PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25698902-5 2015 We also observed through a Western blotting assay that galangin strongly inhibited the TPA-induced protein expressions of protein kinase Calpha (PKCalpha), protein kinase Cdelta (PKCdelta), phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), the phospho-inhibitor of kappaBalpha (phospho-IkappaBalpha), c-Fos, c-Jun, and nuclear factor kappa B (NF-kappaB). Tetradecanoylphorbol Acetate 87-90 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 325-330 28098862-8 2017 Furthermore, rhein significantly inhibited JNK, AP-1 phosphorylation in the cells treated with PMA. Tetradecanoylphorbol Acetate 95-98 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 48-52 27708396-3 2016 Here, we demonstrate that ERK/c-Jun signaling is involved in DNA demethylation of EBV immediate early (IE) gene Zta in response to 12-O-Tetradecanoylphorbol-13-acetate (TPA) stimulation. Tetradecanoylphorbol Acetate 131-167 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 27708396-3 2016 Here, we demonstrate that ERK/c-Jun signaling is involved in DNA demethylation of EBV immediate early (IE) gene Zta in response to 12-O-Tetradecanoylphorbol-13-acetate (TPA) stimulation. Tetradecanoylphorbol Acetate 169-172 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 27708396-8 2016 Thus, TPA activates ERK/c-Jun signaling, which subsequently facilitates Tet1 to bind to Zta promoter, leading to DNA demethylation, gene expression, and EBV reactivation. Tetradecanoylphorbol Acetate 6-9 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-29 26431317-7 2015 Further analysis revealed that TPA+UVC co-exposure caused synergistic perturbation of specific genes associated with p53, AP-1 and inflammatory pathways important in carcinogenesis. Tetradecanoylphorbol Acetate 31-34 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 122-126 25666088-5 2015 Our aim of the present study is to investigate the pro-inflammatory cytokines and pattern of AP-1 factors expressed during activation of lung adenocarcinoma A549 cells by Phorbol-12-myristate-13-acetate (PMA) and to understand the anti-inflammatory effect of apigenin. Tetradecanoylphorbol Acetate 171-202 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-97 25666088-5 2015 Our aim of the present study is to investigate the pro-inflammatory cytokines and pattern of AP-1 factors expressed during activation of lung adenocarcinoma A549 cells by Phorbol-12-myristate-13-acetate (PMA) and to understand the anti-inflammatory effect of apigenin. Tetradecanoylphorbol Acetate 204-207 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-97 25915860-0 2015 12-O-Tetradecanoylphorbol-13-Acetate Induces Up-Regulated Transcription of Variant 1 but Not Variant 2 of VIL2 in Esophageal Squamous Cell Carcinoma Cells via ERK1/2/AP-1/Sp1 Signaling. Tetradecanoylphorbol Acetate 0-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 166-170 25915860-7 2015 AP-1 and Sp1 binding sites within the promoter region of VIL2 V1 acted not only as basal transcriptional elements but also as a composite TPA-responsive element (TRE) for the transcription of VIL2 V1. Tetradecanoylphorbol Acetate 138-141 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 25915860-8 2015 TPA stimulation enhanced c-Jun and Sp1 binding to the TRE via activation of the ERK1/2 pathway and increased protein levels of c-Jun, c-Fos, and Sp1, resulting in over-expression of VIL2 V1, whereas the MEK1/2 inhibitor U0126 blocked these events. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-30 25915860-8 2015 TPA stimulation enhanced c-Jun and Sp1 binding to the TRE via activation of the ERK1/2 pathway and increased protein levels of c-Jun, c-Fos, and Sp1, resulting in over-expression of VIL2 V1, whereas the MEK1/2 inhibitor U0126 blocked these events. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 127-132 25915860-10 2015 Taken together, these results suggest that TPA is able to induce VIL2 V1 over-expression in ESCC cells by activating MEK/ERK1/2 signaling and increasing binding of Sp1 and c-Jun to the TRE of the VIL2 V1 promoter, and that VIL2 is an important TPA-induced effector. Tetradecanoylphorbol Acetate 43-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-177 25530093-8 2015 Moreover, TPA (12-O-tetradecanoylphorbol-13-acetate), a potent inducer of c-Jun, could remarkably promote viral immediate-early gene wsv069 transcription in crayfish hemocytes. Tetradecanoylphorbol Acetate 10-13 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 74-79 25530093-8 2015 Moreover, TPA (12-O-tetradecanoylphorbol-13-acetate), a potent inducer of c-Jun, could remarkably promote viral immediate-early gene wsv069 transcription in crayfish hemocytes. Tetradecanoylphorbol Acetate 15-51 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 74-79 25533502-5 2015 Moreover, butein abolished TNF-alpha- and PMA-induced IkappaBalpha phosphorylation, which participates in NF-kappaB activation, and PMA-induced phosphorylation of c-Jun, a subunit composed of AP-1. Tetradecanoylphorbol Acetate 42-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 192-196 25533502-0 2015 Butein suppresses ICAM-1 expression through the inhibition of IkappaBalpha and c-Jun phosphorylation in TNF-alpha- and PMA-treated HUVECs. Tetradecanoylphorbol Acetate 119-122 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-84 25533502-6 2015 In vitro, butein inhibited the phosphorylation of c-Jun, binding to GST beads, mediated by JNK isolated from PMA-treated cells. Tetradecanoylphorbol Acetate 109-112 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 50-55 25143809-0 2014 The Heterochromatin-1 Phosphorylation Contributes to TPA-Induced AP-1 Expression. Tetradecanoylphorbol Acetate 53-56 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-69 25143809-4 2014 In the present study, we show that heterochromatin 1 gamma (HP1gamma) plays a negative role in TPA-induced c-Jun and c-Fos expression. Tetradecanoylphorbol Acetate 95-98 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 107-112 24753227-4 2014 The 12-O-tetradecanoylphorbol-13-acetate-responsive element, a binding site for c-Jun and c-Fos, was identified as resveratrol-responsive element. Tetradecanoylphorbol Acetate 4-40 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 80-85 24796531-6 2014 c-Jun increased expression of SPPR3 mainly via a PKC/JNK pathway in response to TPA in KYSE450 cells. Tetradecanoylphorbol Acetate 80-83 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 22561169-6 2012 A reporter gene assay revealed that Mn2+ promoted the activity of AP-1 (activator protein-1, a complex of c-Fos and c-Jun) in the presence of PMA. Tetradecanoylphorbol Acetate 142-145 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 66-70 24743307-8 2014 In support of this notion, we observed decreased CSB occupancy of TPA-response elements when c-Jun levels were diminished. Tetradecanoylphorbol Acetate 66-69 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-98 23396363-1 2014 The inducible proto-oncogenic (c-Fos:c-Jun)/AP-1 transcription complex binds 12-O-tetradecanoylphorbol 13-acetate (TPA)-responsive elements (TRE) in its target genes. Tetradecanoylphorbol Acetate 77-113 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-42 23396363-1 2014 The inducible proto-oncogenic (c-Fos:c-Jun)/AP-1 transcription complex binds 12-O-tetradecanoylphorbol 13-acetate (TPA)-responsive elements (TRE) in its target genes. Tetradecanoylphorbol Acetate 115-118 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-42 23647419-5 2013 The AP-1 agonist, tetradeconoyl-12,13-phorbol acetate (TPA), also stimulated hTH promoter activity, and Dex and TPA together further accentuated this response. Tetradecanoylphorbol Acetate 55-58 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-8 23647419-5 2013 The AP-1 agonist, tetradeconoyl-12,13-phorbol acetate (TPA), also stimulated hTH promoter activity, and Dex and TPA together further accentuated this response. Tetradecanoylphorbol Acetate 112-115 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-8 22351517-6 2013 TPA treatment also elevates levels of c-jun (AP-1 component), cyclooxygenase-2 (COX-2), p50 (NF-kappaB component), interleukin-6 (IL-6), and tumor necrosis factor (TNF) in the skin. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-43 22351517-6 2013 TPA treatment also elevates levels of c-jun (AP-1 component), cyclooxygenase-2 (COX-2), p50 (NF-kappaB component), interleukin-6 (IL-6), and tumor necrosis factor (TNF) in the skin. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-49 22505246-5 2012 Juglone significantly suppressed TPA-induced protein kinase B (AKT) and c-Jun phosphorylation and c-fos activation, but not mitogen-activated protein-kinase kinase (MEK), extracellular signaling-regulated kinase (ERK) or 90 kDa ribosomal protein S6 kinase (RSK) phosphorylation. Tetradecanoylphorbol Acetate 33-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 72-77 22561169-6 2012 A reporter gene assay revealed that Mn2+ promoted the activity of AP-1 (activator protein-1, a complex of c-Fos and c-Jun) in the presence of PMA. Tetradecanoylphorbol Acetate 142-145 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 72-91 22561169-6 2012 A reporter gene assay revealed that Mn2+ promoted the activity of AP-1 (activator protein-1, a complex of c-Fos and c-Jun) in the presence of PMA. Tetradecanoylphorbol Acetate 142-145 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-121 22561169-8 2012 These results suggest that Mn2+ promotes PMA-induced IL-2 production by inducing the production and activation of AP-1, at least in part. Tetradecanoylphorbol Acetate 41-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-118 22151918-8 2012 In the nucleus, it has also strongly suppressed TPA-stimulated expression of NF-kappaB, c-Jun and c-Fos. Tetradecanoylphorbol Acetate 48-51 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 88-93 21377232-2 2012 The binding of AP-1 proteins to the 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element can activate target genes and regulate many critical cellular processes. Tetradecanoylphorbol Acetate 36-72 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-19 21377232-2 2012 The binding of AP-1 proteins to the 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element can activate target genes and regulate many critical cellular processes. Tetradecanoylphorbol Acetate 74-77 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-19 21864583-3 2011 In this study, we examined the functional roles of mouse Zac1 (mZac1) in HeLa cells treated with 12-O-tetradecanoylphorbol-13-acetate (PMA), a potent Activator protein 1 (AP-1) activator. Tetradecanoylphorbol Acetate 97-133 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 150-169 22299029-0 2012 Differential role of PKC-induced c-Jun in HTLV-1 LTR activation by 12-O-tetradecanoylphorbol-13-acetate in different human T-cell lines. Tetradecanoylphorbol Acetate 67-103 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 33-38 21864583-3 2011 In this study, we examined the functional roles of mouse Zac1 (mZac1) in HeLa cells treated with 12-O-tetradecanoylphorbol-13-acetate (PMA), a potent Activator protein 1 (AP-1) activator. Tetradecanoylphorbol Acetate 97-133 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 171-175 21864583-3 2011 In this study, we examined the functional roles of mouse Zac1 (mZac1) in HeLa cells treated with 12-O-tetradecanoylphorbol-13-acetate (PMA), a potent Activator protein 1 (AP-1) activator. Tetradecanoylphorbol Acetate 135-138 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 150-169 21864583-3 2011 In this study, we examined the functional roles of mouse Zac1 (mZac1) in HeLa cells treated with 12-O-tetradecanoylphorbol-13-acetate (PMA), a potent Activator protein 1 (AP-1) activator. Tetradecanoylphorbol Acetate 135-138 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 171-175 21106746-5 2011 Site-directed mutagenesis studies indicate that both AP-1 response elements are critical for 12-O-tetradecanoylphorbol-13-acetate (TPA)-enhanced MIEP activity in transient-transfection assays. Tetradecanoylphorbol Acetate 93-129 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-57 21106746-5 2011 Site-directed mutagenesis studies indicate that both AP-1 response elements are critical for 12-O-tetradecanoylphorbol-13-acetate (TPA)-enhanced MIEP activity in transient-transfection assays. Tetradecanoylphorbol Acetate 131-134 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-57 20131957-0 2010 Hyul-Tong-Ryung suppresses PMA-induced MMP-9 expression by inhibiting AP-1-mediated gene expression via ERK 1/2 signaling pathway in MCF-7 human breast cancer cells. Tetradecanoylphorbol Acetate 27-30 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-74 20131957-7 2010 These results indicate that HM inhibits PMA-induced MMP-9 expression by blocking the activation of activator protein-1 (AP-1) via extracellular signal regulated kinase 1/2 (ERK 1/2) signaling pathway. Tetradecanoylphorbol Acetate 40-43 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-118 20131957-7 2010 These results indicate that HM inhibits PMA-induced MMP-9 expression by blocking the activation of activator protein-1 (AP-1) via extracellular signal regulated kinase 1/2 (ERK 1/2) signaling pathway. Tetradecanoylphorbol Acetate 40-43 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 120-124 20025870-7 2010 In contrast, treatment of HASM by PMA induces phosphorylation and activation of Ra, MEK1/2, ERK1/2, JNK, Elk-1, and c-Jun. Tetradecanoylphorbol Acetate 34-37 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-121 20590612-0 2010 Metformin blocks migration and invasion of tumour cells by inhibition of matrix metalloproteinase-9 activation through a calcium and protein kinase Calpha-dependent pathway: phorbol-12-myristate-13-acetate-induced/extracellular signal-regulated kinase/activator protein-1. Tetradecanoylphorbol Acetate 174-205 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 252-271 20590612-6 2010 In these cells, metformin also suppressed phorbol-12-myristate-13-acetate (PMA)-enhanced levels of matrix metalloproteinases-9 (MMP-9) protein, mRNA and transcription activity through suppression of activator protein-1 (AP-1) activation. Tetradecanoylphorbol Acetate 42-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 199-218 20590612-6 2010 In these cells, metformin also suppressed phorbol-12-myristate-13-acetate (PMA)-enhanced levels of matrix metalloproteinases-9 (MMP-9) protein, mRNA and transcription activity through suppression of activator protein-1 (AP-1) activation. Tetradecanoylphorbol Acetate 42-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 220-224 20590612-6 2010 In these cells, metformin also suppressed phorbol-12-myristate-13-acetate (PMA)-enhanced levels of matrix metalloproteinases-9 (MMP-9) protein, mRNA and transcription activity through suppression of activator protein-1 (AP-1) activation. Tetradecanoylphorbol Acetate 75-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 199-218 20590612-6 2010 In these cells, metformin also suppressed phorbol-12-myristate-13-acetate (PMA)-enhanced levels of matrix metalloproteinases-9 (MMP-9) protein, mRNA and transcription activity through suppression of activator protein-1 (AP-1) activation. Tetradecanoylphorbol Acetate 75-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 220-224 20590612-10 2010 CONCLUSIONS AND IMPLICATIONS: Metformin inhibited PMA-induced invasion and migration of human fibrosarcoma cells via Ca(2+)-dependent PKCalpha/ERK and JNK/AP-1-signalling pathways. Tetradecanoylphorbol Acetate 50-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 155-159 20152819-5 2010 DHA suppressed PMA-enhanced expression of MMP-9 protein, mRNA, and transcriptional activity through suppressing NF-kappaB and AP-1 activation without changing the level of tissue inhibitor of metalloproteinase (TIMP)-1. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 126-130 20152819-7 2010 DHA-inhibited PMA-induced NF-kappaB and c-Jun nuclear translocation, which are upstream of PMA-induced MMP-9 expression and invasion. Tetradecanoylphorbol Acetate 14-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-45 20152819-7 2010 DHA-inhibited PMA-induced NF-kappaB and c-Jun nuclear translocation, which are upstream of PMA-induced MMP-9 expression and invasion. Tetradecanoylphorbol Acetate 91-94 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-45 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 280-285 20053986-5 2010 Whereas monomeric c-Fos is highly mobile and distributed evenly with nucleolar exclusion in the nucleus, heterodimerization with c-Jun entails intranuclear redistribution and dramatic reduction in mobility of c-Fos caused by predominant association with the nuclear matrix independently of any binding to AP-1/12-O-tetradecanoylphorbol-13-acetate-responsive element or cAMP-responsive element sequences. Tetradecanoylphorbol Acetate 310-346 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 129-134 19768635-0 2010 Plumbagin inhibits TPA-induced MMP-2 and u-PA expressions by reducing binding activities of NF-kappaB and AP-1 via ERK signaling pathway in A549 human lung cancer cells. Tetradecanoylphorbol Acetate 19-22 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-110 19768635-4 2010 Next, plumbagin also strongly inhibited TPA-induced phosphorylation and degradation of inhibitor of kappaBalpha (IkappaBalpha), and the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun. Tetradecanoylphorbol Acetate 40-43 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 201-206 19853631-6 2010 In addition, the c-Jun mutant blocked the IP activity stimulated by TPA. Tetradecanoylphorbol Acetate 68-71 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 17-22 20492173-4 2010 Next, alpha-mangostin also strongly inhibited TPA-induced degradation of inhibitor of kappaBalpha (IkappaBalpha) and the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun. Tetradecanoylphorbol Acetate 46-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-191 20492175-0 2010 Acacetin inhibits TPA-induced MMP-2 and u-PA expressions of human lung cancer cells through inactivating JNK signaling pathway and reducing binding activities of NF-kappaB and AP-1. Tetradecanoylphorbol Acetate 18-21 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 176-180 20492175-5 2010 Next, acacetin also strongly inhibited TPA-stimulated the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun. Tetradecanoylphorbol Acetate 39-42 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 123-128 20492175-8 2010 Taken together, these results suggest the antimetastatic effects of acacetin on the TPA-induced A549 cells might be by reducing MMP-2 and u-PA expressions through inhibiting phosphorylation of JNK and reducing NF-kappaB and AP-1 binding activities. Tetradecanoylphorbol Acetate 84-87 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 224-228 19541923-12 2009 Ectopic expression of c-Jun/c-Fos or p300 or treatment of cells with phorbol 12-myristate 13-acetate (PMA) stimulated endogenous TFF2 mRNA expression and promoter activity, and p53 inhibited the effects of AP-1 and PMA on TFF2. Tetradecanoylphorbol Acetate 102-105 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 22-27 19164581-4 2009 After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. Tetradecanoylphorbol Acetate 44-80 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 31-35 19130490-6 2009 Electrophoretic mobility shift assays (EMSA), showed that NO specifically interferes with the TPA-induced DNA binding affinity of c-Jun and c-Fos without affecting the TPA-induced increase in the levels of the transcription factors. Tetradecanoylphorbol Acetate 94-97 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 130-135 19176525-5 2009 A serine-to-alanine mutation at position 121 of ATF-2 represses the c-Jun-dependent transcription of AP-1/cyclic AMP-response element reporter genes and also the p300-mediated activation of a Gal4-reporter gene in response to TPA. Tetradecanoylphorbol Acetate 226-229 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 68-73 19176525-6 2009 Our results suggest that the phosphorylation of ATF-2 at Ser-121 plays a key role in the c-Jun-mediated activation of transcription that occurs in response to TPA. Tetradecanoylphorbol Acetate 159-162 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 89-94 19164581-4 2009 After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. Tetradecanoylphorbol Acetate 44-80 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-114 19164581-4 2009 After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. Tetradecanoylphorbol Acetate 44-80 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 157-162 19164581-4 2009 After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. Tetradecanoylphorbol Acetate 82-85 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 31-35 19164581-4 2009 After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. Tetradecanoylphorbol Acetate 82-85 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 110-114 19164581-4 2009 After exposure of cells to the AP-1 agonist 12-O-tetradecanoylphorbol-13-acetate (TPA), CRTC1 is recruited to AP-1 target gene promoters and associates with c-Jun and c-Fos to activate transcription. Tetradecanoylphorbol Acetate 82-85 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 157-162 19018257-6 2008 TAM67 increased dephosphorylation of Akt induced by LY294002 and reduced the TPA response element DNA-binding of phosphorylated c-Jun. Tetradecanoylphorbol Acetate 77-80 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 128-133 19418353-6 2009 PMA induced the translocation of c-jun and p65 to the nucleus; however, IPE inhibited their nuclear translocations induced by PMA in HepG2 cells. