PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27538486-7 2017 In non-Hodgkin B-cell lines, small interfering RNA-mediated PDLIM2 knockdown results in superactivation of TFs NF-kappaB and AP-1 following phorbol 12-myristate 13-acetate (PMA) stimulation. Tetradecanoylphorbol Acetate 140-171 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 125-129 28927117-0 2017 Salvia miltiorrhiza extract inhibits TPA-induced MMP-9 expression and invasion through the MAPK/AP-1 signaling pathway in human breast cancer MCF-7 cells. Tetradecanoylphorbol Acetate 37-40 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 96-100 28927117-10 2017 SME suppressed TPA-induced MMP-9 expression and MCF-7 cell invasion by blocking the transcriptional activation of AP-1. Tetradecanoylphorbol Acetate 15-18 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-118 25051397-6 2014 The expression levels of AP-1 transcription factors were increased in HepG2 cells following induction by phorbol 12-myristate 13-acetate, but ginsenoside Rh2 suppressed this induced AP-1 expression. Tetradecanoylphorbol Acetate 105-136 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-29 27035791-7 2016 Furthermore, Rev-AuNP treatment remarkably downregulated TPA-induced nuclear translocation and transcriptional activation of nuclear transcription factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 57-60 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 177-196 27035791-7 2016 Furthermore, Rev-AuNP treatment remarkably downregulated TPA-induced nuclear translocation and transcriptional activation of nuclear transcription factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 57-60 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 198-202 27035791-12 2016 Our findings revealed that the anti-invasive effects of Rev-AuNPs in response to TPA-stimulation were mediated by the suppression of MMP-9, COX-2, NF-kappaB, AP-1, PI3K/Akt and ERK and/or the activation of HO-1 signaling cascades. Tetradecanoylphorbol Acetate 81-84 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 158-162 23615401-9 2013 Furthermore, TPA-induced extracellular signal-regulated kinase (ERK) 1/2 and Akt phosphorylation and the DNA binding activity of activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) were attenuated by pretreatment with AP and HO-1 end products. Tetradecanoylphorbol Acetate 13-16 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 129-148 24317440-10 2014 Furthermore, in MNK-74 and SC-M1 cells treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) and 5 or 10 microM of ATPR significantly suppressed the activity of the AP-1 reporter as compared to treatment with ATRA (P<0.05). Tetradecanoylphorbol Acetate 52-88 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-171 24317440-10 2014 Furthermore, in MNK-74 and SC-M1 cells treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) and 5 or 10 microM of ATPR significantly suppressed the activity of the AP-1 reporter as compared to treatment with ATRA (P<0.05). Tetradecanoylphorbol Acetate 90-93 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-171 23615401-9 2013 Furthermore, TPA-induced extracellular signal-regulated kinase (ERK) 1/2 and Akt phosphorylation and the DNA binding activity of activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) were attenuated by pretreatment with AP and HO-1 end products. Tetradecanoylphorbol Acetate 13-16 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 150-154 23615401-10 2013 In conclusion, these results suggest that AP inhibits TPA-induced cell migration and invasion by reducing MMP-9 activation, which is mediated mainly by inhibition of the ERK1/2 and phosphatidylinositol 3-kinase/Akt signaling pathways and subsequent AP-1 and NF-kappaB transactivation. Tetradecanoylphorbol Acetate 54-57 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 249-253 20959602-8 2011 Reciprocally, AP-1 TFs were up-regulated by RUNX1 after 12-O-tetradecanoylphorbol-13-acetate induction and recruited to RUNX1-occupied sites lacking AP-1 motifs. Tetradecanoylphorbol Acetate 56-92 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-18 23615261-6 2013 TPA substantially increased NF-kappaB and AP-1 DNA binding activity. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-46 23242121-3 2013 Cis-guggulsterone inhibited TPA-induced MMP expression by blocking IkappaB kinase (IKK)/NF-kappaB signaling, whereas trans-guggulsterone blocked mitogen-activated protein kinase (MAPK)/AP-1 signaling. Tetradecanoylphorbol Acetate 28-31 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 209-213 21381080-2 2011 The stomach isoform of Cldn18, Cldn18a2 is regulated via a PKC/MAPK/AP-1-dependent pathway in PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated gastric cancer cells. Tetradecanoylphorbol Acetate 108-144 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 68-72 21381080-2 2011 The stomach isoform of Cldn18, Cldn18a2 is regulated via a PKC/MAPK/AP-1-dependent pathway in PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated gastric cancer cells. Tetradecanoylphorbol Acetate 146-149 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 68-72 21246637-0 2011 Evodiamine inhibits 12-O-tetradecanoylphorbol-13-acetate-induced activator protein 1 transactivation and cell transformation in human hepatocytes. Tetradecanoylphorbol Acetate 20-56 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-84 21246637-5 2011 The Chang/AP-1 cells were treated with E. rutaecarpa and its bioactive constituents, and challenged with the AP-1 stimulator 12-O-tetradecanoylphorbol-13- acetate (TPA). Tetradecanoylphorbol Acetate 125-162 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 109-113 21246637-6 2011 The present study showed that the methanol extract of E. rutaecarpa decreased the TPA-induced AP-1 transactivation in Chang/AP-1 cells, with an EC50 value of 24.72 mug/mL. Tetradecanoylphorbol Acetate 82-85 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 94-98 21246637-6 2011 The present study showed that the methanol extract of E. rutaecarpa decreased the TPA-induced AP-1 transactivation in Chang/AP-1 cells, with an EC50 value of 24.72 mug/mL. Tetradecanoylphorbol Acetate 82-85 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 124-128 21246637-7 2011 EVO inhibited the TPA-induced AP-1 transactivation and colony formation, with EC50 values of 82 muM and 8.2 muM, respectively. Tetradecanoylphorbol Acetate 18-21 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-34 21246637-9 2011 These results suggested that EVO treatment suppressed the TPA-induced AP-1 activity via the ERKs pathway. Tetradecanoylphorbol Acetate 58-61 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-74 21262201-5 2011 DHAvD also suppressed activation of mitogen-activated protein kinase (MAPK), and MAPK-mediated nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) activations in TPA-treated MCF-7 cells. Tetradecanoylphorbol Acetate 176-179 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 134-153 21262201-5 2011 DHAvD also suppressed activation of mitogen-activated protein kinase (MAPK), and MAPK-mediated nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) activations in TPA-treated MCF-7 cells. Tetradecanoylphorbol Acetate 176-179 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 155-159 21262201-6 2011 The results indicate that DHAvD-mediated inhibition of TPA-induced MMP-9 expression and cell invasion