PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9891065-8 1999 TPA-induced activation of the SRE was partially inhibited by dominant negative c-Raf, ERK1, or ERK2, and constitutively active mutants of PKC-alpha and PKC-epsilon activated the transactivation domain of Elk-1. Tetradecanoylphorbol Acetate 0-3 v-raf-leukemia viral oncogene 1 Mus musculus 79-84 7545901-1 1995 Experiments were carried out to determine Raf-1 protein kinase domain fragments which exhibit a characteristic electrophoretic mobility shift noted with Raf-1 protein kinase in response to serum and phorbol ester (PMA) treatment of serum-deprived NIH 3T3 cells. Tetradecanoylphorbol Acetate 214-217 v-raf-leukemia viral oncogene 1 Mus musculus 42-47 7545901-1 1995 Experiments were carried out to determine Raf-1 protein kinase domain fragments which exhibit a characteristic electrophoretic mobility shift noted with Raf-1 protein kinase in response to serum and phorbol ester (PMA) treatment of serum-deprived NIH 3T3 cells. Tetradecanoylphorbol Acetate 214-217 v-raf-leukemia viral oncogene 1 Mus musculus 153-158 7545901-5 1995 These results suggest that modification(s) within the 33 kDa C-terminal portion of Raf-1 which occur independently of association with Ras may be responsible for the band shift observed with serum and PMA treatment of serum-deprived NIH 3T3 cells. Tetradecanoylphorbol Acetate 201-204 v-raf-leukemia viral oncogene 1 Mus musculus 83-88 7718627-8 1995 Moreover, while both TPA and bFGF stimulated the hyperphosphorylation of c-RAF and the activity of MAP kinase, TPA pretreatment failed to block RAF phosphorylation or the stimulation of MAP kinase activity by bFGF. Tetradecanoylphorbol Acetate 21-24 v-raf-leukemia viral oncogene 1 Mus musculus 73-78 8288587-2 1994 Recently, 12-O-tetradecanoylphorbol 13-acetate has been found to mediate Raf-1 phosphorylation, suggesting that protein kinase C (PKC) may be involved in the Raf-1 activation mechanism(s). Tetradecanoylphorbol Acetate 10-46 v-raf-leukemia viral oncogene 1 Mus musculus 73-78 7534287-4 1995 Comparison of phosphopeptide maps of Raf-1 immunoprecipitated from the two cell types activated by either aFGF or the phorbol ester (12-O-tetradecanoylphorbol-13-acetate) suggests that Raf-1 is phosphorylated by both Ras-dependent and PLC-gamma-dependent mechanisms. Tetradecanoylphorbol Acetate 133-169 v-raf-leukemia viral oncogene 1 Mus musculus 37-42 7534287-4 1995 Comparison of phosphopeptide maps of Raf-1 immunoprecipitated from the two cell types activated by either aFGF or the phorbol ester (12-O-tetradecanoylphorbol-13-acetate) suggests that Raf-1 is phosphorylated by both Ras-dependent and PLC-gamma-dependent mechanisms. Tetradecanoylphorbol Acetate 133-169 v-raf-leukemia viral oncogene 1 Mus musculus 185-190 8288587-2 1994 Recently, 12-O-tetradecanoylphorbol 13-acetate has been found to mediate Raf-1 phosphorylation, suggesting that protein kinase C (PKC) may be involved in the Raf-1 activation mechanism(s). Tetradecanoylphorbol Acetate 10-46 v-raf-leukemia viral oncogene 1 Mus musculus 158-163 8361757-7 1993 As transformation by Ras depends on jun-mediated transcriptional events, we also examined H-ras and c-raf-1 cooperation in transcriptional transactivation of TPA-responsive element (TRE)-dependent reporters. Tetradecanoylphorbol Acetate 158-161 v-raf-leukemia viral oncogene 1 Mus musculus 100-107 8321321-1 1993 The kinase Raf-1 can be activated by treatment of cells with mitogens and by the protein kinase C (PKC) activator 12-O-tetradecanoyl-phorbol-13-acetate (TPA) (reviewed in refs 1,2). Tetradecanoylphorbol Acetate 114-151 v-raf-leukemia viral oncogene 1 Mus musculus 11-16 8321321-1 1993 The kinase Raf-1 can be activated by treatment of cells with mitogens and by the protein kinase C (PKC) activator 12-O-tetradecanoyl-phorbol-13-acetate (TPA) (reviewed in refs 1,2). Tetradecanoylphorbol Acetate 153-156 v-raf-leukemia viral oncogene 1 Mus musculus 11-16 1313769-0 1992 Serum-, TPA-, and Ras-induced expression