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 33-38 18628248-4 2008 Application of QUE significantly suppressed TPA-induced activation of the PKCdelta/ERK/AP-1-signaling cascade. Tetradecanoylphorbol Acetate 44-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 87-91 18024477-0 2008 Lucidenic acid inhibits PMA-induced invasion of human hepatoma cells through inactivating MAPK/ERK signal transduction pathway and reducing binding activities of NF-kappaB and AP-1. Tetradecanoylphorbol Acetate 24-27 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 176-180 18628248-3 2008 A translocation of protein kinase C (PKC)delta from the cytosol to the membrane followed by activation of extracellular signal-regulated kinase (ERK) and c-Jun/activator protein-1 (AP-1) by TPA was demonstrated, and TPA-induced MMP-9 activation and migration were inhibited by the pan PKC inhibitor, GF109203X, the specific PKCdelta inhibitor, rottlerin, an ERK inhibitor (PD98059) and an AP-1 inhibitor (curcumin). Tetradecanoylphorbol Acetate 190-193 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 154-179 18628248-3 2008 A translocation of protein kinase C (PKC)delta from the cytosol to the membrane followed by activation of extracellular signal-regulated kinase (ERK) and c-Jun/activator protein-1 (AP-1) by TPA was demonstrated, and TPA-induced MMP-9 activation and migration were inhibited by the pan PKC inhibitor, GF109203X, the specific PKCdelta inhibitor, rottlerin, an ERK inhibitor (PD98059) and an AP-1 inhibitor (curcumin). Tetradecanoylphorbol Acetate 190-193 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 181-185 18628248-3 2008 A translocation of protein kinase C (PKC)delta from the cytosol to the membrane followed by activation of extracellular signal-regulated kinase (ERK) and c-Jun/activator protein-1 (AP-1) by TPA was demonstrated, and TPA-induced MMP-9 activation and migration were inhibited by the pan PKC inhibitor, GF109203X, the specific PKCdelta inhibitor, rottlerin, an ERK inhibitor (PD98059) and an AP-1 inhibitor (curcumin). Tetradecanoylphorbol Acetate 190-193 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 389-393 18628248-3 2008 A translocation of protein kinase C (PKC)delta from the cytosol to the membrane followed by activation of extracellular signal-regulated kinase (ERK) and c-Jun/activator protein-1 (AP-1) by TPA was demonstrated, and TPA-induced MMP-9 activation and migration were inhibited by the pan PKC inhibitor, GF109203X, the specific PKCdelta inhibitor, rottlerin, an ERK inhibitor (PD98059) and an AP-1 inhibitor (curcumin). Tetradecanoylphorbol Acetate 216-219 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 181-185 18541274-3 2008 Zinc significantly reduced IFN-gamma expression and activator protein-1 (AP-1) signaling in cells activated by phorbol 12-myristate 13-acetate (PMA) and phytohemagglutinin (PHA) without affecting cell viability. Tetradecanoylphorbol Acetate 111-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 52-71 18541274-3 2008 Zinc significantly reduced IFN-gamma expression and activator protein-1 (AP-1) signaling in cells activated by phorbol 12-myristate 13-acetate (PMA) and phytohemagglutinin (PHA) without affecting cell viability. Tetradecanoylphorbol Acetate 111-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-77 18541274-3 2008 Zinc significantly reduced IFN-gamma expression and activator protein-1 (AP-1) signaling in cells activated by phorbol 12-myristate 13-acetate (PMA) and phytohemagglutinin (PHA) without affecting cell viability. Tetradecanoylphorbol Acetate 144-147 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 52-71 18541274-3 2008 Zinc significantly reduced IFN-gamma expression and activator protein-1 (AP-1) signaling in cells activated by phorbol 12-myristate 13-acetate (PMA) and phytohemagglutinin (PHA) without affecting cell viability. Tetradecanoylphorbol Acetate 144-147 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-77 18024477-9 2008 In conclusion, we demonstrated that the anti-invasive effects of the LAB on the PMA-induced HepG(2) cells might be through inhibiting the phosphorylation of ERK1/2 and reducing AP-1 and NF-kappaB DNA-binding activities, leading to downregulation of MMP-9 expression. Tetradecanoylphorbol Acetate 80-83 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 177-181 18024477-7 2008 Moreover, LAB also strongly inhibited PMA-stimulated nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) DNA-binding activities of HepG(2) cells in dose-dependent manners. Tetradecanoylphorbol Acetate 38-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 92-111 18024477-7 2008 Moreover, LAB also strongly inhibited PMA-stimulated nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) DNA-binding activities of HepG(2) cells in dose-dependent manners. Tetradecanoylphorbol Acetate 38-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-117 17215518-1 2007 The c-Jun/Sp1 interaction is essential for growth factor- and phorbol 12-myristate 13-acetate (PMA)-induced genes expression, including human 12(S)-lipoxygenase, keratin 16, cytosolic phospholipase A2, p21(WAF1/CIP1), and neuronal nicotinic acetylcholine receptor beta4. Tetradecanoylphorbol Acetate 62-93 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 17215518-1 2007 The c-Jun/Sp1 interaction is essential for growth factor- and phorbol 12-myristate 13-acetate (PMA)-induced genes expression, including human 12(S)-lipoxygenase, keratin 16, cytosolic phospholipase A2, p21(WAF1/CIP1), and neuronal nicotinic acetylcholine receptor beta4. Tetradecanoylphorbol Acetate 95-98 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 17215518-2 2007 Here, we examined the mechanism underlying the PMA-induced regulation on the interaction between c-Jun and Sp1. Tetradecanoylphorbol Acetate 47-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 97-102 17314023-1 2007 Long-term culture of phorbol ester (TPA)-differentiated and growth-arrested human U937 leukemia cells was associated with expression of c-jun transcription factors and vimentin intermediate filaments until the cells entered a retrodifferentiation program. Tetradecanoylphorbol Acetate 36-39 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 136-141 17215518-3 2007 We found that treatment of cells with PMA induced a dephosphorylation at the C terminus of c-Jun at Ser-243 and a concomitant inhibition of PP2B by using PP2B small interfering RNA, resulting in reduction of PMA-induced gene expression as well as the c-Jun/Sp1 interaction. Tetradecanoylphorbol Acetate 38-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 17215518-3 2007 We found that treatment of cells with PMA induced a dephosphorylation at the C terminus of c-Jun at Ser-243 and a concomitant inhibition of PP2B by using PP2B small interfering RNA, resulting in reduction of PMA-induced gene expression as well as the c-Jun/Sp1 interaction. Tetradecanoylphorbol Acetate 38-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 251-256 17215518-4 2007 The c-Jun mutant TAM-67-3A, which contains three substitute alanines at Thr-231, Ser-243, and Ser-249 compared with TAM-67, binds more efficaciously with Sp1 and is about twice as efficacious as TAM-67 in inhibiting the PMA-induced activation of the 12(S)-lipoxygenase promoter. Tetradecanoylphorbol Acetate 220-223 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 17082637-3 2006 In this study, we report that TNF-alpha stimulates the expression of the FRA-1 protooncogene in human pulmonary epithelial cells using c-Jun, acting via a 12-O-tetradecanoylphorbol-13 acetate response element located at -318. Tetradecanoylphorbol Acetate 155-191 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 135-140 17404068-7 2007 Since the transcription factor activator protein-1 (AP-1) plays a role in tumor promotion and is also known to regulate COX-2 induction, we attempted to determine the effect of KG-135 on TPA-induced activation of AP-1. Tetradecanoylphorbol Acetate 187-190 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 31-50 17404068-7 2007 Since the transcription factor activator protein-1 (AP-1) plays a role in tumor promotion and is also known to regulate COX-2 induction, we attempted to determine the effect of KG-135 on TPA-induced activation of AP-1. Tetradecanoylphorbol Acetate 187-190 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 213-217 17404068-8 2007 Cotreatment with KG-135 resulted in a decrease in TPA-induced DNA binding of AP-1. Tetradecanoylphorbol Acetate 50-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-81 17404068-11 2007 Taken together, the above findings suggest that KG-135 inhibits TPA-induced COX-2 expression in MCF-10A cells by blocking the JNK/AP-1 signaling pathway. Tetradecanoylphorbol Acetate 64-67 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 130-134 16888805-0 2007 Interleukin-1beta and tetradecanoylphorbol acetate-induced biosynthesis of tumor necrosis factor alpha in human hepatoma cells involves the transcription factors ATF2 and c-Jun and stress-activated protein kinases. Tetradecanoylphorbol Acetate 22-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 171-176 16888805-5 2007 Both IL-1beta and TPA triggered phosphorylation and activation of the basic region leucine zipper transcription factors c-Jun and ATF2 and expression of dominant-negative mutants of c-Jun and ATF2-reduced TNFalpha promoter activity and secretion of TNFalpha. Tetradecanoylphorbol Acetate 18-21 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 120-125 16888805-5 2007 Both IL-1beta and TPA triggered phosphorylation and activation of the basic region leucine zipper transcription factors c-Jun and ATF2 and expression of dominant-negative mutants of c-Jun and ATF2-reduced TNFalpha promoter activity and secretion of TNFalpha. Tetradecanoylphorbol Acetate 18-21 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 182-187 16757545-7 2006 Stimulation of PKC using the phorbol ester 12-O-tetradecanoylphorbol 13-acetate caused a rapid, significant (P < or = 0.05) increase in c-Jun and c-Fos concentrations but a significant decrease in mRNA for OTR within 6 h followed by a significant decrease in OT binding by 24 h. Adenoviral infection of the cells with expression vectors for c-Jun and c-Fos increased the AP-1 subunits but had no effect on OTR expression. Tetradecanoylphorbol Acetate 43-79 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 139-144 16757545-7 2006 Stimulation of PKC using the phorbol ester 12-O-tetradecanoylphorbol 13-acetate caused a rapid, significant (P < or = 0.05) increase in c-Jun and c-Fos concentrations but a significant decrease in mRNA for OTR within 6 h followed by a significant decrease in OT binding by 24 h. Adenoviral infection of the cells with expression vectors for c-Jun and c-Fos increased the AP-1 subunits but had no effect on OTR expression. Tetradecanoylphorbol Acetate 43-79 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 344-349 16940435-4 2006 After 1 h, TPA increased total c-jun mRNA by 10.5-fold. Tetradecanoylphorbol Acetate 11-14 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 31-36 16651411-9 2006 In the presence of TPA, whereas ERalpha was not bound to the promoter, a strong association of acetylated and/or phospho-H3, MSK1, and c-Jun was observed. Tetradecanoylphorbol Acetate 19-22 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 135-140 15831482-0 2005 Selective regulation of c-jun gene expression by mitogen-activated protein kinases via the 12-o-tetradecanoylphorbol-13-acetate- responsive element and myocyte enhancer factor 2 binding sites. Tetradecanoylphorbol Acetate 91-127 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-29 16651411-6 2006 Mutation of the activator protein 1 (AP-1) binding site abrogated the TPA-induced transcriptional response of the luciferase reporter gene under the control of the TFF1 promoter, showing the requirement for the AP-1 site. Tetradecanoylphorbol Acetate 70-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-35 16651411-6 2006 Mutation of the activator protein 1 (AP-1) binding site abrogated the TPA-induced transcriptional response of the luciferase reporter gene under the control of the TFF1 promoter, showing the requirement for the AP-1 site. Tetradecanoylphorbol Acetate 70-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-41 16651411-6 2006 Mutation of the activator protein 1 (AP-1) binding site abrogated the TPA-induced transcriptional response of the luciferase reporter gene under the control of the TFF1 promoter, showing the requirement for the AP-1 site. Tetradecanoylphorbol Acetate 70-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 211-215 16480952-0 2006 Differentiation-associated genes regulated by TPA-induced c-Jun expression via a PKC/JNK pathway in KYSE450 cells. Tetradecanoylphorbol Acetate 46-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-63 16480952-3 2006 To further understand how the mitogen-activated protein kinase signaling pathways regulate AP-1 activity and expression of c-Jun target genes, our strategy was based on the use of 12-o-tetradecanoylophorbol-13-acetate (TPA) and pharmacological reagents to induce or block c-Jun expression. Tetradecanoylphorbol Acetate 219-222 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 123-128 16480952-4 2006 The mRNA and protein expression of these genes increased in response to TPA-induced c-Jun/AP-1 expression. Tetradecanoylphorbol Acetate 72-75 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 84-89 16480952-4 2006 The mRNA and protein expression of these genes increased in response to TPA-induced c-Jun/AP-1 expression. Tetradecanoylphorbol Acetate 72-75 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-94 16480952-7 2006 Taken together, these results suggested that differentiation-associated genes were regulated by TPA-induced c-Jun/AP-1 mainly via a PKC/JNK pathway in esophageal cancer cell line KYSE450. Tetradecanoylphorbol Acetate 96-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 108-113 16480952-7 2006 Taken together, these results suggested that differentiation-associated genes were regulated by TPA-induced c-Jun/AP-1 mainly via a PKC/JNK pathway in esophageal cancer cell line KYSE450. Tetradecanoylphorbol Acetate 96-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 114-118 16478997-2 2006 We now show that Sp1 that recruited HDAC1 to the Sp1/cJun complex was constitutively acetylated when cells were exposed to phorbol 12-myristate 13-acetate (PMA) (3 h). Tetradecanoylphorbol Acetate 123-154 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-57 16478997-2 2006 We now show that Sp1 that recruited HDAC1 to the Sp1/cJun complex was constitutively acetylated when cells were exposed to phorbol 12-myristate 13-acetate (PMA) (3 h). Tetradecanoylphorbol Acetate 156-159 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-57 15863510-7 2005 Moreover, transfection of Caki-1 cells with AP-1 decoy oligodeoxynucleotides resulted in the suppression of phorbol 12-myristate 13-acetate-induced MMP-9 expression and invasion. Tetradecanoylphorbol Acetate 108-139 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-48 15806162-11 2005 RNAi-mediated knockdown of endogenous SRF, ELK1 and c-JUN protein expression significantly reduced TPA-stimulated FRA-1 promoter activity. Tetradecanoylphorbol Acetate 99-102 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 52-57 15292277-2 2004 Here, we show that SHP expression increases during monocytic differentiaton with exposure HL-60 leukemia cells to a 12-O-tetradecanoylphorbol-13-acetate (TPA) response element, whose treatment induced the SHP promoter activity dependent on c-Jun expression, which is well known to be involved in the commitment step in the TPA-induced differentiation of HL-60 leukemia cells. Tetradecanoylphorbol Acetate 116-152 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 240-245 15292277-2 2004 Here, we show that SHP expression increases during monocytic differentiaton with exposure HL-60 leukemia cells to a 12-O-tetradecanoylphorbol-13-acetate (TPA) response element, whose treatment induced the SHP promoter activity dependent on c-Jun expression, which is well known to be involved in the commitment step in the TPA-induced differentiation of HL-60 leukemia cells. Tetradecanoylphorbol Acetate 154-157 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 240-245 15292277-4 2004 Electrophoretic mobility shift assays using oligonucleotides derived from the SHP promoter reveal that c-Jun exhibit TPA-induced DNA binding, providing a mechanism for the transcriptional activation of SHP gene expression. Tetradecanoylphorbol Acetate 117-120 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108 15292277-5 2004 It was also found that overexpression of SHP and c-Jun greatly facilitated monocytic differentiation by TPA and surprisingly, that expression of SHP or c-Jun alone was sufficient to make cells differentiate into functionally mature monocytes, but silencing of SHP and c-Jun by RNA interference diminished the TPA-induced monocytic differentiation. Tetradecanoylphorbol Acetate 104-107 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 49-54 15138488-3 2004 In this study, we found that TPA activates the c-Jun NH2-terminal kinase (JNK)/c-Jun/AP-1 pathway. Tetradecanoylphorbol