involves the suppression of the MAPK/NF-kappaB and MAPK/AP-1 pathways in MCF-7 cells. Tetradecanoylphorbol Acetate 55-58 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 158-162 23288142-8 2013 EMSA showed that DHA, LA, PD98059, and wortmannin decreased TPA-induced NF-kappaB and AP-1 DNA-binding activity. Tetradecanoylphorbol Acetate 60-63 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 23151889-5 2013 Surfactin attenuated TPA-induced nuclear translocation and activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 21-24 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 123-142 23151889-5 2013 Surfactin attenuated TPA-induced nuclear translocation and activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Tetradecanoylphorbol Acetate 21-24 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 156-160 21129776-5 2011 Finally, in line with the known TPA pathway, we found that nuclear proteins could bind a sequence corresponding to a unique AP1 site on promoter 2 selectively in the activated cell fraction. Tetradecanoylphorbol Acetate 32-35 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 124-127 20669087-10 2011 Likewise, the constitutive nuclear NF- kappaB (p65) activity as well as phorbol 12-myristate 13-acetate (PMA)- and sodium N-butyrate (SnB)-induced AP-1 binding activity in Raji cells were significantly reduced following treatment with maslinic acid. Tetradecanoylphorbol Acetate 72-103 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-151 20669087-10 2011 Likewise, the constitutive nuclear NF- kappaB (p65) activity as well as phorbol 12-myristate 13-acetate (PMA)- and sodium N-butyrate (SnB)-induced AP-1 binding activity in Raji cells were significantly reduced following treatment with maslinic acid. Tetradecanoylphorbol Acetate 105-108 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-151 20138977-7 2010 Hesperidin suppressed TPA-stimulated NF-kappaB translocation into the nucleus through IkappaB inhibitory signaling pathways and also inhibited TPA-induced AP-1 activity by the inhibitory phosphorylation of p38 kinase and c-Jun N-terminal kinase (JNK) signaling pathways. Tetradecanoylphorbol Acetate 143-146 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 155-159 20550117-7 2010 The EEGC also showed an inhibitory effect on the PMA-induced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and protein kinase B (Akt) in cytosol, as well as the activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) levels in the nucleus of HepG2 cells. Tetradecanoylphorbol Acetate 49-52 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 181-200 20550117-7 2010 The EEGC also showed an inhibitory effect on the PMA-induced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and protein kinase B (Akt) in cytosol, as well as the activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) levels in the nucleus of HepG2 cells. Tetradecanoylphorbol Acetate 49-52 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 202-206 20082219-5 2010 In addition, melittin suppressed the PMA-induced phosphorylations of ERK and JNK mitogen-activated protein kinases, upstream factors involved in Ap-1 and NF-kappaB. Tetradecanoylphorbol Acetate 37-40 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-149 19420016-5 2009 Using specific inhibitors, we confirmed that PMA-induced cell invasion and MMP-9 expression is primarily regulated by nuclear factor-kappa B (NF-kappaB) activation via phosphatidylinositol 3-kinase (PI3K)/Akt and activator protein-1 (AP-1) activation via extracellular signal-regulated kinase (ERK)1/2. Tetradecanoylphorbol Acetate 45-48 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 213-232 20053986-2 2010 To bind to its target AP-1/12-O-tetradecanoylphorbol-13-acetate-responsive element or cAMP-responsive element DNA sequences in gene promoters and exert its transcriptional part, c-Fos must heterodimerize with other bZip proteins, its best studied partners being the Jun proteins (c-Jun, JunB, and JunD). Tetradecanoylphorbol Acetate 27-63 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 287-291 19420016-5 2009 Using specific inhibitors, we confirmed that PMA-induced cell invasion and MMP-9 expression is primarily regulated by nuclear factor-kappa B (NF-kappaB) activation via phosphatidylinositol 3-kinase (PI3K)/Akt and activator protein-1 (AP-1) activation via extracellular signal-regulated kinase (ERK)1/2. Tetradecanoylphorbol Acetate 45-48 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 234-238 19447859-6 2009 Transient transfection experiments also showed that pterostilbene strongly inhibited TPA-stimulated nuclear factor kappa B (NF-kappaB) and activator protein-1 (AP-1)-dependent transcriptional activity in HepG(2) cells. Tetradecanoylphorbol Acetate 85-88 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 139-158 19420016-6 2009 KPS-A decreased PMA-induced transcriptional activation of NF-kappaB and AP-1 and inhibited PMA-induced phosphorylation of ERK1/2 and Akt. Tetradecanoylphorbol Acetate 16-19 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 72-76 19447859-6 2009 Transient transfection experiments also showed that pterostilbene strongly inhibited TPA-stimulated nuclear factor kappa B (NF-kappaB) and activator protein-1 (AP-1)-dependent transcriptional activity in HepG(2) cells. Tetradecanoylphorbol Acetate 85-88 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 160-164 19420016-9 2009 These results suggest that KPS-A inhibits PMA-induced invasion by reducing MMP-9 activation, mainly via the PI3K/Akt/NF-kappaB and PKCdelta/ERK/AP-1 pathways in MCF-7 cells and blocks tumor growth and MMP-9-mediated invasiveness in mice with breast carcinoma. Tetradecanoylphorbol Acetate 42-45 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 144-148 19447859-7 2009 Moreover, pterostilbene can suppress TPA-induced activation of extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase, c-Jun N-terminal kinases 1/2 and phosphatidylinositol 3-kinase/Akt and protein kinase C that are upstream of NF-kappaB and AP-1. Tetradecanoylphorbol Acetate 37-40 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 267-271 18245498-4 2008 The activation of activator protein-1 and nuclear factor-kappaB induced by TPA was dose dependently inhibited by RWE or quercetin treatment. Tetradecanoylphorbol Acetate 75-78 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 18-37 18992303-4 2009 Promoter activities of IL-2, nuclear factor of activated T cells (NFAT), and activator protein-1 (AP-1), after 6 h stimulation with PMA and ionomycin, gradually decreased in high glucose cultures to approximately 20% of those in normal glucose at 12 weeks. Tetradecanoylphorbol Acetate 132-135 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-96 18992303-4 2009 Promoter activities of IL-2, nuclear factor of activated T cells (NFAT), and activator protein-1 (AP-1), after 6 h stimulation with PMA and ionomycin, gradually decreased in high glucose cultures to approximately 20% of those in normal glucose at 12 weeks. Tetradecanoylphorbol Acetate 132-135 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-102 16267831-11 2006 Similarly, AP-1 binding activity showed a transient variation in both cell lines after TPA treatment but with different kinetics. Tetradecanoylphorbol Acetate 87-90 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 11-15 17114644-0 2007 Ascofuranone suppresses PMA-mediated matrix