from Ap-1/Ets-driven promoters requires Raf-1 kinase. Tetradecanoylphorbol Acetate 8-11 v-raf-leukemia viral oncogene 1 Mus musculus 81-86 8426742-11 1993 We conclude that Raf-1 signaling is essential for transformation of NIH/3T3 cells by peripheral oncogenes and for regulation of a subset of early response genes by TPA and serum growth factors. Tetradecanoylphorbol Acetate 164-167 v-raf-leukemia viral oncogene 1 Mus musculus 17-22 1386920-2 1992 We found that mutant Ras blocks serum- and 12-O-tetradecanoyl phorbol 13-acetate-induced activation of Raf-1 kinase in NIH3T3 cells and Raf-1 as well as B-Raf PSK stimulation by nerve growth factor (NGF) in PC12 pheochromocytoma cells. Tetradecanoylphorbol Acetate 43-80 v-raf-leukemia viral oncogene 1 Mus musculus 103-108 1386920-2 1992 We found that mutant Ras blocks serum- and 12-O-tetradecanoyl phorbol 13-acetate-induced activation of Raf-1 kinase in NIH3T3 cells and Raf-1 as well as B-Raf PSK stimulation by nerve growth factor (NGF) in PC12 pheochromocytoma cells. Tetradecanoylphorbol Acetate 43-80 v-raf-leukemia viral oncogene 1 Mus musculus 136-141 1313769-2 1992 We show by use of Raf-1 dominant-negative mutants that Raf-1 is required for serum-, TPA-, and Ras-induced expression from the oncogene-responsive element in the polyomavirus enhancer. Tetradecanoylphorbol Acetate 85-88 v-raf-leukemia viral oncogene 1 Mus musculus 18-23 1313769-2 1992 We show by use of Raf-1 dominant-negative mutants that Raf-1 is required for serum-, TPA-, and Ras-induced expression from the oncogene-responsive element in the polyomavirus enhancer. Tetradecanoylphorbol Acetate 85-88 v-raf-leukemia viral oncogene 1 Mus musculus 55-60 1313769-4 1992 Raf-C4 appears to function by titrating out a Raf-1-activating factor that is induced by Ras following serum or TPA treatment of NIH-3T3 cells. Tetradecanoylphorbol Acetate 112-115 v-raf-leukemia viral oncogene 1 Mus musculus 46-51 2556385-2 1989 Transfection of the c-raf-1 cDNA or addition of TPA to NIH/3T3 cells stimulated the serum response element and TPA response element but not the cAMP response element. Tetradecanoylphorbol Acetate 111-114 v-raf-leukemia viral oncogene 1 Mus musculus 20-27 2556385-0 1989 Activation of the serum response element and 12-O-tetradecanoylphorbol-13-acetate response element by the activated c-raf-1 protein in a manner independent of protein kinase C. Transfection of the cDNA encoding the activated c-raf-1 protein or addition of 12-O-tetradecanoylphorbol-13-acetate (TPA) or dibutyryl cAMP to NIH/3T3 cells activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene. Tetradecanoylphorbol Acetate 45-81 v-raf-leukemia viral oncogene 1 Mus musculus 116-123 2556385-0 1989 Activation of the serum response element and 12-O-tetradecanoylphorbol-13-acetate response element by the activated c-raf-1 protein in a manner independent of protein kinase C. Transfection of the cDNA encoding the activated c-raf-1 protein or addition of 12-O-tetradecanoylphorbol-13-acetate (TPA) or dibutyryl cAMP to NIH/3T3 cells activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene. Tetradecanoylphorbol Acetate 45-81 v-raf-leukemia viral oncogene 1 Mus musculus 225-232 2556385-0 1989 Activation of the serum response element and 12-O-tetradecanoylphorbol-13-acetate response element by the activated c-raf-1 protein in a manner independent of protein kinase C. Transfection of the cDNA encoding the activated c-raf-1 protein or addition of 12-O-tetradecanoylphorbol-13-acetate (TPA) or dibutyryl cAMP to NIH/3T3 cells activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene. Tetradecanoylphorbol Acetate 256-292 v-raf-leukemia viral oncogene 1 Mus musculus 116-123 2556385-0 1989 Activation of the serum response element and 12-O-tetradecanoylphorbol-13-acetate response element by the activated c-raf-1 protein in a manner independent of protein kinase C. Transfection of the cDNA encoding the activated c-raf-1 protein or addition of 12-O-tetradecanoylphorbol-13-acetate (TPA) or dibutyryl cAMP to NIH/3T3 cells activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene. Tetradecanoylphorbol Acetate 256-292 v-raf-leukemia viral oncogene 1 Mus musculus 225-232 2556385-0 1989 Activation of the serum response element and 12-O-tetradecanoylphorbol-13-acetate response element by the activated c-raf-1 protein in a manner independent of protein kinase C. Transfection of the cDNA encoding the activated c-raf-1 protein or addition of 12-O-tetradecanoylphorbol-13-acetate (TPA) or dibutyryl cAMP to NIH/3T3 cells activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene. Tetradecanoylphorbol Acetate 294-297 v-raf-leukemia viral oncogene 1 Mus musculus 116-123 2556385-0 1989 Activation of the serum response element and 12-O-tetradecanoylphorbol-13-acetate response element by the activated c-raf-1 protein in a manner independent of protein kinase C. Transfection of the cDNA encoding the activated c-raf-1 protein or addition of 12-O-tetradecanoylphorbol-13-acetate (TPA) or dibutyryl cAMP to NIH/3T3 cells activated the c-fos gene enhancer linked to the chloramphenicol acetyltransferase or luciferase reporter gene. Tetradecanoylphorbol Acetate 294-297 v-raf-leukemia viral oncogene 1 Mus musculus 225-232 2556385-4 1989 These results indicate that the activated c-raf-1 protein stimulates the serum response element and TPA response element in a manner independent of protein kinase C and cAMP-dependent protein kinase. Tetradecanoylphorbol Acetate 100-103 v-raf-leukemia viral oncogene 1 Mus musculus 42-49 3057494-6 1988 Transformation by v-src, or treatment with platelet-derived growth factor or phorbol 12-myristate 13-acetate, activated the Raf-1-associated serine/kinase activity as measured in immune-complex kinase assays. Tetradecanoylphorbol Acetate 77-108 v-raf-leukemia viral oncogene 1 Mus musculus 124-129 21400615-4 2011 Western blot analysis revealed that 5"-NIO inhibited activities of Raf-1 (S338), MEK1/2, ERK1/2, JNK, and c-Jun induced by EGF or TPA, respectively, whereas it did not affect autophosphorylation of epidermal growth factor receptor (EGFR) induced by EGF or TPA. Tetradecanoylphorbol Acetate 130-133 v-raf-leukemia viral oncogene 1 Mus musculus 67-72 17350626-8 2007 The phosphorylation of MEK1/2 and Raf-1 induced by ET-1 or TPA were also inhibited by EGCG. Tetradecanoylphorbol Acetate 59-62 v-raf-leukemia viral oncogene 1 Mus musculus 34-39 19688047-6 2008 RESULTS: The pharmacological PKC activator phorbol-12-myristate-13-acetate (PMA) and platelet-derived growth factor (PDGF) were able to induce the activation of Raf-1 kinase in the v-H-ras-transformed NIH3T3 fibroblasts. Tetradecanoylphorbol Acetate 43-74 v-raf-leukemia viral oncogene 1 Mus musculus 161-166 19688047-6 2008 RESULTS: The pharmacological PKC activator phorbol-12-myristate-13-acetate (PMA) and platelet-derived growth factor (PDGF) were able to induce the activation of Raf-1 kinase in the v-H-ras-transformed NIH3T3 fibroblasts. Tetradecanoylphorbol Acetate 76-79 v-raf-leukemia viral oncogene 1 Mus musculus 161-166 21400615-6 2011 Importantly, 5"-NIO inhibited Pin1 phosphorylation at serine 16 induced by EGF or TPA, respectively, resulted in the inhibition of interaction between Pin1 and Raf-1. Tetradecanoylphorbol Acetate 82-85 v-raf-leukemia viral oncogene 1 Mus musculus 160-165 21400615-8 2011 Together, these findings suggest that 5"-NIO might act as an anticarcinogene in EGF- or TPA-induced carcinogenesis through the inhibition of interaction between Pin1 and Raf-1. Tetradecanoylphorbol Acetate 88-91 v-raf-leukemia viral oncogene 1 Mus musculus 170-175 18174170-3 2008 Moreover, NIH3T3 cells expressing the 4 CRUs of Ahnak showed enhanced c-Raf, MEK, and Erk phosphorylation in response to phorbol 12-myristate 13-acetate (PMA) compared with parental cells. Tetradecanoylphorbol Acetate 121-152 v-raf-leukemia viral oncogene 1 Mus musculus 70-75 18174170-3 2008 Moreover, NIH3T3 cells expressing the 4 CRUs of Ahnak showed enhanced c-Raf, MEK, and Erk