Acetate 29-32 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 47-52 15289320-3 2004 This cyclopentenone was able to inhibit activator protein1 (AP-1)-dependent transcriptional induction of COX-2 and VEGF promoters induced by phorbol 12-myristate 13-acetate (PMA) or c-Jun overexpression. Tetradecanoylphorbol Acetate 141-172 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-58 15289320-3 2004 This cyclopentenone was able to inhibit activator protein1 (AP-1)-dependent transcriptional induction of COX-2 and VEGF promoters induced by phorbol 12-myristate 13-acetate (PMA) or c-Jun overexpression. Tetradecanoylphorbol Acetate 141-172 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 60-64 15289320-3 2004 This cyclopentenone was able to inhibit activator protein1 (AP-1)-dependent transcriptional induction of COX-2 and VEGF promoters induced by phorbol 12-myristate 13-acetate (PMA) or c-Jun overexpression. Tetradecanoylphorbol Acetate 174-177 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-58 15289320-3 2004 This cyclopentenone was able to inhibit activator protein1 (AP-1)-dependent transcriptional induction of COX-2 and VEGF promoters induced by phorbol 12-myristate 13-acetate (PMA) or c-Jun overexpression. Tetradecanoylphorbol Acetate 174-177 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 60-64 15289320-3 2004 This cyclopentenone was able to inhibit activator protein1 (AP-1)-dependent transcriptional induction of COX-2 and VEGF promoters induced by phorbol 12-myristate 13-acetate (PMA) or c-Jun overexpression. Tetradecanoylphorbol Acetate 174-177 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 182-187 15279563-9 2004 MAO B, but not MAO A gene, could be activated by PMA (phorbol 12-myristate 13-acetate) by protein kinase C, MAPkinase signal transduction pathway involves cJun and Egr-1. Tetradecanoylphorbol Acetate 54-85 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 155-159 15282324-3 2004 We report here that CCND1 promoter activation by estrogens in human breast cancer cells is mediated by recruitment of a c-Jun/c-Fos/estrogen receptor alpha complex to the tetradecanoyl phorbol acetate-responsive element of the gene, together with Oct-1 to a site immediately adjacent. Tetradecanoylphorbol Acetate 171-200 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 120-125 15378003-7 2004 We also show that all KLF6 effects on c-Jun were largely dependent on phorbol ester (TPA/ionomycin) extracellular stimulation, which enhanced KLF6 nuclear translocation and transcriptional activity and modified its phosphorylation status. Tetradecanoylphorbol Acetate 85-88 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-43 15138488-8 2004 Thus, TPA stimulated c-Jun through JNK, and JIP-1 effectively blocked JNK. Tetradecanoylphorbol Acetate 6-9 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 21-26 15138488-14 2004 Taken together, TPA, probably by stimulation of PKC, phosphorylates JNK, which phosphorylates and increases expression of c-Jun leading to AP-1 activity. Tetradecanoylphorbol Acetate 16-19 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 122-127 15138488-4 2004 To explore the possible role that the JNK/c-Jun/AP-1 signal pathway has on TPA-induced apoptosis in LNCaP cells, we stably transfected the scaffold protein, JNK interacting protein 1 (JIP-1), which binds to JNK inhibiting its ability to phosphorylate c-Jun. Tetradecanoylphorbol Acetate 75-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-47 15047839-0 2004 Early activation of the Kaposi"s sarcoma-associated herpesvirus RTA, RAP, and MTA promoters by the tetradecanoyl phorbol acetate-induced AP1 pathway. Tetradecanoylphorbol Acetate 99-128 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 137-140 15180304-7 2004 Both phorbol 12-myristate 13-acetate (PMA; 2.5 mM) and forskolin (FSK; 5 mM) increased the c-fos and c-jun mRNA expressions. Tetradecanoylphorbol Acetate 5-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 101-106 15180304-7 2004 Both phorbol 12-myristate 13-acetate (PMA; 2.5 mM) and forskolin (FSK; 5 mM) increased the c-fos and c-jun mRNA expressions. Tetradecanoylphorbol Acetate 38-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 101-106 15180304-9 2004 When LPS was co-treated with either PMA or FSK, it showed an additive interaction for the induction of c-jun mRNA expression. Tetradecanoylphorbol Acetate 36-39 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-108 15034932-2 2004 The natural product, nordihydroguaiaretic acid (NDGA) shows an inhibitory effect on the binding of jun/AP-1 protein to the AP-1 site in 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated HL60 cells. Tetradecanoylphorbol Acetate 136-172 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-107 15034932-2 2004 The natural product, nordihydroguaiaretic acid (NDGA) shows an inhibitory effect on the binding of jun/AP-1 protein to the AP-1 site in 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated HL60 cells. Tetradecanoylphorbol Acetate 136-172 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 123-127 15034932-2 2004 The natural product, nordihydroguaiaretic acid (NDGA) shows an inhibitory effect on the binding of jun/AP-1 protein to the AP-1 site in 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated HL60 cells. Tetradecanoylphorbol Acetate 174-177 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-107 15034932-2 2004 The natural product, nordihydroguaiaretic acid (NDGA) shows an inhibitory effect on the binding of jun/AP-1 protein to the AP-1 site in 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated HL60 cells. Tetradecanoylphorbol Acetate 174-177 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 123-127 15034932-3 2004 The NDGA inhibits the auto-regulated de novo synthesis of c-jun mRNA in TPA-stimulated HL60 cells. Tetradecanoylphorbol Acetate 72-75 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-63 15047839-5 2004 Treatment with TPA proved to significantly induce both AP1 DNA-binding activity and levels of activated phosphorylated cJUN in PEL cells and ectopic expression of cJUN-plus-cFOS-induced RTA protein expression in PEL cells. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 55-58 15047839-5 2004 Treatment with TPA proved to significantly induce both AP1 DNA-binding activity and levels of activated phosphorylated cJUN in PEL cells and ectopic expression of cJUN-plus-cFOS-induced RTA protein expression in PEL cells. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 119-123 15047839-5 2004 Treatment with TPA proved to significantly induce both AP1 DNA-binding activity and levels of activated phosphorylated cJUN in PEL cells and ectopic expression of cJUN-plus-cFOS-induced RTA protein expression in PEL cells. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 163-167 15047839-6 2004 Cotransfected cJUN plus cFOS or TPA treatment transactivated the KSHV RTA, RAP, and MTA promoters in an AP1-binding site-dependent manner in all three promoters. Tetradecanoylphorbol Acetate 32-35 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-107 15047839-7 2004 Chromatin immunoprecipitation assays confirmed that cJUN associates with these KSHV target promoters in PEL cells as early as 4 h after TPA treatment. Tetradecanoylphorbol Acetate 136-139 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 52-56 15047839-9 2004 Both increased phosphorylated cJUN and AP1 DNA-binding activity was detected as early as 1 h after TPA treatment in PEL cells, suggesting that AP1 activity may be crucial for very early activation of the RAP, MTA, and RTA promoters during the KSHV lytic cycle. Tetradecanoylphorbol Acetate 99-102 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-34 15047839-9 2004 Both increased phosphorylated cJUN and AP1 DNA-binding activity was detected as early as 1 h after TPA treatment in PEL cells, suggesting that AP1 activity may be crucial for very early activation of the RAP, MTA, and RTA promoters during the KSHV lytic cycle. Tetradecanoylphorbol Acetate 99-102 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-42 15047839-9 2004 Both increased phosphorylated cJUN and AP1 DNA-binding activity was detected as early as 1 h after TPA treatment in PEL cells, suggesting that AP1 activity may be crucial for very early activation of the RAP, MTA, and RTA promoters during the KSHV lytic cycle. Tetradecanoylphorbol Acetate 99-102 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 143-146 15047839-11 2004 Therefore, we suggest that the initiating effects of TPA via the AP1 pathway in PEL cells need to be amplified by RTA for full lytic-cycle induction. Tetradecanoylphorbol Acetate 53-56 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-68 15139522-4 2004 The HT-29 C-4 cells were treated for 1 h with various natural chemopreventive agents and challenged with AP-1 stimulators such as 12-O-tetradecanoylphorbol-13-acetate (TPA) or hydrogen peroxide (H2O2) for 6 h. The c-Jun N-terminal kinase (JNK) was examined to understand the effect of these compounds on the upstream signaling activator of AP-1. Tetradecanoylphorbol Acetate 130-166 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 105-109 15139522-7 2004 RESULTS: TPA and H2O2 treatments strongly induced AP-1-luciferase activity as expected. Tetradecanoylphorbol Acetate 9-12 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 50-54 15161022-7 2004 EGCG also abrogated the PMA-induced activation of extracellular-regulated protein kinase (Erk) and c-jun N-terminal kinase (JNK), which are upstream modulators of AP-1. Tetradecanoylphorbol Acetate 24-27 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 163-167 13679379-11 2003 Chromatin immunoprecipitation assays revealed an enhanced recruitment of c-Jun, Jun-D, and Fra-2 to the endogenous fra-1 promoter upon TPA stimulation. Tetradecanoylphorbol Acetate 135-138 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 73-78 14654785-6 2003 Previously, tandem AP1 sites in the promoter were reported to be important for the serum and TPA inducibility of the vimentin gene. Tetradecanoylphorbol Acetate 93-96 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 19-22 12947046-5 2003 In addition, we demonstrated that the E2 repression could be antagonized by phorbol 12-myristate 13-acetate, which stimulated c-Jun phosphorylation on serine 63, a process that is a prerequisite for recruitment of the transcriptional coactivator cAMP response element binding protein (CREB)-binding protein (CBP). Tetradecanoylphorbol Acetate 76-107 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 126-131 13679379-12 2003 These results underscore the regulatory role of c-Jun, Jun-D, and Fra-2 in TPA-inducible fra-1 expression in HBE cells in vivo. Tetradecanoylphorbol Acetate 75-78 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 48-53 12787135-6 2003 GC-rich Sp1 element and activator protein 1 (AP-1) element on MCP-1 promoter were required for constitutive and 12-O-tetradecanoylphorbol-13-acetate-induced transcription, respectively, and involved in transrepression by E2. Tetradecanoylphorbol Acetate 112-148 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-43 12925217-7 2003 Histamine enhanced transcriptional activity and DNA binding of activator protein 1 at the two TPA-response elements. Tetradecanoylphorbol Acetate 94-97 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 63-82 12925217-8 2003 It shifted the TPA-response-element-binding activator protein 1 composition from c-Jun homodimers to c-Fos/c-Jun heterodimers. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-63 12925217-8 2003 It shifted the TPA-response-element-binding activator protein 1 composition from c-Jun homodimers to c-Fos/c-Jun heterodimers. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-86 12925217-8 2003 It shifted the TPA-response-element-binding activator protein 1 composition from c-Jun homodimers to c-Fos/c-Jun heterodimers. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 107-112 14500826-6 2003 When losing the AP-1-dependent hMSH2 promoter activity, either by mutating the AP-1 binding sites of the hMSH2 promoter or by using a dominant negative c-Jun factor, the hMSH2 overexpression induced by TPA is abolished both in vitro and in vivo. Tetradecanoylphorbol Acetate 202-205 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-20 14500826-6 2003 When losing the AP-1-dependent hMSH2 promoter activity, either by mutating the AP-1 binding sites of the hMSH2 promoter or by using a dominant negative c-Jun factor, the hMSH2 overexpression induced by TPA is abolished both in vitro and in vivo. Tetradecanoylphorbol Acetate 202-205 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-83 14500826-6 2003 When losing the AP-1-dependent hMSH2 promoter activity, either by mutating the AP-1 binding sites of the hMSH2 promoter or by using a dominant negative c-Jun factor, the hMSH2 overexpression induced by TPA is abolished both in vitro and in vivo. Tetradecanoylphorbol Acetate 202-205 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 152-157 12787135-6 2003 GC-rich Sp1 element and activator protein 1 (AP-1) element on MCP-1 promoter were required for constitutive and 12-O-tetradecanoylphorbol-13-acetate-induced transcription, respectively, and involved in transrepression by E2. Tetradecanoylphorbol Acetate 112-148 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-49 12787135-7 2003 E2 inhibited constitutive Sp1 and 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 transcriptional activities whereas it did not inhibit DNA binding of Sp1 or AP-1 c-Fos/c-Jun. Tetradecanoylphorbol Acetate 34-70 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-83 12072430-8 2002 We further show that 12-O-tetradecanoylphorbol-13-acetate (TPA) increases BCSG1 mRNA expression and up-regulates BCSG1 promoter activity through the intronic AP1 sites. Tetradecanoylphorbol Acetate 21-57 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 158-161 12651162-8 2003 HEK293 cells stably overexpressing Trespin display increased cell proliferation and partial resistance to growth inhibition and phosphorylation of c-Jun induced by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 182-218 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-152 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 34-54 12592382-6 2003 Inductions of c-fos RNA by both drugs and c-jun phosphorylation by TPA were also significantly reduced by PD98059 pretreatment. Tetradecanoylphorbol Acetate 67-70 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-47 12433930-2 2003 The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) is often used to induce AP-1 activity. Tetradecanoylphorbol Acetate 18-54 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 85-89 12433930-2 2003 The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) is often used to induce AP-1 activity. Tetradecanoylphorbol Acetate 56-59 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 85-89 12433930-8 2003 We demonstrated that c-Fos, c-Jun, and JunD are involved in TPA inhibitory effect due to their ability to bind TRE-ALAS, evidenced by supershift analysis and their capacity to repress promoter activity in transfection assays. Tetradecanoylphorbol Acetate 60-63 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-33 12213569-7 2002 Distinct from serum factors and the tumor promoter TPA-induced MAPKs, which resulted in transcriptional activation of ELK or c-JUN, TCDD-stimulated MAPKs were critical for the induction of AHR-dependent gene transcription and CYP1A1 expression. Tetradecanoylphorbol Acetate 51-54 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 125-130 12592382-3 2003 During this period, phosphorylation of one of the downstream transcriptional factors of MAPK cascade, ATF2, was 3.2- and 2.0-fold induced by TPA and Saikosaponin a, respectively, whereas that of another transcriptional factor, c-jun, was induced by TPA only. Tetradecanoylphorbol Acetate 141-144 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 227-232 12489106-1 2002 The dominant negative c-jun TAM-67 has been shown to inhibit tumor promotion induced by 12-O-tetradecanoylphorbol-13-acetate and okadaic acid (OA). Tetradecanoylphorbol Acetate 88-124 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 22-27 12433834-9 2002 Electrophoretic mobility shift assays and supershift analyses have revealed that activating protein 1 (AP-1) is the transcription factor binding the cAMP-responsive element/12-O-tetradecanoylphorbol 13-acetate-responsive element located in the ACE promoter after PMA stimulation. Tetradecanoylphorbol Acetate 173-209 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 103-107 12433834-12 2002 Our results demonstrate that the two transcription factors, Egr-1 and AP-1, are involved in the PMA-induced ACE transcriptional activation in human endothelial cells via the activation of the extracellular signal-regulated kinase 1/2 signaling pathway. Tetradecanoylphorbol Acetate 96-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-74 12072430-8 2002 We further show that 12-O-tetradecanoylphorbol-13-acetate (TPA) increases BCSG1 mRNA expression and up-regulates BCSG1 promoter activity through the intronic AP1 sites. Tetradecanoylphorbol Acetate 59-62 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 158-161 12072430-9 2002 The effect of TPA on BCSG1 transcription is also demonstrated under in vivo conditions in intact cells by using chromatin immunoprecipitation assays that show the TPA-induced binding of c-Jun to the chromatin region encompassing the intronic AP1 sites. Tetradecanoylphorbol Acetate 14-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-191 12072430-9 2002 The effect of TPA on BCSG1 transcription is also demonstrated under in vivo conditions in intact cells by using chromatin immunoprecipitation assays that show the TPA-induced binding of c-Jun to the chromatin region encompassing the intronic AP1 sites. Tetradecanoylphorbol Acetate 14-17 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 242-245 12072430-9 2002 The effect of TPA on BCSG1 transcription is also demonstrated under in vivo conditions in intact cells by using chromatin immunoprecipitation assays that show the TPA-induced binding of c-Jun to the chromatin region encompassing the intronic AP1 sites. Tetradecanoylphorbol Acetate 163-166 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 186-191 12072430-9 2002 The effect of TPA on BCSG1 transcription is also demonstrated under in vivo conditions in intact cells by using chromatin immunoprecipitation assays that show the TPA-induced binding of c-Jun to the chromatin region encompassing the intronic AP1 sites. Tetradecanoylphorbol Acetate 163-166 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 242-245 12082627-5 2002 The AP-1 activator phorbol 12-myristate 13-acetate (TPA) enhanced the binding of this DR4 AP-1 binding site to protein(s) in a nuclear extract from TPA-treated cells, increased luciferase activity of a reporter construct containing this site and induced DR4 expression at the transcription level. Tetradecanoylphorbol Acetate 52-55 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-8 12187329-6 2002 Whereas TPA treatment resulted in a strong induction of p21(WAF/CIP1), c-Fos and c-Jun levels, neither one of the novel PKC activators altered expression of these proteins. Tetradecanoylphorbol Acetate 8-11 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-86 12076508-4 2002 Short term exposure to phorbol 12-myristate 13-acetate (TPA), a phorbol ester tumour promoter, or hydrogen peroxide (H(2)O(2)) also activates AP-1 and NF-kappa