metalloproteinase-9 gene activation through the Ras/Raf/MEK/ERK- and Ap1-dependent mechanisms. Tetradecanoylphorbol Acetate 24-27 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-116 17114644-6 2007 In addition, ascofuranone suppressed PMA-induced phosphorylation of Ras, Raf, MEK and extracellular signal-regulated kinase (ERK), upstream factors involved in AP-1activation, whereas the phosphorylation of p38 and JNK/mitogen-activated protein kinase was not affected by ascofuranone, suggesting that the primary target of ascofuranone for suppression of the AP-1 induction is present in upstream of ERK signaling pathway. Tetradecanoylphorbol Acetate 37-40 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 160-164 17114644-6 2007 In addition, ascofuranone suppressed PMA-induced phosphorylation of Ras, Raf, MEK and extracellular signal-regulated kinase (ERK), upstream factors involved in AP-1activation, whereas the phosphorylation of p38 and JNK/mitogen-activated protein kinase was not affected by ascofuranone, suggesting that the primary target of ascofuranone for suppression of the AP-1 induction is present in upstream of ERK signaling pathway. Tetradecanoylphorbol Acetate 37-40 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 360-364 17438848-6 2007 The percentage of cells of active AP-1, IL-5 protein in supernatants of allergic rhinitis T lymphocytes stimulated with PMA and curcumin were significantly lower than those of allergic rhinitis T lymphocytes stimulated with PMA (P < 0.01); but significantly higher than those of allergic rhinitis T lymphocytes stimulated without PMA and those of deflection of nasal septum T lymphocytes stimulated. Tetradecanoylphorbol Acetate 120-123 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 34-38 17207890-10 2007 An AP-1 and a NF-kappaB recognition sites were necessary for full induction of IL-8 promoter activity by TNF-alpha and TPA. Tetradecanoylphorbol Acetate 119-122 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 3-7 17207890-12 2007 Immunoblotting experiments showed that TPA was more potent than TNF-alpha to induce in a PKCalpha/beta dependent manner the p44/p42 mitogen-activated protein kinases (MAPK) signaling cascade which controls AP-1 activity. Tetradecanoylphorbol Acetate 39-42 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 206-210 17394101-4 2007 Deerberry fruit extracts also blocked TPA- or UVB-induced phosphorylation of ERKs and MEK 1/2, two upstream regulators of AP-1 and inhibited proliferation of human leukemia HL-60 cancer cells and human lung epithelial cancer A549 cells and induced apoptosis of HL-60 cells. Tetradecanoylphorbol Acetate 38-41 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 122-126 17394101-5 2007 These results suggest that the inhibition of TPA- or UVB-induced AP-1 and NF-kappaB activity, inhibition of HL-60 cells and cancer A549 cells proliferation and induction of apoptotic in human leukemia HL-60 cancer cells may be mediated through the ERKs and MEK 1/2 signal pathway. Tetradecanoylphorbol Acetate 45-48 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-69 15878157-8 2005 Phorbol ester 12-O-teradecanoyl-phorbol-13-acetate (TPA) activated AP-1 in B82L and B82M721 cells, but not B82 cells. Tetradecanoylphorbol Acetate 52-55 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 67-71 15878157-11 2005 Ethanol selectively inhibited TPA-induced phosphorylation of ERK and PKCdelta, and modestly suppressed TPA-stimulated AP-1 activation in B82L and B82M721 cells. Tetradecanoylphorbol Acetate 103-106 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-122 15465640-5 2004 Results in this experiment showed that SNL glycoprotein inhibits 12-O-Tetra decanoylphorbol-13-acetate (TPA; 100 nM)-induced DNA-binding activities of NF-kappaB and AP-1, and enhances NO production in MCF-7 cells. Tetradecanoylphorbol Acetate 104-107 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-169 15797241-1 2005 The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity. Tetradecanoylphorbol Acetate 27-63 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-97 15797241-1 2005 The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity. Tetradecanoylphorbol Acetate 27-63 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-103 15797241-1 2005 The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity. Tetradecanoylphorbol Acetate 65-68 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-97 15797241-1 2005 The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) induces activator protein-1 (AP-1) transcription factors, early response genes involved in a diverse set of transcriptional regulatory processes, and protein kinase C (PKC) activity. Tetradecanoylphorbol Acetate 65-68 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-103 15790882-10 2005 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element. Tetradecanoylphorbol Acetate 15-51 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 163-166 15790882-10 2005 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element. Tetradecanoylphorbol Acetate 15-51 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 185-189 15790882-10 2005 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element. Tetradecanoylphorbol Acetate 15-51 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 216-219 15790882-10 2005 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element. Tetradecanoylphorbol Acetate 53-56 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 163-166 15790882-10 2005 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element. Tetradecanoylphorbol Acetate 53-56 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 185-189 15790882-10 2005 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased AP1 factor (Fra-1 and JunB) binding to the hINV gene AP1-5 response element. Tetradecanoylphorbol Acetate 53-56 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 216-219 15666830-5 2004 TPA but not AII increased the level of the transcription factor JunB in nuclear extracts and the increase was partially abolished by the MEK1 inhibitor PD98059. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-68 15666830-7 2004 Taken together these results suggest that TPA inhibits the AII-dependent activation of CYP11B2 via the p44/42 MAPK signaling pathway leading to an increase of the level of nuclear JunB. Tetradecanoylphorbol Acetate 42-45 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 180-184 15329596-0 2004 Sevoflurane inhibits phorbol-myristate-acetate-induced activator protein-1 activation in human T lymphocytes in vitro: potential role of the p38-stress kinase pathway. Tetradecanoylphorbol Acetate 21-46 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 55-74 15329596-6 2004 Phorbol-myristate-acetate-dependent effects of sevoflurane on the phosphorylation of the mitogen-activated protein kinases were studied using Western blots, the trans-activating potency of AP-1 was determined using reporter gene assays, and the cytokine release was measured using enzyme-linked immunosorbent assays. Tetradecanoylphorbol Acetate 0-25 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 189-193 15627897-4 2004 Here we analyzed the role of AP-1 on the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced human hepatocellular transformation. Tetradecanoylphorbol Acetate 41-77 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 29-33 15627897-4 2004 Here we analyzed the role of AP-1 on the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced human hepatocellular transformation. Tetradecanoylphorbol Acetate 79-82 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 29-33 15627897-5 2004 TPA promoted the formation of anchorage-independent colonies, induced the AP-1 activity, and enhanced the DNA-binding ability of AP-1 in human hepatocytes. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 74-78 15627897-5 2004 TPA promoted the formation of anchorage-independent colonies, induced the AP-1 activity, and enhanced the DNA-binding ability of AP-1 in human hepatocytes. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 129-133 15627897-6 2004 The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway. Tetradecanoylphorbol Acetate 94-97 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-190 15627897-6 2004 The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway. Tetradecanoylphorbol Acetate 106-109 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-122 15627897-6 2004 The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway. Tetradecanoylphorbol Acetate 106-109 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-190 15627897-6 2004 The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway. Tetradecanoylphorbol Acetate 106-109 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 118-122 15627897-6 2004 The phosphorylation of extracellular signal-regulated protein kinases (ERKs) was increased by TPA and the TPA-induced AP-1 activity was inhibited by PD98059, indicating that TPA-induced AP-1 activation was via ERK pathway. Tetradecanoylphorbol Acetate 106-109 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-190 15627897-7 2004 Moreover, retinoic acid and PD98059, which inhibited the AP-1 activity, abolished the TPA-induced transformation. Tetradecanoylphorbol Acetate 86-89 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-61 15627897-8 2004 Our findings indicated that AP-1 and ERKs activations were required for TPA-induced human hepatocellular transformation. Tetradecanoylphorbol Acetate 72-75 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-32 14673171-4 2004 We report here that ATF-3, JunB, and BRG-1 (the ATPase subunit of the 2-MDa human chromatin remodeling machine SWI/SNF) are recruited to the 3" boundary of nuc-1 following phorbol myristate acetate stimulation in Jurkat T cells. Tetradecanoylphorbol Acetate 172-197 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-31 15037572-9 2004 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element. Tetradecanoylphorbol Acetate 15-51 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 171-174 15037572-9 2004 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element. Tetradecanoylphorbol Acetate 15-51 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 217-222 15037572-9 2004 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element. Tetradecanoylphorbol Acetate 53-56 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 171-174 15037572-9 2004 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C activator, increased hINV gene expression, a response that correlates with increased nuclear AP1 factor level and binding to the hINV gene AP1-1 response element. Tetradecanoylphorbol Acetate 53-56 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 217-222 14627504-8 2003 The activation of AP-1 induced by PMA was also extensively inhibited by resveratrol at 0.1, 1, and 10 micromol/L. Tetradecanoylphorbol Acetate 34-37 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 18-22 12592382-4 2003 On the other hand, expressions of proto-oncogene c-jun, junB and c-fos were induced by TPA and Saikosaponin a during 30 min to 6 h of treatment. Tetradecanoylphorbol Acetate 87-90 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 56-60 12123542-3 2002 RESULTS: Transient transfection of RARbeta expression vector into MKN-45 cells resulted in the RARbeta concentration dependent repression of AP-1 activity induced by 12-o-tetradecanoylphorbol-13-acetate (TPA), regardless of the presence of ATRA. Tetradecanoylphorbol Acetate 166-202 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 141-145 12009305-7 2002 For AP-1 binding activity induced by TPA, the repressive effect of ATRA was only observed in BGC-823 and RARalpha and RARbeta stably transfected MKN-45 cells, but not in intact MKN-45 cells. Tetradecanoylphorbol Acetate 37-40 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-8 12123542-3 2002 RESULTS: Transient transfection of RARbeta expression vector into MKN-45 cells resulted in the RARbeta concentration dependent repression of AP-1 activity induced by 12-o-tetradecanoylphorbol-13-acetate (TPA), regardless of the presence of ATRA. Tetradecanoylphorbol Acetate 204-207 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 141-145 11948401-9 2002 The transcriptional activities of full-length JunB and full-length Fra-1, but not the transactivation domain fusions, were increased by TPA treatment and suppressed by RA. Tetradecanoylphorbol Acetate 136-139 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-50 12162432-4 2002 TPA and EGF, acting through the MAP kinase pathway, activate AP-1 and subsequently NF-kappaB proteins and downstream transcription processes that are involved in the transformation response in transformation-sensitive (P+) JB6 cells. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 61-65 11605784-4 2001 NF-kappaB and AP-1 DNA-binding abilities were significantly increased both at baseline and after stimulation by phorbol 12-myristate 13-acetate (TPA) in PBMC from MCNS patients compared with controls, but declined to normal levels after treatment with dexamethasone (DEX). Tetradecanoylphorbol Acetate 145-148 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-18 11751871-3 2002 Further analysis demonstrated that serum or 12-O-tetradecanoylphorbol-13-acetate activation of several immediate early genes including fos, fosB, junB, and egr1 was inhibited by Wnt signaling. Tetradecanoylphorbol Acetate 44-80 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-150 11861377-6 2002 We also demonstrated that nobiletin suppressed the 12-O-tetradecanoylphorbol 13-acetate-induced binding activity of activator protein-1. Tetradecanoylphorbol Acetate 51-87 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-135 12297018-5 2002 Likewise, the TPA-induced DNA binding of the activator protein-1 (AP-1) was inhibited by curcumin pretreatment. Tetradecanoylphorbol Acetate 14-17 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-64 12297018-5 2002 Likewise, the TPA-induced DNA binding of the activator protein-1 (AP-1) was inhibited by curcumin pretreatment. Tetradecanoylphorbol Acetate 14-17 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 66-70 11714372-8 2001 After stimulation by PMA, a dose-dependent inhibition of AP-1 was observed with the six phenolic acids in the 20 nM-20 microM concentration range: gallic acid > caffeic > protocatechic, paracoumaric, sinapic acids > ferulic acid. Tetradecanoylphorbol Acetate 21-24 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-61 11605784-4 2001 NF-kappaB and AP-1 DNA-binding abilities were significantly increased both at baseline and after stimulation by phorbol 12-myristate 13-acetate (TPA) in PBMC from MCNS patients compared with controls, but declined to normal levels after treatment with dexamethasone (DEX). Tetradecanoylphorbol Acetate 112-143 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-18 