phosphorylation in response to phorbol 12-myristate 13-acetate (PMA) compared with parental cells. Tetradecanoylphorbol Acetate 154-157 v-raf-leukemia viral oncogene 1 Mus musculus 70-75 16673205-7 2006 Minodronate inhibited Raf-1, MEK1/2 and p44/p42 MAP kinase phosphorylation induced by TPA. Tetradecanoylphorbol Acetate 86-89 v-raf-leukemia viral oncogene 1 Mus musculus 22-27 12646577-17 2003 Incadronate markedly enhanced the phosphorylation of Raf-1, MEK1/2, and p44/p42 MAPK induced by PGF2 alpha or 12-O-tetradecanoylphorbol-13-acetate, a PKC activator. Tetradecanoylphorbol Acetate 110-146 v-raf-leukemia viral oncogene 1 Mus musculus 53-58 15922088-8 2005 The TPA-induced phosphorylations of Raf-1, MEK1/2 and p44/p42 MAP kinase were inhibited by tiludronate. Tetradecanoylphorbol Acetate 4-7 v-raf-leukemia viral oncogene 1 Mus musculus 36-41 15356004-0 2004 Src tyrosine kinase inhibitor PP2 markedly enhances Ras-independent activation of Raf-1 protein kinase by phorbol myristate acetate and H2O2. Tetradecanoylphorbol Acetate 106-131 v-raf-leukemia viral oncogene 1 Mus musculus 82-87 15356004-14 2004 This PP2 effect resulted in significant and sustained Ras-independent activation of Raf-1 by PMA and H2O2. Tetradecanoylphorbol Acetate 93-96 v-raf-leukemia viral oncogene 1 Mus musculus 84-89 14623285-0 2003 The synergistic activation of Raf-1 kinase by phorbol myristate acetate and hydrogen peroxide in NIH3T3 cells. Tetradecanoylphorbol Acetate 46-71 v-raf-leukemia viral oncogene 1 Mus musculus 30-35 14623285-1 2003 We have previously demonstrated that a 33kDa C-terminal fragment of c-Raf-1 underwent a mobility shift in response to hydrogen peroxide (H(2)O(2)) and phorbol myristate acetate (PMA), respectively. Tetradecanoylphorbol Acetate 151-176 v-raf-leukemia viral oncogene 1 Mus musculus 68-73 14623285-1 2003 We have previously demonstrated that a 33kDa C-terminal fragment of c-Raf-1 underwent a mobility shift in response to hydrogen peroxide (H(2)O(2)) and phorbol myristate acetate (PMA), respectively. Tetradecanoylphorbol Acetate 178-181 v-raf-leukemia viral oncogene 1 Mus musculus 68-73 14623285-4 2003 Interestingly, H(2)O(2) produced synergistic increase of PMA-stimulated Raf-1 kinase activation after simultaneous treatment of PMA and H(2)O(2). Tetradecanoylphorbol Acetate 57-60 v-raf-leukemia viral oncogene 1 Mus musculus 72-77 14623285-4 2003 Interestingly, H(2)O(2) produced synergistic increase of PMA-stimulated Raf-1 kinase activation after simultaneous treatment of PMA and H(2)O(2). Tetradecanoylphorbol Acetate 128-131 v-raf-leukemia viral oncogene 1 Mus musculus 72-77 14623285-6 2003 Taken together, our data suggest that the synergistic activation of Raf-1 kinase in response to PMA and H(2)O(2) occurs via mechanisms that involve an interaction of Raf-1 kinase and PKC-epsilon, along with a transient phosphorylation of both Raf-1 kinase and PKC. Tetradecanoylphorbol Acetate 96-99 v-raf-leukemia viral oncogene 1 Mus musculus 68-73 14623285-6 2003 Taken together, our data suggest that the synergistic activation of Raf-1 kinase in response to PMA and H(2)O(2) occurs via mechanisms that involve an interaction of Raf-1 kinase and PKC-epsilon, along with a transient phosphorylation of both Raf-1 kinase and PKC. Tetradecanoylphorbol Acetate 96-99 v-raf-leukemia viral oncogene 1 Mus musculus 166-171 14623285-6 2003 Taken together, our data suggest that the synergistic activation of Raf-1 kinase in response to PMA and H(2)O(2) occurs via mechanisms that involve an interaction of Raf-1 kinase and PKC-epsilon, along with a transient phosphorylation of both Raf-1 kinase and PKC. Tetradecanoylphorbol Acetate 96-99 v-raf-leukemia viral oncogene 1 Mus musculus 166-171 12134072-3 2002 In normal NIH 3T3 cells, (Raf-1[51-220]GFP) showed minimal membrane localization that was enhanced after stimulation with platelet-derived growth factor or phorbol-12-myristate-13-acetate. Tetradecanoylphorbol Acetate 156-187 v-raf-leukemia viral oncogene 1 Mus musculus 26-31