B binding. Tetradecanoylphorbol Acetate 23-54 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 142-146 12076508-4 2002 Short term exposure to phorbol 12-myristate 13-acetate (TPA), a phorbol ester tumour promoter, or hydrogen peroxide (H(2)O(2)) also activates AP-1 and NF-kappa B binding. Tetradecanoylphorbol Acetate 56-59 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 142-146 12091247-2 2002 We have recently shown that phorbol 13-myristate 12-acetate (PMA)-stimulated SPRR1B transcription in Clara-like H441 cells is mainly mediated by activator protein-1 (AP-1) and c-Jun N-terminal kinase-1 (JNK1). Tetradecanoylphorbol Acetate 61-64 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-164 12091247-2 2002 We have recently shown that phorbol 13-myristate 12-acetate (PMA)-stimulated SPRR1B transcription in Clara-like H441 cells is mainly mediated by activator protein-1 (AP-1) and c-Jun N-terminal kinase-1 (JNK1). Tetradecanoylphorbol Acetate 61-64 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 166-170 12082627-5 2002 The AP-1 activator phorbol 12-myristate 13-acetate (TPA) enhanced the binding of this DR4 AP-1 binding site to protein(s) in a nuclear extract from TPA-treated cells, increased luciferase activity of a reporter construct containing this site and induced DR4 expression at the transcription level. Tetradecanoylphorbol Acetate 19-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-8 12082627-5 2002 The AP-1 activator phorbol 12-myristate 13-acetate (TPA) enhanced the binding of this DR4 AP-1 binding site to protein(s) in a nuclear extract from TPA-treated cells, increased luciferase activity of a reporter construct containing this site and induced DR4 expression at the transcription level. Tetradecanoylphorbol Acetate 52-55 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-94 12082627-5 2002 The AP-1 activator phorbol 12-myristate 13-acetate (TPA) enhanced the binding of this DR4 AP-1 binding site to protein(s) in a nuclear extract from TPA-treated cells, increased luciferase activity of a reporter construct containing this site and induced DR4 expression at the transcription level. Tetradecanoylphorbol Acetate 19-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-94 12082627-5 2002 The AP-1 activator phorbol 12-myristate 13-acetate (TPA) enhanced the binding of this DR4 AP-1 binding site to protein(s) in a nuclear extract from TPA-treated cells, increased luciferase activity of a reporter construct containing this site and induced DR4 expression at the transcription level. Tetradecanoylphorbol Acetate 148-151 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-8 12082627-5 2002 The AP-1 activator phorbol 12-myristate 13-acetate (TPA) enhanced the binding of this DR4 AP-1 binding site to protein(s) in a nuclear extract from TPA-treated cells, increased luciferase activity of a reporter construct containing this site and induced DR4 expression at the transcription level. Tetradecanoylphorbol Acetate 148-151 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-94 11719466-10 2001 Taken together, this study shows that a PKC-epsilon-Raf-1-MEK-ERK-AP1 signaling cascade acts on a 12-O-tetradecanoylphorbol-13-acetate response element-like element to mediate hypoxia-induced GRP78 expression in human gastric cancer cells. Tetradecanoylphorbol Acetate 98-134 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 66-69 11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tetradecanoylphorbol Acetate 137-140 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 164-183 11980644-1 2002 Treatment with retinoic acid (RA) or carnosol, two structurally unrelated compounds with anticancer properties, inhibited phorbol ester (PMA)-mediated induction of activator protein-1 (AP-1) activity and cyclooxygenase-2 (COX-2) expression in human mammary epithelial cells. Tetradecanoylphorbol Acetate 137-140 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 185-189 11980644-2 2002 The induction of COX-2 transcription by PMA was mediated by increased binding of AP-1 to the cyclic AMP response element (CRE) of the COX-2 promoter. Tetradecanoylphorbol Acetate 40-43 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 81-85 11980644-10 2002 Overexpressing c-Jun but not CBP/p300 reversed the suppressive effect of carnosol on PMA-mediated stimulation of COX-2 promoter activity. Tetradecanoylphorbol Acetate 85-88 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-20 11914583-1 2002 The functional role of mitogen-activated protein kinase (MAPK) signaling and c-Jun induction in phorbol 12-myristate 13-acetate (PMA)-induced human 12(S)-lipoxygenase gene expression was studied in human epidermoid carcinoma A431 cells. Tetradecanoylphorbol Acetate 96-127 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-82 11914583-1 2002 The functional role of mitogen-activated protein kinase (MAPK) signaling and c-Jun induction in phorbol 12-myristate 13-acetate (PMA)-induced human 12(S)-lipoxygenase gene expression was studied in human epidermoid carcinoma A431 cells. Tetradecanoylphorbol Acetate 129-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-82 11914583-7 2002 Enhancement of binding between the c-Jun-Sp1 complex and the Sp1 oligonucleotide was observed in cells treated with PMA, suggesting the possible interaction of c-Jun-Sp1 with GC-rich binding sites in the gene promoter. Tetradecanoylphorbol Acetate 116-119 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 35-40 11914583-7 2002 Enhancement of binding between the c-Jun-Sp1 complex and the Sp1 oligonucleotide was observed in cells treated with PMA, suggesting the possible interaction of c-Jun-Sp1 with GC-rich binding sites in the gene promoter. Tetradecanoylphorbol Acetate 116-119 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 160-165 11950097-3 2002 DNA binding of AP-1 to the target 12-O-tetradecanoylphorbol-13-acetate response element sequence was maximally induced 1-3 h after irradiation. Tetradecanoylphorbol Acetate 34-70 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 15-19 11716547-5 2001 Considering that TPA is a potent activator of AP-1, we hypothesized that this transcription factor might also be required for p38 pathway-dependent MMP-9 regulation. Tetradecanoylphorbol Acetate 17-20 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-50 11502881-8 2001 Furthermore, the PMA-induced extracellular signal-regulated kinase 1/2 and c-Jun amino-terminal kinase activities that contributed to AP-1 activity and MCP-1 gene induction were obviously attenuated after pretreating ECs with Wog. Tetradecanoylphorbol Acetate 17-20 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 75-80 11479211-4 2001 TPA- or EGF-induced phosphorylation of c-Jun, but not extracellular signal-regulated kinases or p38 kinases, was also blocked by the compounds, indicating that c-Jun N-terminal kinases were critical in mediating TPA- or EGF-induced AP-1 activity and subsequent cell transformation in JB6 cells. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-44 11479211-4 2001 TPA- or EGF-induced phosphorylation of c-Jun, but not extracellular signal-regulated kinases or p38 kinases, was also blocked by the compounds, indicating that c-Jun N-terminal kinases were critical in mediating TPA- or EGF-induced AP-1 activity and subsequent cell transformation in JB6 cells. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 160-165 11479211-4 2001 TPA- or EGF-induced phosphorylation of c-Jun, but not extracellular signal-regulated kinases or p38 kinases, was also blocked by the compounds, indicating that c-Jun N-terminal kinases were critical in mediating TPA- or EGF-induced AP-1 activity and subsequent cell transformation in JB6 cells. Tetradecanoylphorbol Acetate 212-215 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-44 11479211-4 2001 TPA- or EGF-induced phosphorylation of c-Jun, but not extracellular signal-regulated kinases or p38 kinases, was also blocked by the compounds, indicating that c-Jun N-terminal kinases were critical in mediating TPA- or EGF-induced AP-1 activity and subsequent cell transformation in JB6 cells. Tetradecanoylphorbol Acetate 212-215 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 160-165 11749832-8 2001 Interestingly, TPA-induced c-fos/c-jun mRNA expression in endothelial cells was also inhibited by triptolide. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 33-38 11461775-2 2001 The metal-vitamin complex was shown able to strongly potentiate AP-1 binding as induced by phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 91-122 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-68 11461775-2 2001 The metal-vitamin complex was shown able to strongly potentiate AP-1 binding as induced by phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 124-127 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-68 11461775-7 2001 In fact, protein synthesis inhibitor cycloheximide (CHX) prevented the stimulation of AP-1 nuclear binding due to PMA and ascorbate plus PMA. Tetradecanoylphorbol Acetate 114-117 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 11461775-7 2001 In fact, protein synthesis inhibitor cycloheximide (CHX) prevented the stimulation of AP-1 nuclear binding due to PMA and ascorbate plus PMA. Tetradecanoylphorbol Acetate 137-140 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 86-90 11408617-3 2001 Pretreatment of HeLa cells with resveratrol inhibited the transcription of AP-1 reporter gene by UVC and phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 105-136 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 75-79 11408617-3 2001 Pretreatment of HeLa cells with resveratrol inhibited the transcription of AP-1 reporter gene by UVC and phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 138-141 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 75-79 10934195-7 2000 Forskolin and phorbol myristate acetate acted synergistically to enhance transcription of an AP1(-73COL)-luciferase construct. Tetradecanoylphorbol Acetate 14-39 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-96 11226521-4 2001 Promoter deletion analyses revealed that the activator protein-1 (AP-1) transcription factor site was crucial for 12-O-tetradecanoyl phorbol 13-acetate (TPA)-mediated GSTP1 gene transcription. Tetradecanoylphorbol Acetate 114-151 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-64 11226521-4 2001 Promoter deletion analyses revealed that the activator protein-1 (AP-1) transcription factor site was crucial for 12-O-tetradecanoyl phorbol 13-acetate (TPA)-mediated GSTP1 gene transcription. Tetradecanoylphorbol Acetate 114-151 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 66-70 11226521-4 2001 Promoter deletion analyses revealed that the activator protein-1 (AP-1) transcription factor site was crucial for 12-O-tetradecanoyl phorbol 13-acetate (TPA)-mediated GSTP1 gene transcription. Tetradecanoylphorbol Acetate 153-156 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 45-64 11226521-4 2001 Promoter deletion analyses revealed that the activator protein-1 (AP-1) transcription factor site was crucial for 12-O-tetradecanoyl phorbol 13-acetate (TPA)-mediated GSTP1 gene transcription. Tetradecanoylphorbol Acetate 153-156 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 66-70 11226521-5 2001 Electrophoretic mobility shift assays and transient transfection analysis demonstrated that both DNA binding and transactivation activities of AP-1 were induced by TPA. Tetradecanoylphorbol Acetate 164-167 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 143-147 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-170 11356008-3 2001 Here, we report that IL-6 and 12-O-tetradecanoylphorbol-13-acetate (TPA) synergistically transactivate the IRE in HepG2 cells, which is coupled to a strong upregulation of c-Jun and c-Fos expression by TPA via the mitogen-activated protein kinase (MAPK) pathway. Tetradecanoylphorbol Acetate 30-66 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-177 11356008-3 2001 Here, we report that IL-6 and 12-O-tetradecanoylphorbol-13-acetate (TPA) synergistically transactivate the IRE in HepG2 cells, which is coupled to a strong upregulation of c-Jun and c-Fos expression by TPA via the mitogen-activated protein kinase (MAPK) pathway. Tetradecanoylphorbol Acetate 68-71 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-177 11356008-3 2001 Here, we report that IL-6 and 12-O-tetradecanoylphorbol-13-acetate (TPA) synergistically transactivate the IRE in HepG2 cells, which is coupled to a strong upregulation of c-Jun and c-Fos expression by TPA via the mitogen-activated protein kinase (MAPK) pathway. Tetradecanoylphorbol Acetate 202-205 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-177 11278336-12 2001 Bisphenol A diglycidyl ether, a compound that binds to PPARgamma but lacks the ability to activate transcription, also inhibited PMA-mediated induction of AP-1 activity and COX-2. Tetradecanoylphorbol Acetate 129-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 155-159 11050091-8 2001 PMA could also activate a signaling pathway involving MEK1/ERK2/c-Jun-dependent uPA expression. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-69 10775801-8 2000 The high AP1 activities observed during proliferative state or induced in TPA-treated polarized cells, exert a repressive effect on androgen action. Tetradecanoylphorbol Acetate 74-77 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-12 10918063-13 2000 dn-c-Jun mutants abolished PMA-stimulated expression supporting an important role for AP-1 proteins in SPRR1B expression. Tetradecanoylphorbol Acetate 27-30 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 3-8 10871606-2 2000 12-O-Tetradecanoylphorbol-13-acetate (TPA) induction of the FGF-BP gene occurs through transcriptional mechanisms involving Sp1, AP-1, and CCAATT/enhancer-binding protein sites in the proximal FGF-BP gene promoter. Tetradecanoylphorbol Acetate 0-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 129-133 10871606-2 2000 12-O-Tetradecanoylphorbol-13-acetate (TPA) induction of the FGF-BP gene occurs through transcriptional mechanisms involving Sp1, AP-1, and CCAATT/enhancer-binding protein sites in the proximal FGF-BP gene promoter. Tetradecanoylphorbol Acetate 38-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 129-133 10930293-9 2000 These observations demonstrate that, C/EBPbeta and c-Jun contribute to the regulation of the TNF-alpha gene in normal macrophages following treatment with PMA. Tetradecanoylphorbol Acetate 155-158 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-56 10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tetradecanoylphorbol Acetate 132-168 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 177-181 10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tetradecanoylphorbol Acetate 132-168 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 221-226 10866321-5 2000 In a transient transfection assay, all three RAR subtypes, RARalpha, RARbeta, and RARgamma, could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity and the activity of oncogenes c-Jun and c-Fos on AP-1 containing reporter genes in the presence of retinoic acid (RA). Tetradecanoylphorbol Acetate 132-168 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 240-244 10344756-3 1999 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced immediate early genes, such as c-Jun, c-Fos, and Egr-1 in activated Ki-ras-disrupted clones, whereas c-Jun induction was rare in HCT116. Tetradecanoylphorbol Acetate 0-36 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 82-87 10673028-4 1999 Gel supershift assays were performed to detect association of all seven AP-1 family members with their DNA binding site in TPA-treated and -untreated P+ and P- cells. Tetradecanoylphorbol Acetate 123-126 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 72-76 10508860-7 1999 By monitoring fluorescent recombinant protein and by gel mobility shift assays, PS1 was shown to accelerate the translocation of QM from the cytoplasm to the nucleus and to thereby suppress the binding of c-Jun homodimer to 12-O-tetradecanoylphorbol-13- acetate (TPA)-responsive element (TRE). Tetradecanoylphorbol Acetate 224-261 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 205-210 10508860-7 1999 By monitoring fluorescent recombinant protein and by gel mobility shift assays, PS1 was shown to accelerate the translocation of QM from the cytoplasm to the nucleus and to thereby suppress the binding of c-Jun homodimer to 12-O-tetradecanoylphorbol-13- acetate (TPA)-responsive element (TRE). Tetradecanoylphorbol Acetate 263-266 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 205-210 10454570-5 1999 The analysis of two distinct mitogen-activated protein kinase pathways shows that stress-activated protein kinase-Jun N-terminal kinase activation, resulting in the phosphorylation of ATF-2, c-Jun, and JunD, is required not only for the IL-1- but also for the TPA-dependent induction, while the extracellular signal-related kinase 1 (ERK-1) and ERK-2 activation is involved in the TPA- but not in the IL-1-dependent stimulation of the uPA enhancer. Tetradecanoylphorbol Acetate 260-263 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 191-196 10454570-5 1999 The analysis of two distinct mitogen-activated protein kinase pathways shows that stress-activated protein kinase-Jun N-terminal kinase activation, resulting in the phosphorylation of ATF-2, c-Jun, and JunD, is required not only for the IL-1- but also for the TPA-dependent induction, while the extracellular signal-related kinase 1 (ERK-1) and ERK-2 activation is involved in the TPA- but not in the IL-1-dependent stimulation of the uPA enhancer. Tetradecanoylphorbol Acetate 381-384 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 191-196 10489901-2 1999 MATERIALS AND METHODS: The induction of c-jun transcripts by IR, by phorbol 12-myristate 13-acetate (PMA), interleukin 1 (IL-1) and epidermal growth factor (EGF) in normal and A-T lymphoblasts was measured. Tetradecanoylphorbol Acetate 68-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-45 10344756-3 1999 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced immediate early genes, such as c-Jun, c-Fos, and Egr-1 in activated Ki-ras-disrupted clones, whereas c-Jun induction was rare in HCT116. Tetradecanoylphorbol Acetate 38-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 82-87 9733728-8 1998 Co-transfection of the hINV promoter with dominant negative forms of Ras, MEKK1, MEK1, MEK7, MEK3, p38/RK, and c-Jun inhibit the TPA-dependent increase. Tetradecanoylphorbol Acetate 129-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 111-116 10228559-6 1999 TPA stimulation of A2780/CP70 cells also resulted in a rapid but transient induction of c-jun and c-fos as determined by Northern and Western blot analyses, which peaked about 2 h before the peak in ERCC-1 expression. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 88-93 10228559-11 1999 These data suggest that AP-1 may contribute to the upregulation of ERCC-1 in response to TPA in human ovarian cancer cells. Tetradecanoylphorbol Acetate 89-92 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-28 9988737-10 1999 The expression of this mutant form of c-Jun also completely blocks 12-O-tetradecanoylphorbol-13-acetate-induced M-CSF receptor promoter activity during monocytic differentiation. Tetradecanoylphorbol Acetate 67-103 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-43 9885901-5 1998 By contrast, phorbol myristate acetate (PMA) and/or ionomycin-induced apoptosis had much slower kinetics, were preceded by an early increase of NF-kappaB/RelA-p50, AP-1 and NUR-77 activities, and were insensitive to proteasome inhibition. Tetradecanoylphorbol Acetate 13-38 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 164-168 9885901-5 1998 By contrast, phorbol myristate acetate (PMA) and/or ionomycin-induced apoptosis had much slower kinetics, were preceded by an early increase of NF-kappaB/RelA-p50, AP-1 and NUR-77 activities, and were insensitive to proteasome inhibition. Tetradecanoylphorbol Acetate 40-43 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 164-168 10359012-5 1999 Furthermore, PD98059 completely blocked the TPA-induced differentiation of ML-1 cells, as assessed by a number of features associated with mononuclear differentiation including changes in morphology, nonspecific esterase activity, phagocytic ability, NADPH oxidase activity, mitochondrial respiration, and c-jun mRNA inducibility. Tetradecanoylphorbol Acetate 44-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 306-311 9888864-6 1999 This region of the PAI-1 promoter was previously found to contain a tetradecanoyl phorbol acetate-response element (TRE; between -58 and -50) necessary for PMA responsiveness and with a high affinity for c-Jun homodimers. Tetradecanoylphorbol Acetate 68-97 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 204-209 9670939-9 1998 The intracellular incorporation of Abs specific for c-Fos and c-Jun family members by scrape loading inhibited the production and intracellular accumulation of IL-2 within 6 h of costimulation with PMA/ionomycin, or costimulation by CD28 and CD3 ligation. Tetradecanoylphorbol Acetate 198-201 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 62-67 9743233-8 1998 Moreover, phorbol 12-myristate 13-acetate, H2O2, or the combination of H2O2 and sodium orthovanadate (vanadate) activated c-Jun-activating kinase. Tetradecanoylphorbol Acetate 10-41 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 122-127 9716184-0 1998 v-Jun represses c-jun proto-oncogene expression in vivo through a 12-O-tetradecanoylphorbol-13-acetate-responsive element in the proximal gene promoter. Tetradecanoylphorbol Acetate 66-102 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 16-21 9514905-3 1998 Furthermore, expression of the immediate early genes c-fos and c-jun was up-regulated by TPA only in LNCaP and DU-145 cells, whereas PC-3 cells failed to express c-fos mRNA. Tetradecanoylphorbol Acetate 89-92 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 63-68 9573531-2 1998 The promoter regions of certain ECM genes contain TPA (phorbol ester)-responsive element (TRE) motifs that bind the transcription factor, activator protein-1 (AP-1), a complex of Jun and other phosphoproteins. Tetradecanoylphorbol Acetate 50-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 138-157 9573531-2 1998 The promoter regions of certain ECM genes contain TPA (phorbol ester)-responsive element (TRE) motifs that bind the transcription factor, activator protein-1 (AP-1), a complex of Jun and other phosphoproteins. Tetradecanoylphorbol Acetate 50-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 159-163 9566900-9 1998 U937 cells expressing ectopic wild-type c-Jun or TAM-67 secreted over threefold more TNF alpha than the control line in response to PMA plus lipopolysaccharide. Tetradecanoylphorbol Acetate 132-135 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-45 9478937-5 1998 Functional activation of the JNKK/SEK1-JNK/SAPK-c-Jun cascade (where JNKK/SEK1 is JNK kinase/SAPK kinase) was demonstrated by activation of a 12-O-tetradecanoylphorbol-13-acetate response element (TRE) reporter construct in a c-Jun dependent fashion. Tetradecanoylphorbol Acetate 142-178 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-231 9202001-7 1997 This differential substrate specificity of MKP-1 can be functionally extended to nuclear transcriptional events in that PMA-induced c-Jun transcriptional activity was more sensitive to inhibition by MKP-1 than either Elk-1 or c-Myc. Tetradecanoylphorbol Acetate 120-123 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-137 9478937-5 1998 Functional activation of the JNKK/SEK1-JNK/SAPK-c-Jun cascade (where JNKK/SEK1 is JNK kinase/SAPK kinase) was demonstrated by activation of a 12-O-tetradecanoylphorbol-13-acetate response element (TRE) reporter construct in a c-Jun dependent fashion. Tetradecanoylphorbol Acetate 142-178 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 48-53 9710361-8 1998 This response was transient, as the level returned to the control level after 6 h. Forskolin and TPA evoked similar increases, but their effects appeared after 30 min and reached their maxima after 2 h. In contrast, GRF and forskolin, but not TPA, increased the GH mRNA level 2-fold after 24 h. The cJun mRNA level showed no significant change in response to these agents over 24 h and GRF and TPA increased the cFos mRNA level 1.4 and 2.3-fold, respectively, after 30 min. Tetradecanoylphorbol Acetate 97-100 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 299-303 9409785-0 1997 Cooperation of two PEA3/AP1 sites in uPA gene induction by TPA and FGF-2. Tetradecanoylphorbol Acetate 59-62 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 24-27 9211894-1 1997 In exploring the possible mechanisms of androgen independence of prostate-specific antigen (PSA) gene expression, we investigated the effect of elevating AP-1 by both 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment and transfection of the c-Jun expression vector in LNCaP cells. Tetradecanoylphorbol Acetate 167-203 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 154-158 9211894-1 1997 In exploring the possible mechanisms of androgen independence of prostate-specific antigen (PSA) gene expression, we investigated the effect of elevating AP-1 by both 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment and transfection of the c-Jun expression vector in LNCaP cells. Tetradecanoylphorbol Acetate 205-208 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 154-158 9211894-6 1997 Specifically, c-Jun inhibited the formation of AR.ARE complexes and conversely that AR-glutathione S-transferase proteins inhibited the formation of c-Jun.TPA-responsive element (TRE) complexes. Tetradecanoylphorbol Acetate 155-158 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 149-154 9467952-3 1998 Expression of immediate-early genes of the c-fos and c-jun families, whose transcription and activation are regulated by MAP kinases, is differentially induced by insulin and TPA. Tetradecanoylphorbol Acetate 175-178 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 53-58 9270011-6 1997 In this study, we present evidence that RME can down-regulate AP-1 activity induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, insulin, growth factors, and the nuclear proto-oncogenes c-Jun and c-Fos. Tetradecanoylphorbol Acetate 106-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 62-66 9270011-9 1997 Furthermore, using gel retardation assay, we show that 12-O-tetradecanoylphorbol-13-acetate- and epidermal growth factor-induced AP-1 binding activity in breast cancer cells is inhibited by RME. Tetradecanoylphorbol Acetate 55-91 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 129-133 9301678-5 1997 Expression of the c-myc gene was down-regulated and c-jun and c-fms transcripts increased following exposure to 5-500 nM TPA. Tetradecanoylphorbol Acetate 121-124 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 52-57 9218873-8 1997 This TRE bound TPA induced specific nuclear complexes in vitro containing junD, c-jun, c-fos, and fra2 but not cAMP-responsive element binding/activating transcription factor family proteins. Tetradecanoylphorbol Acetate 15-18 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 80-85 9202234-11 1997 The pattern of steroid responses was retained in the presence of the c-Jun activator phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 85-116 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 69-74 9301678-6 1997 In contrast, exposure to 0.5 nM TPA decreased c-myc expression and increased c-jun transcripts only transiently between 4 and 8 h while little if any effect was detectable on c-fms mRNA expression and subsequent differentiation. Tetradecanoylphorbol Acetate 32-35 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-82 9177393-5 1997 The c-jun and c-fos mRNA stimulation elicited by TPA was reduced by the PKC inhibitors, chelerythrine and staurosporine, and could not be mimicked by 4alpha-phorbol 12,13-didecanoate (a phorbol ester that fails to activate PKC), whereas the stimulation induced by EGF was diminished by the PTK inhibitor, genistein. Tetradecanoylphorbol Acetate 49-52 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 4-9 9177393-8 1997 Addition of TSH (0.1-0.5 mU/mL), however, to either TPA or EGF dose dependently inhibited the c-jun and c-fos mRNA elicited by these agents. Tetradecanoylphorbol Acetate 52-55 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 94-99 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 34-39 9067545-6 1997 Overexpression of MnSOD led to a significant decrease in c-jun and c-fos expression in response to treatment with TPA or the oxidant promoter superoxide. Tetradecanoylphorbol Acetate 114-117 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62 9121495-5 1996 TPA stimulation of the human GnRH gene is mediated by a consensus AP-1 site located at -402 to -396 bp, TGACTCA, which specifically binds c-fos and c-jun in Gn11 and NLT cells and recombinant c-jun in gel mobility shift studies. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 148-153 9121495-5 1996 TPA stimulation of the human GnRH gene is mediated by a consensus AP-1 site located at -402 to -396 bp, TGACTCA, which specifically binds c-fos and c-jun in Gn11 and NLT cells and recombinant c-jun in gel mobility shift studies. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 192-197 9142914-5 1997 Gastrin stimulation increased c-fos and c-jun mRNA abundance and AP-1-dependent transcriptional activity, as assessed by a reporter construct in which the CAT reporter gene is under the control of a 12-O-tetradecanoylphorbol-13-acetate response element multimer. Tetradecanoylphorbol Acetate 199-235 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 40-45 9142914-5 1997 Gastrin stimulation increased c-fos and c-jun mRNA abundance and AP-1-dependent transcriptional activity, as assessed by a reporter construct in which the CAT reporter gene is under the control of a 12-O-tetradecanoylphorbol-13-acetate response element multimer. Tetradecanoylphorbol Acetate 199-235 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-69 9121495-4 1996 In contrast, TPA treatment stimulated expression of a human GnRH-luciferase reporter construct, correlating with the expression of the protoon-cogenes c-fos and c-jun. Tetradecanoylphorbol Acetate 13-16 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 161-166 8797597-2 1996 c-Jun and v-Jun bind specifically to 12-O-tetradecanoylphorbol-13-acetate responsive elements [TREs, also called activator protein 1 (AP-1) motifs]. Tetradecanoylphorbol Acetate 37-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 8797597-2 1996 c-Jun and v-Jun bind specifically to 12-O-tetradecanoylphorbol-13-acetate responsive elements [TREs, also called activator protein 1 (AP-1) motifs]. Tetradecanoylphorbol Acetate 37-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 10-15 8797597-2 1996 c-Jun and v-Jun bind specifically to 12-O-tetradecanoylphorbol-13-acetate responsive elements [TREs, also called activator protein 1 (AP-1) motifs]. Tetradecanoylphorbol Acetate 37-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 113-132 8797597-2 1996 c-Jun and v-Jun bind specifically to 12-O-tetradecanoylphorbol-13-acetate responsive elements [TREs, also called activator protein 1 (AP-1) motifs]. Tetradecanoylphorbol Acetate 37-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 134-138 8761946-2 1996 Since fos/jun and steroid hormones interact to regulate gene expression, we asked whether phorbol-12-myristate-13-acetate (PMA), which stimulates binding of fos/jun to AP1 sites, transactivates the avian beta 3 integrin gene and, if so, does the phorbol ester modulate 1,25(OH)2D3 induction of the gene. Tetradecanoylphorbol Acetate 90-121 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 168-171 8761946-2 1996 Since fos/jun and steroid hormones interact to regulate gene expression, we asked whether phorbol-12-myristate-13-acetate (PMA), which stimulates binding of fos/jun to AP1 sites, transactivates the avian beta 3 integrin gene and, if so, does the phorbol ester modulate 1,25(OH)2D3 induction of the gene. Tetradecanoylphorbol Acetate 123-126 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 168-171 8793856-4 1996 Reverse transcription-polymerase chain reaction (RT-PCR) analysis was performed to estimate the c-jun and c-fos mRNA contents in GnRH-, forskolin- (cAMP activator) and tetradecanoyl phorbol acetate- (TPA; protein kinase C activator) treated primary cultures of porcine anterior pituitary cells. Tetradecanoylphorbol Acetate 200-203 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 96-101 8793856-5 1996 Densitometric quantification demonstrated that GnRH and TPA treatment increased c-jun and c-fos mRNA levels significantly, whereas forskolin reduced the levels of both. Tetradecanoylphorbol Acetate 56-59 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 80-85 8701784-4 1996 In these cells, 12-0-tetra-decanoylphorbol-13-acetate (TPA) increased c-fos and c-jun expression as did estradiol. Tetradecanoylphorbol Acetate 55-58 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 80-85 8530360-6 1995 Phorbol 12-myristate 13-acetate did not activate the JNKs although it activated ERK1 and ERK2, which phosphorylated the c-Jun transactivation domain in vitro. Tetradecanoylphorbol Acetate 0-31 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 120-125 7775415-2 1995 The long terminal repeat (LTR) of Mo-MuLV affects the regulation of a number of cellular genes, including collagenase IV, monocyte chemoattractant protein-1, and c-jun genes, all of which contain 12-O-tetradecanoylphorbol-13-acetate-responsive element consensus sites within their promoters. Tetradecanoylphorbol Acetate 196-232 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 162-167 7490476-10 1995 Northern blot analysis revealed that c-jun mRNA was induced by IFN-gamma plus anti-Fas antibody treatment as well as by TPA treatment; the addition of IFN-gamma alone to the incubation medium had no effect on the expression of c-jun mRNA. Tetradecanoylphorbol Acetate 120-123 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-42 7592995-2 1995 In this work, we demonstrate that the levels of c-jun mRNA, c-Jun protein, and DNA binding activity of a nuclear transcription factor AP-1 to 12-o-tetradecanoylphorbol 13-acetate responsive elements all increased following treatment with the cell-permeable ceramide, N-acetylsphingosine in human leukemia HL-60 cells. Tetradecanoylphorbol Acetate 142-178 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 48-53 7592995-2 1995 In this work, we demonstrate that the levels of c-jun mRNA, c-Jun protein, and DNA binding activity of a nuclear transcription factor AP-1 to 12-o-tetradecanoylphorbol 13-acetate responsive elements all increased following treatment with the cell-permeable ceramide, N-acetylsphingosine in human leukemia HL-60 cells. Tetradecanoylphorbol Acetate 142-178 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 134-138 7592861-5 1995 TPA-dependent stimulation can also be demonstrated by co-transfection with plasmid DNAs that overexpress the JUN family of proteins, especially c-JUN. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 144-149 7539928-6 1995 Induction of c-fos and c-jun expression by TPA was inhibited by both herbimycin A and calphostin C, suggesting that both PKC and TK pathways are necessary for the induction of the TPA-induced transcription factor AP1, which is a known TPA-inducible early immediate gene product. Tetradecanoylphorbol Acetate 43-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 23-28 7539928-6 1995 Induction of c-fos and c-jun expression by TPA was inhibited by both herbimycin A and calphostin C, suggesting that both PKC and TK pathways are necessary for the induction of the TPA-induced transcription factor AP1, which is a known TPA-inducible early immediate gene product. Tetradecanoylphorbol Acetate 180-183 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 23-28 7539928-6 1995 Induction of c-fos and c-jun expression by TPA was inhibited by both herbimycin A and calphostin C, suggesting that both PKC and TK pathways are necessary for the induction of the TPA-induced transcription factor AP1, which is a known TPA-inducible early immediate gene product. Tetradecanoylphorbol Acetate 180-183 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 23-28 7867590-5 1995 Secondly, in prolonged (4-day) treatments of MTLN (ER-positive) cells, low antiestrogen concentrations (nanomolar) decreased the basal AP-1 response by about 2 and increased the 12-O-tetradecanoyl-phorbol-13-acetate-stimulated AP-1 response by about 3-4. Tetradecanoylphorbol Acetate 178-215 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 227-231 7774103-4 1995 By contrast, PMA-induced production of IL-1 beta was impaired in RA patients and was preceded by the disregulated expression of c-Fos and c-Jun proteins when compared with healthy donors. Tetradecanoylphorbol Acetate 13-16 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 138-143 8788311-3 1995 Twelve-0-tetradecanoylphorbol-13-acetate (TPA) increased c-fos and c-jun expressions in endometrial fibroblasts as estradiol did, and pretreatment with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) reduced the estrogen-inducible c-fos and c-jun expressions. Tetradecanoylphorbol Acetate 42-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 67-72 8788311-3 1995 Twelve-0-tetradecanoylphorbol-13-acetate (TPA) increased c-fos and c-jun expressions in endometrial fibroblasts as estradiol did, and pretreatment with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) reduced the estrogen-inducible c-fos and c-jun expressions. Tetradecanoylphorbol Acetate 42-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 261-266 21043585-7 1995 Treatment of cells with TPA was associated with induction of c-jun and junB mRN A within 1-4 h. The protein products of these transcription factors are known to be part of the transcription factor complex Activator protein 1 (AP-1). Tetradecanoylphorbol Acetate 24-27 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 61-66 21043585-7 1995 Treatment of cells with TPA was associated with induction of c-jun and junB mRN A within 1-4 h. The protein products of these transcription factors are known to be part of the transcription factor complex Activator protein 1 (AP-1). Tetradecanoylphorbol Acetate 24-27 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 205-224 21043585-7 1995 Treatment of cells with TPA was associated with induction of c-jun and junB mRN A within 1-4 h. The protein products of these transcription factors are known to be part of the transcription factor complex Activator protein 1 (AP-1). Tetradecanoylphorbol Acetate 24-27 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-230 21043585-8 1995 Indeed, our data prove a rapid induction of AP-1 protein after TPA stimulation, as shown by mobility shift assays. Tetradecanoylphorbol Acetate 63-66 