11145168-1 2000 Interaction between a tumor promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA), and ligands of nuclear receptors has been interpreted as the result of crosstalk between the nuclear receptors and oncogenic transcription factor AP-1. Tetradecanoylphorbol Acetate 38-74 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 228-232 11532088-5 2001 The effect of LMW heparin on the binding of nuclear proteins to a regulatory activator protein-1 (AP-1) site, which mediates the high glucose and PMA responsiveness of the TGF-beta 1 promoter, was studied by electrophoretic mobility shift assays. Tetradecanoylphorbol Acetate 146-149 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-96 11532088-5 2001 The effect of LMW heparin on the binding of nuclear proteins to a regulatory activator protein-1 (AP-1) site, which mediates the high glucose and PMA responsiveness of the TGF-beta 1 promoter, was studied by electrophoretic mobility shift assays. Tetradecanoylphorbol Acetate 146-149 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-102 11448162-0 2001 12-O-tetradecanoylphorbol-13-acetate induces Epstein-Barr virus reactivation via NF-kappaB and AP-1 as regulated by protein kinase C and mitogen-activated protein kinase. Tetradecanoylphorbol Acetate 0-36 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 95-99 11448162-6 2001 Electrophoretic mobility shift assays demonstrated that transcription factors NF-kappaB and AP-1 were also activated by TPA in a time-dependent manner. Tetradecanoylphorbol Acetate 120-123 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 92-96 11448162-10 2001 These results show that TPA induces EBV reactivation via NF-kappaB and AP-1 and that PKC is an important mediator in regulating gene expression leading to EBV reactivation after TPA treatment of GT38 cells. Tetradecanoylphorbol Acetate 24-27 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-75 11145168-1 2000 Interaction between a tumor promoter, 12-O-tetradecanoylphorbol 13-acetate (TPA), and ligands of nuclear receptors has been interpreted as the result of crosstalk between the nuclear receptors and oncogenic transcription factor AP-1. Tetradecanoylphorbol Acetate 76-79 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 228-232 11121152-6 2000 Atopic dermatitis keratinocyte nuclear lysates had higher constitutive levels of c-Jun, and phorbol myristate acetate promoted an earlier and stronger expression of c-Jun, JunB, and of the phosphorylated forms of c-Fos. Tetradecanoylphorbol Acetate 92-117 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-176 10807873-8 2000 Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele. Tetradecanoylphorbol Acetate 0-31 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-77 10807873-8 2000 Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele. Tetradecanoylphorbol Acetate 0-31 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-108 10807873-8 2000 Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele. Tetradecanoylphorbol Acetate 33-36 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-77 10807873-8 2000 Phorbol 12-myristate 13-acetate (PMA) and insulin, 2 known activators of AP-1, increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele. Tetradecanoylphorbol Acetate 33-36 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-108 10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tetradecanoylphorbol Acetate 25-28 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 11216470-8 2000 Likewise, both compounds inhibited NF-kappaB and AP-1 activation in cultured human promyelocytic leukemia (HL-60) cells stimulated with TPA. Tetradecanoylphorbol Acetate 136-139 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 49-53 10514454-9 1999 However, it inhibited TPA-induced AP-1 activity in ZR75-1 cells and the constitutive AP-1 activity in H460 and H292 cells. Tetradecanoylphorbol Acetate 22-25 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 34-38 10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tetradecanoylphorbol Acetate 70-73 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tetradecanoylphorbol Acetate 70-73 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 10329043-7 1999 RESULTS: The CCA reporter line exhibited a radiation dose-responsive induction of AP-1 activity that was decreased by 5 microM 9cRA and increased by 50 ng/ml TPA. Tetradecanoylphorbol Acetate 158-161 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 82-86 10329043-8 1999 Simultaneous treatment with TPA and 9cRA prevented 9cRA repression of AP-1 and resulted in AP-1 activity above basal level. Tetradecanoylphorbol Acetate 28-31 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-74 10329043-8 1999 Simultaneous treatment with TPA and 9cRA prevented 9cRA repression of AP-1 and resulted in AP-1 activity above basal level. Tetradecanoylphorbol Acetate 28-31 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-95 10329043-11 1999 CONCLUSION: Although TPA prevented AP-1 repression by 9cRA, it did not prevent radiosensitization in CCA cultures, therefore the mechanism of radiosensitization of CCA by 9cRA is independent of AP-1 repression. Tetradecanoylphorbol Acetate 21-24 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 35-39 9356353-1 1997 Activating protein-1 (AP-1) binding TPA responsive elements (TRE) are located downstream of the transcription initiation site in the U5 region of the HIV-1 long terminal repeat (LTR). Tetradecanoylphorbol Acetate 36-39 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 22-26 9837861-9 1998 The results showed that TPA induced endogenous MnSOD expression and inhibited both AP-1 and NF-kappaB. Tetradecanoylphorbol Acetate 24-27 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-87 9419345-2 1998 Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells. Tetradecanoylphorbol Acetate 63-66 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-149 9419345-5 1998 TPA and EGF induce transactivation of AP-1 activity in P+ cells but not in P- cells. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-42 9419345-7 1998 Stable transfection of wild-type MAPK (Erk2) into P- cells restored its response to TPA and EGF for both AP-1 activation and cell transformation. Tetradecanoylphorbol Acetate 84-87 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-109 9434740-10 1997 In vitro DNA binding studies confirmed strong AP-1 activation under conditions where NF kappa B is blocked but the MnSOD transcript is strongly induced (e.g., PMA treatment in the presence of PDTC). Tetradecanoylphorbol Acetate 159-162 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-50 9377579-0 1997 Re-expression of elafin in 21MT2 breast carcinomas by phorbol 12-myristate 13-acetate is mediated by the Ap1 site in the elafin promoter. Tetradecanoylphorbol Acetate 54-85 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-108 9377579-4 1997 By deletion analysis and mutagenesis, we have identified the Ap1 site in the promoter as the cis element mediating transcriptional activation of elafin in 70N normal breast cells and its induction by phorbol 12-myristate 13-acetate (PMA) in 21MT2 breast tumors. Tetradecanoylphorbol Acetate 200-231 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 61-64 9377579-4 1997 By deletion analysis and mutagenesis, we have identified the Ap1 site in the promoter as the cis element mediating transcriptional activation of elafin