PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32505192-9 2020 Subsequently, PMA induced MMP-9 expression via PKCdelta-mediated reactive oxygen species (ROS) generation, extracellular signal-regulated kinase 1/2 (ERK1/2) activation, and then induced c-Fos/AP-1 signaling pathway. Tetradecanoylphorbol Acetate 14-17 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 193-197 14967736-7 2004 Electrophoretic mobility shift assay revealed that fenofibrate significantly decreased the ET-1-stimulated or phorbol 12-myristate 13-acetate-stimulated AP-1 DNA binding activity, and the nuclear extract probe complex was supershifted by anti-c-Jun antibody. Tetradecanoylphorbol Acetate 110-141 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 153-157 12670703-1 2003 Several treatments which regulate tyrosine hydroxylase (TH) transcription, such as stress in vivo, or 12-O-tetradecanoylphorbol-13-acetate (TPA) in cell culture, induce both Egr1 and AP1 factors. Tetradecanoylphorbol Acetate 102-138 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 183-186 12670703-1 2003 Several treatments which regulate tyrosine hydroxylase (TH) transcription, such as stress in vivo, or 12-O-tetradecanoylphorbol-13-acetate (TPA) in cell culture, induce both Egr1 and AP1 factors. Tetradecanoylphorbol Acetate 140-143 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 183-186 12670703-6 2003 Electrophoretic mobility shift assays with nuclear extracts from TPA treated cells were used to identify the composition of the factors which bound the AP1/Ebox motif and whether there is competition with factors which bind the Sp1/Egr1 motif. Tetradecanoylphorbol Acetate 65-68 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 152-155 11333365-6 2001 Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. Tetradecanoylphorbol Acetate 53-84 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 117-120 11333365-6 2001 Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. Tetradecanoylphorbol Acetate 53-84 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 232-235 11333365-6 2001 Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. Tetradecanoylphorbol Acetate 86-89 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 117-120 11333365-6 2001 Further in vitro study showed that NAMDA potentiated phorbol-12 myristate-13 acetate (PMA)-induced c-Fos expression, AP1 binding activity, and late gene expression determined by chloramphenicol acetyltransferase (CAT) activity from AP1 containing tyrosine hydroxylase promoter-CAT fusion gene in SK-N-BE(2)C neurons. Tetradecanoylphorbol Acetate 86-89 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 232-235 11238722-2 2001 Mutagenesis of either the cAMP responsive element (CRE) or the activator protein-1 element (AP1) within the TH gene proximal promoter leads to a dramatic inhibition of the TPA response. Tetradecanoylphorbol Acetate 172-175 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 63-82 11238722-2 2001 Mutagenesis of either the cAMP responsive element (CRE) or the activator protein-1 element (AP1) within the TH gene proximal promoter leads to a dramatic inhibition of the TPA response. Tetradecanoylphorbol Acetate 172-175 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 92-95 11238722-3 2001 The TH CRE and TH AP1 sites are also independently responsive to TPA in minimal promoter constructs. Tetradecanoylphorbol Acetate 65-68 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 18-21 11238722-8 2001 Our results support the hypothesis that TPA stimulates the TH gene promoter via signaling pathways that activate either the TH AP1 or TH CRE sites. Tetradecanoylphorbol Acetate 40-43 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 127-130 11138725-5 2000 Furthermore, TAS-301 inhibited PDGF-induced activation of protein kinase C (PKC) and the phorbol 12-myristate 13-acetate-mediated induction of activator protein 1 (AP-1) in a concentration-dependent manner. Tetradecanoylphorbol Acetate 89-120 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 143-162 11138725-5 2000 Furthermore, TAS-301 inhibited PDGF-induced activation of protein kinase C (PKC) and the phorbol 12-myristate 13-acetate-mediated induction of activator protein 1 (AP-1) in a concentration-dependent manner. Tetradecanoylphorbol Acetate 89-120 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 164-168 9555062-3 1998 Both AP-1 and ENKCRE-2 DNA binding activities were markedly increased at 1-4 h by PMA treatment and these PMA-induced responses were inhibited by pre-treatment with CHX, showing that the increase of proENK mRNA level was well correlated with the AP-1 and ENKCRE-2 DNA binding activities. Tetradecanoylphorbol Acetate 82-85 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 5-9 9555062-3 1998 Both AP-1 and ENKCRE-2 DNA binding activities were markedly increased at 1-4 h by PMA treatment and these PMA-induced responses were inhibited by pre-treatment with CHX, showing that the increase of proENK mRNA level was well correlated with the AP-1 and ENKCRE-2 DNA binding activities. Tetradecanoylphorbol Acetate 82-85 