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-48 8063812-2 1994 We demonstrate using a human glial cell line (1321N1) that activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases beta-APP mRNA levels, induces known components of the transcription factor activator protein-1 (AP-1), and increases protein-DNA binding activity to AP-1 sequences within the beta-APP promoter. Tetradecanoylphorbol Acetate 101-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 224-243 7713192-7 1994 The phorbol ester, phorbol myristate acetate (PMA), caused a significant 2-3 fold increase in AP-1 DNA binding, which was sustained for 24 h and completely attenuated by co-incubation with dexamethasone. Tetradecanoylphorbol Acetate 19-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 94-98 7713192-7 1994 The phorbol ester, phorbol myristate acetate (PMA), caused a significant 2-3 fold increase in AP-1 DNA binding, which was sustained for 24 h and completely attenuated by co-incubation with dexamethasone. Tetradecanoylphorbol Acetate 46-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 94-98 7955078-0 1994 Effect of curcumin on 12-O-tetradecanoylphorbol-13-acetate- and ultraviolet B light-induced expression of c-Jun and c-Fos in JB6 cells and in mouse epidermis. Tetradecanoylphorbol Acetate 22-58 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111 7955078-3 1994 Treatment of quiescent JB6 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) (10 ng/ml) for 24 h markedly stimulated the formation of c-Jun and caused morphological changes. Tetradecanoylphorbol Acetate 38-74 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 138-143 7955078-3 1994 Treatment of quiescent JB6 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) (10 ng/ml) for 24 h markedly stimulated the formation of c-Jun and caused morphological changes. Tetradecanoylphorbol Acetate 76-79 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 138-143 7955078-6 1994 The increased expression of c-Jun and morphological changes observed at 24 h after treatment of JB6 cells with TPA (10 ng/ml) was inhibited by curcumin (10 nmol/ml). Tetradecanoylphorbol Acetate 111-114 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-33 7955078-11 1994 Topical application of 10 mumol curcumin together with 5 nmol TPA once a day for 5 days strongly inhibited TPA-induced epidermal hyperplasia and c-Jun and c-Fos expression. Tetradecanoylphorbol Acetate 62-65 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-150 7875527-7 1994 Consequently, the binding activity of c-Jun protein to the TPA-responsive element increases, and this causes the induction of PPET-1 mRNA. Tetradecanoylphorbol Acetate 59-62 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-43 8063812-2 1994 We demonstrate using a human glial cell line (1321N1) that activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases beta-APP mRNA levels, induces known components of the transcription factor activator protein-1 (AP-1), and increases protein-DNA binding activity to AP-1 sequences within the beta-APP promoter. Tetradecanoylphorbol Acetate 101-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 245-249 8063812-2 1994 We demonstrate using a human glial cell line (1321N1) that activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases beta-APP mRNA levels, induces known components of the transcription factor activator protein-1 (AP-1), and increases protein-DNA binding activity to AP-1 sequences within the beta-APP promoter. Tetradecanoylphorbol Acetate 101-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 298-302 8063812-2 1994 We demonstrate using a human glial cell line (1321N1) that activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases beta-APP mRNA levels, induces known components of the transcription factor activator protein-1 (AP-1), and increases protein-DNA binding activity to AP-1 sequences within the beta-APP promoter. Tetradecanoylphorbol Acetate 134-137 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 224-243 8063812-2 1994 We demonstrate using a human glial cell line (1321N1) that activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases beta-APP mRNA levels, induces known components of the transcription factor activator protein-1 (AP-1), and increases protein-DNA binding activity to AP-1 sequences within the beta-APP promoter. Tetradecanoylphorbol Acetate 134-137 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 245-249 8063812-2 1994 We demonstrate using a human glial cell line (1321N1) that activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases beta-APP mRNA levels, induces known components of the transcription factor activator protein-1 (AP-1), and increases protein-DNA binding activity to AP-1 sequences within the beta-APP promoter. Tetradecanoylphorbol Acetate 134-137 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 298-302 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 193-198 8035787-5 1994 This superinduction was blocked by preincubation of cells with the glutathione precursor N-acetyl cysteine or with phorbol 12-myristate 13-acetate, which indicates redox control of c-jun expression and probable involvement of protein kinase C. By gel retardation assay, no increase in AP-1 DNA binding activity was found to be concomitant with the transcriptional activation of c-jun. Tetradecanoylphorbol Acetate 115-146 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 181-186 8035787-5 1994 This superinduction was blocked by preincubation of cells with the glutathione precursor N-acetyl cysteine or with phorbol 12-myristate 13-acetate, which indicates redox control of c-jun expression and probable involvement of protein kinase C. By gel retardation assay, no increase in AP-1 DNA binding activity was found to be concomitant with the transcriptional activation of c-jun. Tetradecanoylphorbol Acetate 115-146 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 285-289 8035787-5 1994 This superinduction was blocked by preincubation of cells with the glutathione precursor N-acetyl cysteine or with phorbol 12-myristate 13-acetate, which indicates redox control of c-jun expression and probable involvement of protein kinase C. By gel retardation assay, no increase in AP-1 DNA binding activity was found to be concomitant with the transcriptional activation of c-jun. Tetradecanoylphorbol Acetate 115-146 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 378-383 8020141-1 1994 Rapid transient induction of the human c-jun proto-oncogene by 12-O-tetradecanoylphorbol-13-acetate (TPA) and UV irradiation requires the presence of two cis-acting elements, Jun1 and Jun2. Tetradecanoylphorbol Acetate 63-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-44 8020141-1 1994 Rapid transient induction of the human c-jun proto-oncogene by 12-O-tetradecanoylphorbol-13-acetate (TPA) and UV irradiation requires the presence of two cis-acting elements, Jun1 and Jun2. Tetradecanoylphorbol Acetate 101-104 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-44 8174632-11 1994 PMA also induced c-fos and c-jun with a time course similar to that of serum or thrombin. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-32 8036019-2 1994 Although S63 and S73 are conserved in the mutant v-Jun oncoprotein, they are not phosphorylated by two enzymes which target the corresponding residues in c-Jun in vitro; namely a partially purified c-Jun kinase from TPA-stimulated U937 cells and purified p54 mitogen activated protein (MAP) kinase. Tetradecanoylphorbol Acetate 216-219 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 198-203 8036020-5 1994 Following activation of PKC, the effects of TPA are known to act through the transcription factor AP-1. Tetradecanoylphorbol Acetate 44-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-102 8020141-2 1994 Using dimethyl sulfate (DMS) genomic footprinting, in vivo, all protein binding sites in the c-jun promoter, including Jun1 and Jun2, are already fully occupied before induction and the protein--DNA contacts are unchanged during gene activation by TPA and UV and subsequent repression. Tetradecanoylphorbol Acetate 248-251 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-98 8020141-7 1994 The lack of detectable changes in DNA binding and factor composition strongly suggests that transcriptional activation and subsequent inactivation of c-jun promoter activity by TPA or UV is mediated by post-translational modifications of prebound cJun and possibly ATF-2. Tetradecanoylphorbol Acetate 177-180 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 150-155 8020141-7 1994 The lack of detectable changes in DNA binding and factor composition strongly suggests that transcriptional activation and subsequent inactivation of c-jun promoter activity by TPA or UV is mediated by post-translational modifications of prebound cJun and possibly ATF-2. Tetradecanoylphorbol Acetate 177-180 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 247-251 8179594-2 1994 The AP-1 complex consists of distinct protein heterodimers encoded by the proto-oncogene c-fos and c-jun mRNA whose gene expression can be induced by TPA, cyclic AMP and growth factors. Tetradecanoylphorbol Acetate 150-153 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 99-104 8179594-3 1994 Recent findings suggest an involvement of reactive oxygen species in the pathway of TPA and protein kinase C leading to expression of c-fos and c-jun mRNA. Tetradecanoylphorbol Acetate 84-87 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 144-149 8289787-4 1994 Ablation of epidermal growth factor-, tetradecanoyl phorbol acetate-, or anisomycin-stimulated S6 phosphorylation by using the p70/85S6k inhibitor rapamycin has no effect on histone H3 and HMG-like protein phosphorylation or on the induction and superinduction of c-fos and c-jun. Tetradecanoylphorbol Acetate 38-67 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 274-279 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 67-72 7841543-9 1994 The above studies suggest that (1) the repression of androgen induction of gene expression by TPA-activated PKC is at least in part due to overexpression of c-jun and c-fos and (2) PKC may be a negative growth regulator in prostate cells. Tetradecanoylphorbol Acetate 94-97 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 157-162 8288641-7 1994 Treatment of HL-60, but not HL-525, cells with TPA was associated with increased MAP kinase activity as determined by phosphorylation of myelin basic protein and the c-Jun Y peptide. Tetradecanoylphorbol Acetate 47-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 166-171 8247013-2 1993 These proteins enhance trans-activation by c-jun, and the c-erbA receptors in the presence of thyroid hormone repress TPA and c-jun induction of transcription. Tetradecanoylphorbol Acetate 118-121 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 43-48 8204956-1 1993 Jun and Fos are major components of the transcriptional complex AP-1 (Activator Protein-1), a collection of dimeric transcriptional activators composed of members of the Jun and Fos family of bZIP proteins, that bind to a common site known as TRE (TPA Responsive Element) or the AP-1 site. Tetradecanoylphorbol Acetate 248-251 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-68 8204956-1 1993 Jun and Fos are major components of the transcriptional complex AP-1 (Activator Protein-1), a collection of dimeric transcriptional activators composed of members of the Jun and Fos family of bZIP proteins, that bind to a common site known as TRE (TPA Responsive Element) or the AP-1 site. Tetradecanoylphorbol Acetate 248-251 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-89 8204956-1 1993 Jun and Fos are major components of the transcriptional complex AP-1 (Activator Protein-1), a collection of dimeric transcriptional activators composed of members of the Jun and Fos family of bZIP proteins, that bind to a common site known as TRE (TPA Responsive Element) or the AP-1 site. Tetradecanoylphorbol Acetate 248-251 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 279-283 8204956-2 1993 Transcription of c-jun is rapidly induced by exposure to different extra-cellular signals like growth factors, cytokines, tumor promoters (TPA), UV and other DNA-damaging agents. Tetradecanoylphorbol Acetate 139-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 17-22 8389757-11 1993 Activity of the mitogen-activated protein kinase family with associated phosphorylation of c-Jun Y-peptide was markedly diminished in TPA-treated HL-60/vinc cells, but not in response to okadaic acid. Tetradecanoylphorbol Acetate 134-137 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 91-96 8391009-2 1993 Monocytic differentiation of HL-60 cells by TPA (12-0-tetradecanoyl phorbol-13-acetate) has been reported to be paralleled by increased AP-1 binding to DNA and by elevated c-jun expression, suggesting transcriptional level of control. Tetradecanoylphorbol Acetate 44-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 136-140 8391009-2 1993 Monocytic differentiation of HL-60 cells by TPA (12-0-tetradecanoyl phorbol-13-acetate) has been reported to be paralleled by increased AP-1 binding to DNA and by elevated c-jun expression, suggesting transcriptional level of control. Tetradecanoylphorbol Acetate 44-47 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-177 8384354-1 1993 Expression of immediate-early genes involving the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-responsive element (TRE) is modulated by post-translational modification of pre-existing activator protein 1 (AP-1) constituents. Tetradecanoylphorbol Acetate 89-92 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 183-202 8390855-7 1993 Because Ha-Ras requires isoprenylation for membrane binding, we examined the effect of the isoprenylation inhibitors lovastatin and perillic acid on PMA-induced c-Jun phosphorylation. Tetradecanoylphorbol Acetate 149-152 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 161-166 8386622-1 1993 In many different cell types treatment with phorbol esters (e.g. 4 beta-phorbol 12-myristate 13-acetate, PMA) leads to the activation of protein-kinase C (PKC) and subsequently to the activation of the activator-protein-1(AP-1)-responsive gene expression. Tetradecanoylphorbol Acetate 67-103 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 202-221 8386622-1 1993 In many different cell types treatment with phorbol esters (e.g. 4 beta-phorbol 12-myristate 13-acetate, PMA) leads to the activation of protein-kinase C (PKC) and subsequently to the activation of the activator-protein-1(AP-1)-responsive gene expression. Tetradecanoylphorbol Acetate 67-103 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 222-226 8386622-1 1993 In many different cell types treatment with phorbol esters (e.g. 4 beta-phorbol 12-myristate 13-acetate, PMA) leads to the activation of protein-kinase C (PKC) and subsequently to the activation of the activator-protein-1(AP-1)-responsive gene expression. Tetradecanoylphorbol Acetate 105-108 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 202-221 8386622-1 1993 In many different cell types treatment with phorbol esters (e.g. 4 beta-phorbol 12-myristate 13-acetate, PMA) leads to the activation of protein-kinase C (PKC) and subsequently to the activation of the activator-protein-1(AP-1)-responsive gene expression. Tetradecanoylphorbol Acetate 105-108 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 222-226 8386622-7 1993 The functional role of the increased AP-1 DNA-binding activity was studied by transfecting THP-1 cells with reporter constructs containing AP-1 sites [Col-TREx5/TK-CAT and IL-1 beta-X-CAT, which contains the putative 12-O-tetradecanoyl-phorbol-13-acetate(TPA)-responsive element of the IL-1 beta gene]. Tetradecanoylphorbol Acetate 217-254 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-41 8386622-7 1993 The functional role of the increased AP-1 DNA-binding activity was studied by transfecting THP-1 cells with reporter constructs containing AP-1 sites [Col-TREx5/TK-CAT and IL-1 beta-X-CAT, which contains the putative 12-O-tetradecanoyl-phorbol-13-acetate(TPA)-responsive element of the IL-1 beta gene]. Tetradecanoylphorbol Acetate 255-258 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-41 8384354-1 1993 Expression of immediate-early genes involving the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-responsive element (TRE) is modulated by post-translational modification of pre-existing activator protein 1 (AP-1) constituents. Tetradecanoylphorbol Acetate 50-87 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 183-202 8384354-1 1993 Expression of immediate-early genes involving the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-responsive element (TRE) is modulated by post-translational modification of pre-existing activator protein 1 (AP-1) constituents. Tetradecanoylphorbol Acetate 50-87 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 204-208 8384354-1 1993 Expression of immediate-early genes involving the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-responsive element (TRE) is modulated by post-translational modification of pre-existing activator protein 1 (AP-1) constituents. Tetradecanoylphorbol Acetate 89-92 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 204-208 8352882-8 1993 After treatment with TPA, MEK cultures produced a large induction of both c-jun and c-fos mRNA by 60 min, as determined by northern blot analysis, and a large induction of ODC mRNA and enzyme activity by 6 h. TPA treatment of cultured HEKs, however, did not induce ODC activity; in fact, less activity, compared with that of control cultures, was observed. Tetradecanoylphorbol Acetate 21-24 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 74-79 8442767-7 1993 The finding that induction of c-jun expression by ethanol was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggested that this effect is mediated by protein kinase C. Furthermore, down-regulation of protein kinase C by prolonged exposure to 12-O-tetradecanoylphorbol-13-acetate was associated with a block in ethanol-induced c-jun expression. Tetradecanoylphorbol Acetate 271-307 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 8416791-3 1993 In this work we investigated c-fos and c-jun gene expression and AP-1-(12-O-tetradecanoylphorbol-13-acetate)-responsive enhancer element (TRE) binding activity during keratinocyte differentiation utilizing both authentic and in culture-reconstituted human epidermis. Tetradecanoylphorbol Acetate 71-107 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 65-69 8352882-1 1993 The goal of this study was to compare the response of mouse epidermal keratinocytes (MEKs) and human epidermal keratinocytes (HEKs) to 12-O-tetradecanoylphorbol-13-acetate (TPA) with respect to the activation and downregulation of protein kinase C (PKC), the expression of c-jun and c-fos, and the expression and induction of ornithine decarboxylase (ODC) activity. Tetradecanoylphorbol Acetate 135-171 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 273-278 1429597-2 1992 AP-1 binds to 12-O-tetradecanoylphorbol-13-acetate-responsive elements (TREs) palindromic sequences. Tetradecanoylphorbol Acetate 14-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 1421569-3 1992 Phosphorylation of serine 243 markedly decreases the binding of c-Jun to oligonucleotides containing the 12-O-tetradecanoylphorbol-13-acetate response element. Tetradecanoylphorbol Acetate 105-141 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 64-69 1331936-1 1992 The product of the c-jun proto-oncogene is the major