in 70N normal breast cells and its induction by phorbol 12-myristate 13-acetate (PMA) in 21MT2 breast tumors. Tetradecanoylphorbol Acetate 233-236 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 61-64 9668098-8 1998 Further mutational analysis revealed that full TPA induction required interplay between several regulatory elements with homology to Ets, AP-1, and CAATT/enhancer binding protein C/EBP sites. Tetradecanoylphorbol Acetate 47-50 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 138-142 9668098-9 1998 In addition, deletion or mutation of a 10-base pair region juxtaposed to the AP-1 site dramatically increased TPA induced FGF-BP gene expression. Tetradecanoylphorbol Acetate 110-113 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-81 9668098-11 1998 Gel shift analysis showed specific and TPA-inducible protein binding to the Ets, AP-1, and C/EBP sites. Tetradecanoylphorbol Acetate 39-42 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-85 9523597-8 1998 These effects are compatible with (but likely not exclusively due to) an effect on the DNA binding of the 12-O-tetradecanoylphorbol 13-acetate response element to the AP-1 family of transcription factors. Tetradecanoylphorbol Acetate 106-142 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-171 9419345-2 1998 Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells. Tetradecanoylphorbol Acetate 25-61 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 124-143 9419345-2 1998 Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells. Tetradecanoylphorbol Acetate 25-61 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-149 9419345-2 1998 Tumor promoters, such as 12-O-tetradecanoylphorbol 13-acetate (TPA) or epidermal growth factor (EGF), induce high levels of activator protein 1 (AP-1) activity and large, tumorigenic, anchorage-independent colonies in soft agar at a high frequency in JB6 P+ cells, but not in JB6 P- cells. Tetradecanoylphorbol Acetate 63-66 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 124-143 9467952-4 1998 Whereas insulin stimulates prolonged induction of c-jun, but not of junB mRNA, resulting in c-jun expression during the entire G1 period, the growth inhibitor TPA induces junB much longer than c-jun. Tetradecanoylphorbol Acetate 159-162 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 171-175 9467952-5 1998 Inhibition of the Erk2 pathway by PD98059, specific for the upstream MAP kinase kinase (MEK1), abolishes TPA-stimulated junB but not insulin-induced c-jun. Tetradecanoylphorbol Acetate 105-108 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 120-124 9388222-5 1997 However, AP1 induction by 4beta-phorbol 12-myristate 13-acetate, which up-regulates Ras activity in a protein kinase C-dependent, TCR/tyrosine kinase-independent manner, was not affected by Cbl overexpression. Tetradecanoylphorbol Acetate 26-63 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-12 9176246-9 1997 The GR antagonist RU-486 inhibited the repressive effect of Dex on TNF-alpha-induced NF-kappa B activity by 81% but only counteracted the repressive effect of Dex on TPA-induced AP-1 activity by 43%. Tetradecanoylphorbol Acetate 166-169 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 178-182 9108029-8 1997 This process seems to be essential for AP-1 activation by redox modification because co-overexpression of TRX and Ref-1 in COS-7 cells potentiated AP-1 activity only after TRX was transported into the nucleus by phorbol 12-myristate 13 acetate treatment. Tetradecanoylphorbol Acetate 212-243 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-43 9138284-3 1997 The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 250-275 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-23 9138284-3 1997 The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 250-275 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-29 9138284-3 1997 The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 277-280 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-23 9138284-3 1997 The Activator Protein-1 (AP-1) site at approximately -70 bp upstream of the transcriptional start site has long been thought to play a dominant role in the transcriptional activation of the MMP promoters, particularly in response to stimulation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 277-280 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-29 8955111-3 1996 A series of deletion and mutation analyses of the enhancer sequences defined the 45-base pair core region (DR-1 core) containing two short elements with similarity to AP-1 (12-O-tetradecanoylphorbol-13-acetate response element; TRE) and CREB/ATF (cyclic AMP response element; CRE) binding sites, both of which were necessary for full enhancer activity. Tetradecanoylphorbol Acetate 173-209 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-171 8649827-5 1996 In cultured ovarian cancer cells, c-jun and jun-B expression is inducible by serum and TPA and is therefore not constitutive. Tetradecanoylphorbol Acetate 87-90 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-49 7898939-1 1995 The product of the junB gene is a member of the AP-1 family of transcription factors that activate transcription by binding to TPA-responsive elements (TREs) within the promoters of target genes. Tetradecanoylphorbol Acetate 127-130 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 19-23 11725057-7 1995 Both the AP-1/AP-2/SP-1 dyad protein binding region and, to a lesser extent, the YY1 tandem-repeat cluster conferred responsiveness to TPA when placed upstream of a heterologous promoter in transient expression assays. Tetradecanoylphorbol Acetate 135-138 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-13 8631129-10 1996 TCDD did not increase mRNA of c-fos, c-jun, junB or junD (in contrast to TPA which markedly increased the expression of c-fos and junB), nor did TCDD increase AP-1 activity. Tetradecanoylphorbol Acetate 73-76 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 130-134 7864072-3 1995 TNF-alpha, IL-1 beta and phorbol myristate acetate (PMA) treatment increased AP-1 and NF kappa B DNA binding by up to 200% but decreased CREB binding (38%) over a 60-min time course. Tetradecanoylphorbol Acetate 25-50 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-81 7864072-3 1995 TNF-alpha, IL-1 beta and phorbol myristate acetate (PMA) treatment increased AP-1 and NF kappa B DNA binding by up to 200% but decreased CREB binding (38%) over a 60-min time course. Tetradecanoylphorbol Acetate 52-55 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-81 7982981-0 1994 In vitro study of functional involvement of Sp1, NF-kappa B/Rel, and AP1 in phorbol 12-myristate 13-acetate-mediated HIV-1 long terminal repeat activation. Tetradecanoylphorbol Acetate 76-107 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 69-72 8180129-6 1994 AP-1 binding activity was enhanced by 12-O-tetradecanoylphorbol-13-acetate (TPA) and in a temporally dependent manner, with conversion of a high to low mobility band shift occurring after a 12-h exposure to TPA. Tetradecanoylphorbol Acetate 38-74 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 8001557-4 1994 Hydrogen peroxide prevented phorbol-myristate-acetate-stimulated AP-1 binding to DNA but stimulated it if protein kinase C was down-regulated or inhibited. Tetradecanoylphorbol Acetate 28-53 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-69 8171009-4 1994 Within this sequence