fos, AP-1, and HO genes was observed during this period, with the maximal transcriptional activities after TPA treatment for 0.5, 1, and 1.5 h, respectively. Tetradecanoylphorbol Acetate 150-153 jun proto-oncogene Mus musculus 48-52 2121513-5 1990 As the rat HO gene is known to have a TPA-sensitive element in its promoter region, this gene was suggested to be activated by a fos-AP-1 complex protein. Tetradecanoylphorbol Acetate 38-41 jun proto-oncogene Mus musculus 133-137 2167455-2 1990 This gene and the related cellular genes c-jun, jun B and jun D, encode transactivating (or repressing) DNA-binding proteins that form homo- or heterodimeric (Jun-Jun and Jun-Fos) complexes which recognize the AP-1 consensus sequence TGACTCA, a response element that confers sensitivity to the tumour-promoting phorbol ester TPA. Tetradecanoylphorbol Acetate 325-328 jun proto-oncogene Mus musculus 41-46 2138707-1 1990 Proto-oncogene products c-Fos and c-Jun form a complex which binds with high affinity to the 12-O-tetradecanoylphorbol-13-acetate (TPA) response DNA element and which stimulates transcription of phorbol ester- inducible genes. Tetradecanoylphorbol Acetate 93-129 jun proto-oncogene Mus musculus 34-39 2138707-1 1990 Proto-oncogene products c-Fos and c-Jun form a complex which binds with high affinity to the 12-O-tetradecanoylphorbol-13-acetate (TPA) response DNA element and which stimulates transcription of phorbol ester- inducible genes. Tetradecanoylphorbol Acetate 131-134 jun proto-oncogene Mus musculus 34-39 2150599-5 1990 In the c-jun promoter the 12-0-tetradecanoyl-phorbol-13-acetate (TPA) response element (TRE) mediates this effect. Tetradecanoylphorbol Acetate 65-68 jun proto-oncogene Mus musculus 7-12 2138707-8 1990 mXBP-c-Jun complexes can coexist with c-Fos-c-Jun complexes and can bind with high affinity to CRE, but not to TPA response DNA element, sequences. Tetradecanoylphorbol Acetate 111-114 jun proto-oncogene Mus musculus 5-10 34724217-3 2022 Interestingly, 50 mmHg mechanical stressing induced the nuclear localization of NFAT1; but conversely decreased C-Jun and inhibited the expression of CD69 in lymphocytes under lipopolysaccharide or phorbol 12-myristate 13-acetate/ionomycin stimulation. Tetradecanoylphorbol Acetate 198-229 jun proto-oncogene Mus musculus 112-117 7818761-1 1995 This study was undertaken to assess the effects of a single or two sequential topical applications of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the expression of c-fos, c-jun, junB, c-myc, and ornithine decarboxylase (ODC) in promotion-sensitive SSIN mice and the relatively promotion-resistant C57BL/6 strain. Tetradecanoylphorbol Acetate 102-138 jun proto-oncogene Mus musculus 173-178 7818761-1 1995 This study was undertaken to assess the effects of a single or two sequential topical applications of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the expression of c-fos, c-jun, junB, c-myc, and ornithine decarboxylase (ODC) in promotion-sensitive SSIN mice and the relatively promotion-resistant C57BL/6 strain. Tetradecanoylphorbol Acetate 140-143 jun proto-oncogene Mus musculus 173-178 2562123-3 1989 The proto-oncogenes jun B, c-fos, and to a lesser extent jun D were stimulated by increasing the intracellular concentration of cAMP, whereas the TPA stimulation of c-jun and c-myc was inhibited under these conditions. Tetradecanoylphorbol Acetate 146-149 jun proto-oncogene Mus musculus 165-170 34645824-0 2021 Phorbol-12-myristate 13-acetate inhibits Nephronectin gene expression via Protein kinase C alpha and c-Jun/c-Fos transcription factors. Tetradecanoylphorbol Acetate 0-31 jun proto-oncogene Mus musculus 101-106 2457172-0 1988 Induction of proto-oncogene JUN/AP-1 by serum and TPA. Tetradecanoylphorbol Acetate 50-53 jun proto-oncogene Mus musculus 32-36 2547991-0 1989 Loss of responsiveness of an AP1-related factor, PEBP1, to 12-O-tetradecanoylphorbol-13-acetate after transformation of NIH 3T3 cells by the Ha-ras oncogene. Tetradecanoylphorbol Acetate 59-95 jun proto-oncogene Mus musculus 29-32 2504580-4 1989 Truncated c-Jun and JunD proteins containing the C-terminus recognize the same DNA sequences which were defined as the PEA1/AP1 binding sequence or TPA response element (TRE). Tetradecanoylphorbol Acetate 148-151 jun proto-oncogene Mus musculus 10-15 2504580-6 1989 Contrary to c-jun and junB transcription, which are strongly stimulated by serum or TPA treatment of quiescent 3T3 cells, junD transcription is not significantly stimulated in these conditions. Tetradecanoylphorbol Acetate 84-87 jun proto-oncogene Mus musculus 12-17 2457172-7 1988 We report that mouse c-jun gene transcription is rapidly induced by serum and phorbol-ester 12-o-tetradecanoyl phorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 131-134 jun proto-oncogene Mus musculus 21-26 2453058-1 1988 Transcription factor activator protein 1 (AP1) interacts with the promoter region of a number of genes that are stimulated by growth factors present in serum or by agents such as phorbol 12-myristate 13-acetate (PMA) that partially mimic their action. Tetradecanoylphorbol Acetate 179-210 jun proto-oncogene Mus musculus 21-40 2453058-1 1988 Transcription factor activator protein 1 (AP1) interacts with the promoter region of a number of genes that are stimulated by growth factors present in serum or by agents such as phorbol 12-myristate 13-acetate (PMA) that partially mimic their action. Tetradecanoylphorbol Acetate 179-210 jun proto-oncogene Mus musculus 42-45 2453058-1 1988 Transcription factor activator protein 1 (AP1) interacts with the promoter region of a number of genes that are stimulated by growth factors present in serum or by agents such as phorbol 12-myristate 13-acetate (PMA) that partially mimic their action. Tetradecanoylphorbol Acetate 212-215 jun proto-oncogene Mus musculus 21-40 2453058-1 1988 Transcription factor activator protein 1 (AP1) interacts with the promoter region of a number of genes that are stimulated by growth factors present in serum or by agents such as phorbol 12-myristate 13-acetate (PMA) that partially mimic their action. Tetradecanoylphorbol Acetate 212-215 jun proto-oncogene Mus musculus 42-45 2453058-4 1988 A 2- to 3-fold activation was found after treatment with PMA or dibutyryl-cAMP, suggesting that different signal-transducing pathways could activate AP1 factor in these cells. Tetradecanoylphorbol Acetate 57-60 jun proto-oncogene Mus musculus 149-152