component of the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-inducible transcription factor AP-1. Tetradecanoylphorbol Acetate 70-107 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 19-24 1331936-1 1992 The product of the c-jun proto-oncogene is the major component of the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-inducible transcription factor AP-1. Tetradecanoylphorbol Acetate 70-107 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-149 1331936-1 1992 The product of the c-jun proto-oncogene is the major component of the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-inducible transcription factor AP-1. Tetradecanoylphorbol Acetate 109-112 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 19-24 1331936-1 1992 The product of the c-jun proto-oncogene is the major component of the 12-O-tetradecanoyl phorbol 13-acetate (TPA)-inducible transcription factor AP-1. Tetradecanoylphorbol Acetate 109-112 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-149 1331936-2 1992 Jun binds to the TPA-responsive elements (TREs) present in a large number of TPA-inducible genes, thereby regulating their expression in response to activation of protein kinase C. Previously we have shown that Jun/AP-1 can also activate cAMP-responsive elements (CREs), indicating the existence of cross-talk in signal transduction at the transcriptional level. Tetradecanoylphorbol Acetate 17-20 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 215-219 1331936-2 1992 Jun binds to the TPA-responsive elements (TREs) present in a large number of TPA-inducible genes, thereby regulating their expression in response to activation of protein kinase C. Previously we have shown that Jun/AP-1 can also activate cAMP-responsive elements (CREs), indicating the existence of cross-talk in signal transduction at the transcriptional level. Tetradecanoylphorbol Acetate 77-80 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 215-219 1406636-10 1992 Double mutation of the RSRF and AP-1 sites suggests that there is an additional TPA-responsive element between -80 and +150 in the c-jun promoter. Tetradecanoylphorbol Acetate 80-83 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 131-136 1437149-1 1992 Transcription factor AP-1 is constituted by the various products of the fos and jun proto-oncogene family members, which associate as dimers to bind with variable efficiency to 12-O-tetradecanoyl phorbol 13-acetate (TPA)-responsive promoter elements (TREs). Tetradecanoylphorbol Acetate 177-214 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-25 1437149-1 1992 Transcription factor AP-1 is constituted by the various products of the fos and jun proto-oncogene family members, which associate as dimers to bind with variable efficiency to 12-O-tetradecanoyl phorbol 13-acetate (TPA)-responsive promoter elements (TREs). Tetradecanoylphorbol Acetate 216-219 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-25 1437150-0 1992 Differential induction of c-fos and c-jun proto-oncogenes and AP-1 activity by tumor promoter 12-O-tetradecanoyl phorbol 13-acetate in cells at different stages of tumor promotion in vitro. Tetradecanoylphorbol Acetate 94-131 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 36-41 1406636-6 1992 In this study, we mapped the sequences in the c-jun promoter responsible for epidermal growth factor (EGF), serum, and 12-O-tetradecanoylphorbol-13-acetate (TPA) induction by deletion and point mutational analysis. Tetradecanoylphorbol Acetate 119-155 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-51 1406636-6 1992 In this study, we mapped the sequences in the c-jun promoter responsible for epidermal growth factor (EGF), serum, and 12-O-tetradecanoylphorbol-13-acetate (TPA) induction by deletion and point mutational analysis. Tetradecanoylphorbol Acetate 157-160 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-51 1406636-10 1992 Double mutation of the RSRF and AP-1 sites suggests that there is an additional TPA-responsive element between -80 and +150 in the c-jun promoter. Tetradecanoylphorbol Acetate 80-83 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 32-36 1416026-5 1992 Studies on the protooncogene-encoded transcription factor c-Jun employing this assay revealed a TPA-inducible protein dephosphorylation event that strongly increases the DNA-binding potential of the protein. Tetradecanoylphorbol Acetate 96-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-63 19912882-7 1992 Incubation of neuroblastoma cells with the active phorbol ester, phorbol 12-myristate 13-acetate (PMA), increased expression of CAT from pTH(-245/+2 1)CAT over 6-fold and was accompanied by induction of c-fos and c-jun mRNAs and proteins. Tetradecanoylphorbol Acetate 65-96 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 213-218 19912882-7 1992 Incubation of neuroblastoma cells with the active phorbol ester, phorbol 12-myristate 13-acetate (PMA), increased expression of CAT from pTH(-245/+2 1)CAT over 6-fold and was accompanied by induction of c-fos and c-jun mRNAs and proteins. Tetradecanoylphorbol Acetate 98-101 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 213-218 1525167-4 1992 The results demonstrate that these cells express low levels of PKC alpha and PKC beta transcripts and exhibit an attenuated induction of c-jun expression following treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 179-215 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 137-142 1525167-4 1992 The results demonstrate that these cells express low levels of PKC alpha and PKC beta transcripts and exhibit an attenuated induction of c-jun expression following treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 217-220 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 137-142 1542579-1 1992 To understand the mechanism by which phorbol esters (PMA) stimulate c-jun transcription in human leukemic cell line U937, we have mutated specific enhancer sequences within the c-jun promoter. Tetradecanoylphorbol Acetate 53-56 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 68-73 1510878-4 1992 PMA, which directly activates PKC, mimicked the effect of the lectins on c-Fos and c-Jun, but elevation of either intracellular Ca2+ or cAMP levels had little or no effect. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-88 1542579-1 1992 To understand the mechanism by which phorbol esters (PMA) stimulate c-jun transcription in human leukemic cell line U937, we have mutated specific enhancer sequences within the c-jun promoter. Tetradecanoylphorbol Acetate 53-56 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 177-182 1738590-1 1992 The TPA-inducible transcription factor AP-1, consisting of homo- or hetero-dimers of members of the Jun- and Fos-families, regulates transcription of a wide variety of genes containing the TPA response element (TRE). Tetradecanoylphorbol Acetate 4-7 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-43 1737349-6 1992 Down-regulation of PKC by prolonged pretreatment with 12-O-tetradecanoylphorbol-13-acetate was also associated with inhibition of CDDP-induced c-jun expression. Tetradecanoylphorbol Acetate 54-90 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 143-148 1738590-1 1992 The TPA-inducible transcription factor AP-1, consisting of homo- or hetero-dimers of members of the Jun- and Fos-families, regulates transcription of a wide variety of genes containing the TPA response element (TRE). Tetradecanoylphorbol Acetate 189-192 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 39-43 1909627-1 1991 The differentiation into macrophages of the U937 and HL60 human cell lines induced by 4 beta-phorbol 12-myristate 13-acetate (PMA) was accompanied by induction of the expression of the proto-oncogenes c-jun, jun B and jun D. However, expression of the three jun genes was regulated differently during induction of cell differentiation in both U937 and HL60 cells, with the three jun family members being expressed distinctly at different stages of cell differentiation. Tetradecanoylphorbol Acetate 86-124 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 201-206 1731522-5 1992 Within 48 hours after induction with phorbol ester (TPA), both parent lines exhibited markedly increased expression of c-fos/c-jun. Tetradecanoylphorbol Acetate 52-55 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 125-130 1731522-14 1992 Expression of c-fos/c-jun also was noted in a subpopulation of H-RS cells in tissues; and this expression also was enhanced when these cells were treated with TPA in culture. Tetradecanoylphorbol Acetate 159-162 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 20-25 1915667-3 1991 In this paper we show that epidermal growth factor (EGF)- and 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced expression of the c-fos and c-jun protooncogenes is decreased in microgravity, while no effect of gravity changes was observed on A23187- and forskolin-induced expression of these genes. Tetradecanoylphorbol Acetate 62-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 142-147 1915667-3 1991 In this paper we show that epidermal growth factor (EGF)- and 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced expression of the c-fos and c-jun protooncogenes is decreased in microgravity, while no effect of gravity changes was observed on A23187- and forskolin-induced expression of these genes. Tetradecanoylphorbol Acetate 101-104 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 142-147 1939341-1 1991 Previous studies have shown that treatment of human myeloid leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of monocytic differentiation and expression of the c-jun and c-fos early response genes. Tetradecanoylphorbol Acetate 80-116 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 203-208 1939341-1 1991 Previous studies have shown that treatment of human myeloid leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of monocytic differentiation and expression of the c-jun and c-fos early response genes. Tetradecanoylphorbol Acetate 118-121 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 203-208 1939341-2 1991 The present work demonstrates that the glucocorticoid dexamethasone inhibits TPA-induced increases in c-jun and c-fos mRNA levels in U-937 leukemia cells. Tetradecanoylphorbol Acetate 77-80 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 102-107 1939341-4 1991 Other studies have demonstrated that TPA-induced monocytic differentiation and expression of the c-jun and c-fos genes in myeloid leukemia cells are regulated by protein kinase C (PKC). Tetradecanoylphorbol Acetate 37-40 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 97-102 1939341-6 1991 Nuclear run-on assays demonstrate that: (1) induction of c-jun and c-fos expression by TPA is regulated by transcriptional mechanisms, (2) TPA-induced expression of c-jun and c-fos does not require protein synthesis, and (3) TPA-induced expression of both genes is inhibited at the transcriptional level by dexamethasone. Tetradecanoylphorbol Acetate 87-90 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62 1939341-6 1991 Nuclear run-on assays demonstrate that: (1) induction of c-jun and c-fos expression by TPA is regulated by transcriptional mechanisms, (2) TPA-induced expression of c-jun and c-fos does not require protein synthesis, and (3) TPA-induced expression of both genes is inhibited at the transcriptional level by dexamethasone. Tetradecanoylphorbol Acetate 87-90 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-170 1939341-6 1991 Nuclear run-on assays demonstrate that: (1) induction of c-jun and c-fos expression by TPA is regulated by transcriptional mechanisms, (2) TPA-induced expression of c-jun and c-fos does not require protein synthesis, and (3) TPA-induced expression of both genes is inhibited at the transcriptional level by dexamethasone. Tetradecanoylphorbol Acetate 139-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62 1662987-6 1991 An analysis of defined elements in different promoters suggests that serine/threonine phosphoprotein phosphatases are involved in the regulation of the c-jun and the collagenase 12-O-tetradecanoyl phorbol-13-acetate (TPA) response element (TRE) as well as the c-fos serum response element (SRE). Tetradecanoylphorbol Acetate 217-220 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 152-157 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 127-132 1450490-5 1992 Immunoprecipitation experiments also demonstrate a TPA induced increase in the c-jun protein in both sensitive and resistant cells. Tetradecanoylphorbol Acetate 51-54 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 79-84 1791843-3 1991 It recently has been reported that certain nuclear receptors can antagonize the tumor promoter 12-O-tetradeconylphorbol-13-acetate (TPA) by direct interaction with the transcription factor AP-1, and that the AP-1 constituents cJun and cFos can inhibit receptor activity. Tetradecanoylphorbol Acetate 132-135 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 189-193 1791843-3 1991 It recently has been reported that certain nuclear receptors can antagonize the tumor promoter 12-O-tetradeconylphorbol-13-acetate (TPA) by direct interaction with the transcription factor AP-1, and that the AP-1 constituents cJun and cFos can inhibit receptor activity. Tetradecanoylphorbol Acetate 132-135 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 208-212 1791843-3 1991 It recently has been reported that certain nuclear receptors can antagonize the tumor promoter 12-O-tetradeconylphorbol-13-acetate (TPA) by direct interaction with the transcription factor AP-1, and that the AP-1 constituents cJun and cFos can inhibit receptor activity. Tetradecanoylphorbol Acetate 132-135 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-230 1814434-9 1991 Activation of PKC has been implicated in the regulation of certain immediate early response genes, and in the present studies, TPA rapidly induced c-fos and c-jun gene expression. Tetradecanoylphorbol Acetate 127-130 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 157-162 1814434-11 1991 Staurosporine, a nonspecific inhibitor of PKC, partially blocked TPA-induced adherence and growth inhibition and concomitantly prevented TPA-induced c-fos and c-jun gene expression. Tetradecanoylphorbol Acetate 137-140 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 159-164 1801783-5 1991 Depletion of PKC by prolonged TPA treatment resulted in inhibition of c-jun expression. Tetradecanoylphorbol Acetate 30-33 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 70-75 1939341-6 1991 Nuclear run-on assays demonstrate that: (1) induction of c-jun and c-fos expression by TPA is regulated by transcriptional mechanisms, (2) TPA-induced expression of c-jun and c-fos does not require protein synthesis, and (3) TPA-induced expression of both genes is inhibited at the transcriptional level by dexamethasone. Tetradecanoylphorbol Acetate 139-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-170 1939341-6 1991 Nuclear run-on assays demonstrate that: (1) induction of c-jun and c-fos expression by TPA is regulated by transcriptional mechanisms, (2) TPA-induced expression of c-jun and c-fos does not require protein synthesis, and (3) TPA-induced expression of both genes is inhibited at the transcriptional level by dexamethasone. Tetradecanoylphorbol Acetate 139-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 57-62 1939341-6 1991 Nuclear run-on assays demonstrate that: (1) induction of c-jun and c-fos expression by TPA is regulated by transcriptional mechanisms, (2) TPA-induced expression of c-jun and c-fos does not require protein synthesis, and (3) TPA-induced expression of both genes is inhibited at the transcriptional level by dexamethasone. Tetradecanoylphorbol Acetate 139-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 165-170 1939341-10 1991 These findings suggest that dexamethasone down-regulates TPA-induced transcription of the c-jun gene during monocytic differentiation by inhibiting activation of the AP-1 site. Tetradecanoylphorbol Acetate 57-60 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 90-95 1909627-1 1991 The differentiation into macrophages of the U937 and HL60 human cell lines induced by 4 beta-phorbol 12-myristate 13-acetate (PMA) was accompanied by induction of the expression of the proto-oncogenes c-jun, jun B and jun D. However, expression of the three jun genes was regulated differently during induction of cell differentiation in both U937 and HL60 cells, with the three jun family members being expressed distinctly at different stages of cell differentiation. Tetradecanoylphorbol Acetate 126-129 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 201-206 1907719-5 1991 The mutant Jun lacks an activation domain and blocks stimulation of transcription by several oncoproteins, including Ras, v-Src, polyoma middle T, c-Jun and c-Fos, as well as by the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 198-234 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-152 1907719-5 1991 The mutant Jun lacks an activation domain and blocks stimulation of transcription by several oncoproteins, including Ras, v-Src, polyoma middle T, c-Jun and c-Fos, as well as by the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 236-239 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-152 1904283-6 1991 Both TPA and 1,25(OH)2D3, which induce HL-60 cells to differentiate to macrophages, resulted in marked increases in c-jun mRNA; while RA and DMSO, which induce HL-60 cells to differentiate to granulocytes, did not greatly alter c-jun mRNA expression. Tetradecanoylphorbol Acetate 5-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 116-121 1648385-12 1991 The induction of t-PA mRNA by PMA was dependent on protein synthesis and was preceded by a strong transient increase in c-jun and c-fos mRNA levels; the induction of c-fos but not of c-jun was potentiated by forskolin. Tetradecanoylphorbol Acetate 30-33 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 120-125 1904283-6 1991 Both TPA and 1,25(OH)2D3, which induce HL-60 cells to differentiate to macrophages, resulted in marked increases in c-jun mRNA; while RA and DMSO, which induce HL-60 cells to differentiate to granulocytes, did not greatly alter c-jun mRNA expression. Tetradecanoylphorbol Acetate 5-8 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 228-233 1901948-7 1991 This preferential response of the c-jun gene is mediated by its 5" control region and requires the TPA response element, suggesting that this element also serves as an early target for the signal transduction pathway elicited by DNA damage. Tetradecanoylphorbol Acetate 99-102 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 34-39 1851743-7 1991 Similar to its effect on the induction of AP1 by okadaic acid, PMA inhibits the induction of c-jun mRNA by okadaic acid. Tetradecanoylphorbol Acetate 63-66 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-45 1851743-7 1991 Similar to its effect on the induction of AP1 by okadaic acid, PMA inhibits the induction of c-jun mRNA by okadaic acid. Tetradecanoylphorbol Acetate 63-66 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-98 2011401-4 1991 In contrast, accumulation of mRNAs for the C-FOS, C-JUN, and EGR-1 genes increased markedly in TPA-treated cells and preceded the induction of IL2R-alpha mRNA. Tetradecanoylphorbol Acetate 95-98 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 50-55 1902229-10 1991 Experiments using phorbol ester (phorbol 12-myristate 13-acetate) in combination with the Ca2+ ionophore ionomycin confirm