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 246-250 9555062-3 1998 Both AP-1 and ENKCRE-2 DNA binding activities were markedly increased at 1-4 h by PMA treatment and these PMA-induced responses were inhibited by pre-treatment with CHX, showing that the increase of proENK mRNA level was well correlated with the AP-1 and ENKCRE-2 DNA binding activities. Tetradecanoylphorbol Acetate 106-109 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 5-9 9555062-3 1998 Both AP-1 and ENKCRE-2 DNA binding activities were markedly increased at 1-4 h by PMA treatment and these PMA-induced responses were inhibited by pre-treatment with CHX, showing that the increase of proENK mRNA level was well correlated with the AP-1 and ENKCRE-2 DNA binding activities. Tetradecanoylphorbol Acetate 106-109 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 246-250 8654580-3 1996 The Fos and Jun components of AP1 were induced rapidly and transiently in PC12 cells following the addition of phorbol ester (phorbol 12-myristate 13-acetate, PMA). Tetradecanoylphorbol Acetate 126-157 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 30-33 8654580-3 1996 The Fos and Jun components of AP1 were induced rapidly and transiently in PC12 cells following the addition of phorbol ester (phorbol 12-myristate 13-acetate, PMA). Tetradecanoylphorbol Acetate 159-162 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 30-33 8848234-1 1995 We examined age-related changes in composition of transcription factor, activator protein-1 (AP-1) which binds to TPA responsive element (TRE) in the non-stimulated rat brain, using electrophoretic mobility-shift assay with immunodepletion/supershift assay. Tetradecanoylphorbol Acetate 114-117 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 72-91 8848234-1 1995 We examined age-related changes in composition of transcription factor, activator protein-1 (AP-1) which binds to TPA responsive element (TRE) in the non-stimulated rat brain, using electrophoretic mobility-shift assay with immunodepletion/supershift assay. Tetradecanoylphorbol Acetate 114-117 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 93-97 7631795-5 1995 The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulated both AP-1 binding and transcriptional activity in GH3 cells and the somatostatin analogue octreotide inhibited this response by 40-70%. Tetradecanoylphorbol Acetate 18-54 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 77-81 7631795-5 1995 The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulated both AP-1 binding and transcriptional activity in GH3 cells and the somatostatin analogue octreotide inhibited this response by 40-70%. Tetradecanoylphorbol Acetate 56-59 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 77-81 8777434-5 1995 All trans-retinoic acid (RA) abolished the transformation of the 43C line and TPA-treated RELcJ1 cells, suggesting that RA could decrease AP1 activity in these cells despite c-fos or c-jun overexpression. Tetradecanoylphorbol Acetate 78-81 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 138-141 7914348-4 1994 We find that activation of the second messenger pathway leading from protein kinase C to the transcription factor AP-1 by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) impairs induction of the TAT gene both by glucocorticoid hormones and cAMP. Tetradecanoylphorbol Acetate 140-177 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 114-118 7914348-4 1994 We find that activation of the second messenger pathway leading from protein kinase C to the transcription factor AP-1 by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA) impairs induction of the TAT gene both by glucocorticoid hormones and cAMP. Tetradecanoylphorbol Acetate 179-182 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 114-118 19912806-0 1991 Variation in the composition of the AP1 complex in PC12 cells following induction by NGF and TPA. Tetradecanoylphorbol Acetate 93-96 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 36-39 19912806-6 1991 The AP1 binding activity can be further induced in all PC12 cells studied by NGF or TPA. Tetradecanoylphorbol Acetate 84-87 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 4-7 19912806-7 1991 The analysis of c-jun, c-fos, and the fos-related antigens that can constitute the AP1 complex demonstrated compositional variation of this complex by passage in culture and by exposure to NGF or TPA. Tetradecanoylphorbol Acetate 196-199 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 83-86 2176152-6 1990 We show also that RA represses the transcriptional activity of a reporter gene containing a TPA responding AP1 binding site driving the HSV tk promoter. Tetradecanoylphorbol Acetate 92-95 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 107-110 2537468-7 1989 This prolonged induction of jun contrasts with its transient activation by the phorbol ester TPA and provides a physiological example of the ability of jun/AP-1 to stimulate its own transcription. Tetradecanoylphorbol Acetate 93-96 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 156-160