there is a 12-O-tetradecanoylphorbol 13-acetate (TPA)-responsive element (TRE) which is essential for T1 promoter induction in response to the forced expression of the transcription factor AP-1 in NIH 3T3 fibroblasts and F9 teratocarcinoma cells. Tetradecanoylphorbol Acetate 32-68 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 210-214 8171009-4 1994 Within this sequence there is a 12-O-tetradecanoylphorbol 13-acetate (TPA)-responsive element (TRE) which is essential for T1 promoter induction in response to the forced expression of the transcription factor AP-1 in NIH 3T3 fibroblasts and F9 teratocarcinoma cells. Tetradecanoylphorbol Acetate 70-73 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 210-214 8114743-5 1994 We demonstrate that tetradecanoyl phorbol acetate treatment results in a marked and prolonged increase in AP-1 binding activity on these elements, which can be accounted for almost entirely by c-jun and junB. Tetradecanoylphorbol Acetate 20-49 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-110 8114743-5 1994 We demonstrate that tetradecanoyl phorbol acetate treatment results in a marked and prolonged increase in AP-1 binding activity on these elements, which can be accounted for almost entirely by c-jun and junB. Tetradecanoylphorbol Acetate 20-49 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 203-207 8180129-6 1994 AP-1 binding activity was enhanced by 12-O-tetradecanoylphorbol-13-acetate (TPA) and in a temporally dependent manner, with conversion of a high to low mobility band shift occurring after a 12-h exposure to TPA. Tetradecanoylphorbol Acetate 76-79 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 8180129-6 1994 AP-1 binding activity was enhanced by 12-O-tetradecanoylphorbol-13-acetate (TPA) and in a temporally dependent manner, with conversion of a high to low mobility band shift occurring after a 12-h exposure to TPA. Tetradecanoylphorbol Acetate 207-210 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 8180129-7 1994 After a 72-h exposure, AP-1 binding activity was maximally increased by 1 nM TPA and remained elevated to a similar degree even after treatment with 600 nM TPA. Tetradecanoylphorbol Acetate 77-80 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 23-27 8180129-7 1994 After a 72-h exposure, AP-1 binding activity was maximally increased by 1 nM TPA and remained elevated to a similar degree even after treatment with 600 nM TPA. Tetradecanoylphorbol Acetate 156-159 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 23-27 8180129-8 1994 Enhanced AP-1 binding activity was dependent upon continuous exposure to TPA and was not secondary to differentiation. Tetradecanoylphorbol Acetate 73-76 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-13 8180129-9 1994 A 72-h treatment with one nM TPA maximally increased expression of c-jun, krox-24, and jun-B mRNA transcripts. Tetradecanoylphorbol Acetate 29-32 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 87-92 8404639-4 1993 In K562 cells, this selective junB mRNA induction was synergistically augmented by treatment with 12-O-tetradecanoyl phorbol-13-acetate but not affected by forskolin. Tetradecanoylphorbol Acetate 98-135 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-34 8396805-10 1993 The response to the phorbol ester TPA also required a cooperation of M33 and AP1. Tetradecanoylphorbol Acetate 34-37 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-80 8389757-8 1993 Other studies further demonstrate that the jun-B and fra-1 genes are induced by TPA in both HL-60/vinc and HL-60/vinc/R cells, whereas c-fos expression is attenuated in the HL-60/vinc line. Tetradecanoylphorbol Acetate 80-83 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 43-48 1445798-4 1992 junB and fosB were rapidly induced following stimulation with TPA. Tetradecanoylphorbol Acetate 62-65 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 7860222-2 1993 The promoter and adjacent regulatory sequences of the 92-kD type IV collagenase have been identified previously and three cis-acting elements homologous to the binding sites for AP-1, NF-KB and SP-1 proteins contributed to induction of the promoter activity by 12-O-tetradecanoylphorbol 13-acetate (TPA) and tumor necrosis factor (TNF-alpha) in HT1080 cells. Tetradecanoylphorbol Acetate 261-297 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 178-182 7860222-2 1993 The promoter and adjacent regulatory sequences of the 92-kD type IV collagenase have been identified previously and three cis-acting elements homologous to the binding sites for AP-1, NF-KB and SP-1 proteins contributed to induction of the promoter activity by 12-O-tetradecanoylphorbol 13-acetate (TPA) and tumor necrosis factor (TNF-alpha) in HT1080 cells. Tetradecanoylphorbol Acetate 299-302 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 178-182 1445798-6 1992 The expression of fos and jun during T-cell activation was accompanied by increased specific binding of JunB, FosB, and fos-related antigen containing complexes to the TPA responsive element. Tetradecanoylphorbol Acetate 168-171 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-108 1634545-0 1992 Interaction of AP-1-, AP-2-, and Sp1-like proteins with two distinct sites in the upstream regulatory region of the plasminogen activator inhibitor-1 gene mediates the phorbol 12-myristate 13-acetate response. Tetradecanoylphorbol Acetate 168-199 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-19 1450490-4 1992 Thus, treatment of cells with TPA results in a reduction in the levels of c-myb and c-myc mRNA, while the expression of c-fos, c-jun, and junB is greatly enhanced. Tetradecanoylphorbol Acetate 30-33 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 138-142 1738590-4 1992 Induction of jun B can be mimicked in wild type P19 EC cells by the synergistic action of the phorbol ester TPA and the calcium ionophore A23187, through activation of signal transduction pathways, that are activated simultaneously by EGF. Tetradecanoylphorbol Acetate 108-111 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-18 1653238-11 1991 Two putative 12-O-tetradecanoyl-phorbol-13-acetate (TPA) response elements, that might serve as binding sites for the transcription factor AP-1 and a consensus sequence of a transforming growth factor beta 1 (TGF-beta 1) inhibitory element were found in the promoter region. Tetradecanoylphorbol Acetate 13-50 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 139-143 1655978-8 1991 TPA induced c-fos and junB mRNAs transiently and preceding NGF mRNA induction but c-jun mRNA remained undetectable. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 22-26 1653238-11 1991 Two putative 12-O-tetradecanoyl-phorbol-13-acetate (TPA) response elements, that might serve as binding sites for the transcription factor AP-1 and a consensus sequence of a transforming growth factor beta 1 (TGF-beta 1) inhibitory element were found in the promoter region. Tetradecanoylphorbol Acetate 52-55 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 139-143 1711045-8 1991 The promoter region also contains several potential binding sites for the transcription factors AP-1 and AP-2; consistent with the presence of these sites, Northern blot analysis demonstrated that the level of VEGF transcripts is elevated in cultured vascular smooth muscle cells after treatment with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate. Tetradecanoylphorbol Acetate 319-356 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 96-100 34114342-5 2021 The NF-kB /AP-1 transcription factors mediated effects of LPS and TPA on 20alpha-HSD gene transcription. Tetradecanoylphorbol Acetate 66-69 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 11-15 2007095-3 1991 The present studies have examined the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of jun-B gene expression during induction of monocytic differentiation. Tetradecanoylphorbol Acetate 49-85 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-118 2007095-3 1991 The present studies have examined the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) on the regulation of jun-B gene expression during induction of monocytic differentiation. Tetradecanoylphorbol Acetate 87-90 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-118 2007095-5 1991 In contrast, treatment with TPA was associated with rapid increases in jun-B mRNA levels that were maximal at 3 h and remained elevated at 48 h. The induction of jun-B expression by TPA in these cells preceded that of the c-jun and c-fos genes. Tetradecanoylphorbol Acetate 28-31 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-76 2007095-5 1991 In contrast, treatment with TPA was associated with rapid increases in jun-B mRNA levels that were maximal at 3 h and remained elevated at 48 h. The induction of jun-B expression by TPA in these cells preceded that of the c-jun and c-fos genes. Tetradecanoylphorbol Acetate 182-185 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 71-76 2007095-9 1991 In contrast, inhibition of protein synthesis was associated with superinduction of TPA-induced jun-B mRNA levels and an increase in stability of this transcript. Tetradecanoylphorbol Acetate 83-86 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 95-100 1900155-6 1991 The role of Jun-containing TRE binding proteins in promoting B cell cycle progression remains uncertain inasmuch as Jun-B has been associated with transcriptional inhibition of the TPA response element, rather than activation as produced by c-Jun. Tetradecanoylphorbol Acetate 181-184 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-121 1901643-3 1991 This fragment contains a sequence with a high degree of similarity to the binding site for the transcription factor activator protein-1 (AP-1) and indeed, the AP-1 sequence of this fragment is necessary but not sufficient for the maximal response to phorbol 12-myristate 13-acetate (phorbol) or interleukin-1. Tetradecanoylphorbol Acetate 250-281 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-135 1901643-3 1991 This fragment contains a sequence with a high degree of similarity to the binding site for the transcription factor activator protein-1 (AP-1) and indeed, the AP-1 sequence of this fragment is necessary but not sufficient for the maximal response to phorbol 12-myristate 13-acetate (phorbol) or interleukin-1. Tetradecanoylphorbol Acetate 250-281 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 137-141 1901643-3 1991 This fragment contains a sequence with a high degree of similarity to the binding site for the transcription factor activator protein-1 (AP-1) and indeed, the AP-1 sequence of this fragment is necessary but not sufficient for the maximal response to phorbol 12-myristate 13-acetate (phorbol) or interleukin-1. Tetradecanoylphorbol Acetate 250-281 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 159-163 34093777-6 2021 The results demonstrated that triptolide decreased the expression of MMP-9 through inhibition of the TPA-induced phosphorylation of extracellular signal-regulated kinase (ERK) and the downregulation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) activity. Tetradecanoylphorbol Acetate 101-104 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 240-259 3034432-3 1987 Footprinting analysis indicated that these TPA-responsive elements (TREs) are recognized by a common cellular protein: the previously described transcription factor AP-1. Tetradecanoylphorbol Acetate 43-46 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-169 2513128-1 1989 c-Jun, Jun-B, and Jun-D proteins bind to the TPA response element (TRE) either as homodimers or as Jun-Fos heterodimers. Tetradecanoylphorbol Acetate 45-48 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 7-12 2513129-2 1989 jun-B is less potent that c-jun in transforming and immortalizing primary rat embryo cells in cooperation with activated ras (effects enhanced by c-fos and TPA); unlike c-jun, jun-B does not transform Rat-1A cells alone. Tetradecanoylphorbol Acetate 156-159 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 29371085-0 2018 (E)-2-Methoxy-4-(3-(4-methoxyphenyl) prop-1-en-1-yl) phenol attenuates PMA-induced inflammatory responses in human monocytic cells through PKCdelta/JNK/AP-1 pathways. Tetradecanoylphorbol Acetate 71-74 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 152-156 33760219-0 2021 Bruton"s agammaglobulinemia tyrosine kinase (Btk) regulates TPA-induced breast cancer cell invasion via PLCgamma2/PKCbeta/NF-kappaB/AP-1-dependent matrix metalloproteinase-9 activation. Tetradecanoylphorbol Acetate 60-63 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-136 30466990-0 2018 Orientin inhibits invasion by suppressing MMP-9 and IL-8 expression via the PKCalpha/ ERK/AP-1/STAT3-mediated signaling pathways in TPA-treated MCF-7 breast cancer cells. Tetradecanoylphorbol Acetate 132-135 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-94 30466990-7 2018 TPA-induced membrane translocation of protein kinase C alpha (PKCalpha), phosphorylation of extracellular signal regulated kinase (ERK), and nuclear translocations of activator protein-1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) were downregulated by orientin. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-186 30466990-7 2018 TPA-induced membrane translocation of protein kinase C alpha (PKCalpha), phosphorylation of extracellular signal regulated kinase (ERK), and nuclear translocations of activator protein-1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) were downregulated by orientin. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 188-192 30133131-6 2018 TPA-induced membrane translocation of PKCalpha, phosphorylation of JNK, and the nuclear translocations of AP-1 and NF-kappaB were downregulated by mLU8C-PU in MCF-7 cells. Tetradecanoylphorbol Acetate 0-3 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-110 30133131-8 2018 These results indicate that mLU8C-PU inhibits migratory and invasive responses in MCF-7 breast cancer cells by suppressing MMP-9 and IL-8 expression through mitigating TPA-induced PKCalpha, JNK activation, and the nuclear translocation of AP-1 and NF-kappaB. Tetradecanoylphorbol Acetate 168-171 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 239-243 29371085-6 2018 MMPP inhibited PMA-induced membrane translocation of PKCdelta, phosphorylation of JNK, and nuclear translocation of AP-1, resulting in downregulation of cyclooxygenase-2 and chemokine ligand 5 production. Tetradecanoylphorbol Acetate 15-18 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-120 29371085-7 2018 These findings indicate that MMPP inhibits inflammatory responses in THP-1 cells by mitigating PMA-induced activation of PKCdelta and JNK and nuclear translocation of AP-1. Tetradecanoylphorbol Acetate 95-98 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 167-171