that activation of protein kinase C induces c-fos and c-jun expression and that a concomitant increase in cytosolic [Ca2+] potentiates the induction of c-fos while repressing that of c-jun. Tetradecanoylphorbol Acetate 33-64 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 177-182 1902229-10 1991 Experiments using phorbol ester (phorbol 12-myristate 13-acetate) in combination with the Ca2+ ionophore ionomycin confirm that activation of protein kinase C induces c-fos and c-jun expression and that a concomitant increase in cytosolic [Ca2+] potentiates the induction of c-fos while repressing that of c-jun. Tetradecanoylphorbol Acetate 33-64 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 306-311 1899335-2 1991 Upon functional activation of granulocytes by 4 beta-phorbol 12-myristate 13-acetate (PMA), the levels of c-jun, jun B and jun D transcripts were increased. Tetradecanoylphorbol Acetate 46-84 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111 1851138-5 1991 Under these conditions, dbcAMP was found to interfere with the TPA + ionomycin-mediated induction of c-jun encoding the JUN/AP-1 transcription factor. Tetradecanoylphorbol Acetate 63-66 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 101-106 1899335-2 1991 Upon functional activation of granulocytes by 4 beta-phorbol 12-myristate 13-acetate (PMA), the levels of c-jun, jun B and jun D transcripts were increased. Tetradecanoylphorbol Acetate 86-89 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 106-111 2227262-7 1990 We presented results showing that DNA-protein complexes with a 23 bp DNA are similar to but distinct from those with a TPA-responsive element DNA, the recognition site for c-jun/fos products. Tetradecanoylphorbol Acetate 119-122 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 172-177 1822395-1 1991 We show here that TPA treatment of MCF-7 cells represses estrogen receptor dependent transcriptional activity, while increasing the AP1 binding activity. Tetradecanoylphorbol Acetate 18-21 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 132-135 1822395-5 1991 Our results suggest that the inhibition of TPA of the estrogen dependent growth of the MCF-7 cells is caused by over expression of cJun and cFos. Tetradecanoylphorbol Acetate 43-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 131-135 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 222-227 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 222-227 1824713-4 1991 AP-1 binds to 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive elements (TREs); therefore, E1A might modulate a specific signal transduction pathway normally induced by activation of the protein kinase C. Binding of jun/AP-1 to a TRE is induced in all cell types studied when E1A is expressed. Tetradecanoylphorbol Acetate 14-50 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 1824713-4 1991 AP-1 binds to 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive elements (TREs); therefore, E1A might modulate a specific signal transduction pathway normally induced by activation of the protein kinase C. Binding of jun/AP-1 to a TRE is induced in all cell types studied when E1A is expressed. Tetradecanoylphorbol Acetate 52-55 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-4 1824713-4 1991 AP-1 binds to 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive elements (TREs); therefore, E1A might modulate a specific signal transduction pathway normally induced by activation of the protein kinase C. Binding of jun/AP-1 to a TRE is induced in all cell types studied when E1A is expressed. Tetradecanoylphorbol Acetate 52-55 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 225-229 2112105-7 1990 A putative TRE (TPA responsive element or AP-1 recognition sequence) strategically situated upstream from the GST pi tsp (-69 to -63) was examined by TPA treatment of HeLa cells transfected with GST-cat DNA. Tetradecanoylphorbol Acetate 150-153 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 42-46 2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tetradecanoylphorbol Acetate 35-72 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 92-97 2178224-5 1990 In addition, we show that IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate transiently induce c-jun and c-fos expression and that retinoic acid inhibits IL-1 and 12-O-tetradecanoyl-phorbol-13-acetate induction of c-fos, but not c-jun. Tetradecanoylphorbol Acetate 35-72 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 226-231 2113601-4 1990 Upon treatment with TPA or Bryo, the steady-state levels of c-jun mRNA increased rapidly, reached a maximum at 0.5 or 1 hr, and then decreased in the B-CLL cells from all five patients analyzed; this reaction was augmented by the addition of A23187. Tetradecanoylphorbol Acetate 20-23 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 60-65 7669726-7 1995 Staurosporine and H7, however, inhibit the increase in c-jun mRNA by TPA. Tetradecanoylphorbol Acetate 69-72 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 55-60 2320002-4 1990 This protein, HB16, displays structural similarity to CREB and to c-Jun and c-Fos, which bind the related 12-O-tetradecanoylphorbol-13-acetate response element (TRE). Tetradecanoylphorbol Acetate 106-142 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 66-71 2107494-0 1990 Cross-talk in signal transduction: TPA-inducible factor jun/AP-1 activates cAMP-responsive enhancer elements. Tetradecanoylphorbol Acetate 35-38 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 60-64 2154599-6 1990 In addition, the Zta protein, which possesses a similar basic domain to the conserved DNA-binding region of the c-Fos, c-Jun, GCN4, and CREB protein family, proved to bind directly to the consensus AP-1 site in the collagenase 12-O-tetradecanoylphorbol-13-acetate response element. Tetradecanoylphorbol Acetate 227-263 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 119-124 2154599-6 1990 In addition, the Zta protein, which possesses a similar basic domain to the conserved DNA-binding region of the c-Fos, c-Jun, GCN4, and CREB protein family, proved to bind directly to the consensus AP-1 site in the collagenase 12-O-tetradecanoylphorbol-13-acetate response element. Tetradecanoylphorbol Acetate 227-263 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 198-202 2154599-8 1990 Cellular AP-1 binding activity proved to be low in latently EBV-infected Raji cells but was induced (together with the Zta protein) after activation of the lytic cycle with 12-O-tetradecanoylphorbol-13-acetate. Tetradecanoylphorbol Acetate 173-209 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-13 2154605-6 1990 A distinct TPA-responsive element (ZII) is located near the TATA box and shares homology with the AP-1-binding site in the c-jun promoter. Tetradecanoylphorbol Acetate 11-14 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 123-128 2105946-1 1990 AP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 189-225 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 33-38 2105946-1 1990 AP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 227-230 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 33-38 2105946-2 1990 We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Tetradecanoylphorbol Acetate 26-29 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 51-56 2105946-3 1990 Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Tetradecanoylphorbol Acetate 176-179 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 14-19 2105946-4 1990 Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Tetradecanoylphorbol Acetate 39-42 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 20-25 2105946-7 1990 TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Tetradecanoylphorbol Acetate 0-3 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 100-105 2105946-10 1990 The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. Tetradecanoylphorbol Acetate 70-73 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 17-22 2105946-11 1990 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate 43-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 2105946-11 1990 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate 43-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 178-183 2105946-11 1990 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate 204-207 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-35 2105946-11 1990 In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms. Tetradecanoylphorbol Acetate 204-207 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 178-183 2158073-1 1990 The nuclear oncoproteins fos and jun are associated as a heterodimer which binds to TPA (PMA or TPA: phorbol 12-myristate 13-acetate)- responsive promoter elements (TRE), the recognition site for the transcription factor AP-1. Tetradecanoylphorbol Acetate 84-87 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 221-225 2158073-1 1990 The nuclear oncoproteins fos and jun are associated as a heterodimer which binds to TPA (PMA or TPA: phorbol 12-myristate 13-acetate)- responsive promoter elements (TRE), the recognition site for the transcription factor AP-1. Tetradecanoylphorbol Acetate 89-92 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 221-225 2158073-1 1990 The nuclear oncoproteins fos and jun are associated as a heterodimer which binds to TPA (PMA or TPA: phorbol 12-myristate 13-acetate)- responsive promoter elements (TRE), the recognition site for the transcription factor AP-1. Tetradecanoylphorbol Acetate 96-99 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 221-225 2158073-1 1990 The nuclear oncoproteins fos and jun are associated as a heterodimer which binds to TPA (PMA or TPA: phorbol 12-myristate 13-acetate)- responsive promoter elements (TRE), the recognition site for the transcription factor AP-1. Tetradecanoylphorbol Acetate 101-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 221-225 2157183-7 1990 In fact, the expression of E1A rendered the c-jun gene hypersensitive to TPA induction. Tetradecanoylphorbol Acetate 73-76 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 44-49 34512147-7 2021 We further demonstrate that c-Jun, AR, and DNA methyltransferase-1 (DNMT1) form a complex in the 12-O-tetradecanoyl phorbol-13-acetate (TPA) response elements (TREs) region of the NDRG1 promoter, which suppresses NDRG1 transcription through DNA hypermethylation. Tetradecanoylphorbol Acetate 136-139 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-33 34512147-7 2021 We further demonstrate that c-Jun, AR, and DNA methyltransferase-1 (DNMT1) form a complex in the 12-O-tetradecanoyl phorbol-13-acetate (TPA) response elements (TREs) region of the NDRG1 promoter, which suppresses NDRG1 transcription through DNA hypermethylation. Tetradecanoylphorbol Acetate 97-134 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-33 2531661-3 1989 Consistent with studies demonstrating that the AP1 site mediates signal transduction in response to 12-O-tetradecanoylphorbol 13-acetate (TPA) we have shown that TPA can activate Ad-EIII expression and overcome the requirement for EIa. Tetradecanoylphorbol Acetate 100-136 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 47-50 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 0-5 2513129-3 1989 However, cotransfection of c-jun and jun-B into primary rat embryo cells with c-Ha-ras results in a significant decrease in transformation compared with c-jun alone, an event reversed by TPA. Tetradecanoylphorbol Acetate 187-190 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 27-32 2513129-3 1989 However, cotransfection of c-jun and jun-B into primary rat embryo cells with c-Ha-ras results in a significant decrease in transformation compared with c-jun alone, an event reversed by TPA. Tetradecanoylphorbol Acetate 187-190 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 153-158 2531661-3 1989 Consistent with studies demonstrating that the AP1 site mediates signal transduction in response to 12-O-tetradecanoylphorbol 13-acetate (TPA) we have shown that TPA can activate Ad-EIII expression and overcome the requirement for EIa. Tetradecanoylphorbol Acetate 138-141 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 47-50 2531661-3 1989 Consistent with studies demonstrating that the AP1 site mediates signal transduction in response to 12-O-tetradecanoylphorbol 13-acetate (TPA) we have shown that TPA can activate Ad-EIII expression and overcome the requirement for EIa. Tetradecanoylphorbol Acetate 162-165 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 47-50 2531661-6 1989 An EIII promoter construct, in which sequences upstream of the TATA box had been replaced with four AP1 sites, was responsive to TPA and EIa and in combination promoted the synergistic effect. Tetradecanoylphorbol Acetate 129-132 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 100-103 28970848-10 2017 CONCLUSION: The results indicated that the inhibitory effects of CFE against TPA-induced MMP-9 expression and MCF-7 cell invasion were dependent on the protein kinase C delta/p38/c-Jun N-terminal kinase/AP-1 pathway. Tetradecanoylphorbol Acetate 77-80 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 203-207 2541502-2 1989 Functional activation of the transacting transcription factor AP-1 by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) may play an essential role in this process. Tetradecanoylphorbol Acetate 126-129 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 62-66 3142689-1 1988 Binding of the human transcription factor Jun/AP-1 to a conserved 8 bp nucleotide sequence (TRE) is responsible for increased transcription of different cellular genes in response to tumor promoters, such as TPA, and serum factors. Tetradecanoylphorbol Acetate 208-211 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 46-50 3142689-2 1988 Enhanced Jun/AP-1 activity in TPA-stimulated cells is regulated by two different mechanisms: a posttranslational event acting on pre-existing Jun/AP-1 molecules, and transcriptional activation of jun gene expression leading to an increase in the total amount of Jun/AP-1. Tetradecanoylphorbol Acetate 30-33 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 13-17 3142689-2 1988 Enhanced Jun/AP-1 activity in TPA-stimulated cells is regulated by two different mechanisms: a posttranslational event acting on pre-existing Jun/AP-1 molecules, and transcriptional activation of jun gene expression leading to an increase in the total amount of Jun/AP-1. Tetradecanoylphorbol Acetate 30-33 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-150 3142689-2 1988 Enhanced Jun/AP-1 activity in TPA-stimulated cells is regulated by two different mechanisms: a posttranslational event acting on pre-existing Jun/AP-1 molecules, and transcriptional activation of jun gene expression leading to an increase in the total amount of Jun/AP-1. Tetradecanoylphorbol Acetate 30-33 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 146-150 3142689-3 1988 Induction of jun transcription in response to TPA is mediated by binding of Jun/AP-1 to a high-affinity AP-1 binding site in the jun promoter region. Tetradecanoylphorbol Acetate 46-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 80-84 3142689-3 1988 Induction of jun transcription in response to TPA is mediated by binding of Jun/AP-1 to a high-affinity AP-1 binding site in the jun promoter region. Tetradecanoylphorbol Acetate 46-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-108 3142689-4 1988 Site-specific mutagenesis of this binding site prevents TPA induction and trans-activation by Jun/AP-1. Tetradecanoylphorbol Acetate 56-59 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 98-102 28970848-0 2017 Crotonis Fructus Extract Inhibits 12-O-Tetradecanoylphorbol-13-Acetate-Induced Expression of Matrix Metalloproteinase-9 via the Activator Protein-1 Pathway in MCF-7 Cells. Tetradecanoylphorbol Acetate 34-70 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 128-147 28970848-9 2017 Furthermore, CFE attenuated the TPA-induced activation of AP-1. Tetradecanoylphorbol Acetate 32-35 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-62 2548844-3 1989 One of them (ZRE-M) overlaps with a consensus TPA responsive element (TRE) defined as an AP-1/c-jun/c-fos binding site and is located in an EBV promoter controlling the expression of the post-transcriptional activator EB2. Tetradecanoylphorbol Acetate 46-49 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 94-99 2648396-7 1989 Furthermore, formation of foci of transformed RECs by the c-jun/ras combination was augmented 3-fold by the tumor promoter phorbol 12-tetradecanoate 13-acetate. Tetradecanoylphorbol Acetate 123-159 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 58-63 2665635-0 1989 Human immunodeficiency virus long terminal repeat responds to transformation by the mutant T24 H-ras1 oncogene and it contains multiple AP-1 binding TPA-inducible consensus sequence elements. Tetradecanoylphorbol Acetate 149-152 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 136-140 2665635-5 1989 We have noted four motifs in the HIV-1 LTR region which resemble TPA-inducible and AP-1 binding consensus sequences. Tetradecanoylphorbol Acetate 65-68 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 83-87 2665635-6 1989 Since H-ras1 fos and jun/AP-1 respond to TPA and T24 H-ras1 is known to induce both fos and jun/AP-1 nuclear transcriptional factors, it is possible that the latter genes play a role in HIV-1 transcription. Tetradecanoylphorbol Acetate 41-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 25-29 2665635-6 1989 Since H-ras1 fos and jun/AP-1 respond to TPA and T24 H-ras1 is known to induce both fos and jun/AP-1 nuclear transcriptional factors, it is possible that the latter genes play a role in HIV-1 transcription. Tetradecanoylphorbol Acetate 41-44 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 96-100 3034433-0 1987 Purified transcription factor AP-1 interacts with TPA-inducible enhancer elements. Tetradecanoylphorbol Acetate 50-53 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 30-34 3034433-5 1987 Here we demonstrate that multiple synthetic copies of the consensus AP-1-binding site can act as TPA-inducible enhancers in various plasmid constructs after transfection into HeLa cells. Tetradecanoylphorbol Acetate 97-100 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 68-72 3034433-6 1987 These findings suggest that AP-1 is a transcription factor that functions by interacting with a specific enhancer element, and that its activities may be modulated by treatment of cells with TPA, known to stimulate protein kinase C. Tetradecanoylphorbol Acetate 191-194 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 28-32 33307168-11 2021 Finally, c-jun and c-fos were required for TPA-induced expression of the migration-related genes and a novel microRNA, miR-6134, was responsible for TPA-induced suppression of CCNE1. Tetradecanoylphorbol Acetate 43-46 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 9-14 31194000-0 2019 Forskolin and Phorbol 12-myristate 13-acetate modulates the expression pattern of AP-1 factors and cell cycle regulators in estrogen-responsive MCF-7 cells. Tetradecanoylphorbol Acetate 14-45 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 82-86 29660338-7 2018 It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA. Tetradecanoylphorbol Acetate 18-21 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-152 29660338-7 2018 It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA. Tetradecanoylphorbol Acetate 182-185 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 147-152