PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15634742-6 2005 In contrast, pretreatment of monolayers with a PKC inhibitor (bisindolylmaleimide I; GF109203x; 1 microM) almost completely blocked the PMA-induced decrease in I(sc), but did not alter the EGF- or ATP-induced inhibition of I(sc). Tetradecanoylphorbol Acetate 136-139 epidermal growth factor Mus musculus 189-192 14573593-5 2004 Similarly, blockade of the effect of HB-EGF with the selective inhibitor CRM197 or a neutralizing antibody attenuated signals generated by GnRH and phorbol 12-myristate 13-acetate, but not those stimulated by EGF. Tetradecanoylphorbol Acetate 148-179 epidermal growth factor Mus musculus 40-43 8635491-2 1996 Chronic treatment with low doses (0.1-0.5 nM) of phorbol 12-myristate 13-acetate (PMA) had no mitogenic action when given alone, but significantly enhanced epidermal growth factor (EGF)-induced growth. Tetradecanoylphorbol Acetate 49-80 epidermal growth factor Mus musculus 156-179 11375402-7 2001 In contrast, insertion of both the EGF domain and the MPR confers susceptibility to both slow constitutive shedding and the rapid proteolytic cleavage induced by phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 162-193 epidermal growth factor Mus musculus 35-38 9496939-6 1998 Pretreatment of cells with phorbol 12-myristate 13-acetate, known to down-regulate protein kinase C expression, blocked EGF-induced cell migration. Tetradecanoylphorbol Acetate 27-58 epidermal growth factor Mus musculus 120-123 9586065-2 1997 EGF increased the binding activity in nuclear extracts of MC3T3-E1 cells to TPA-responsive element (TRE). Tetradecanoylphorbol Acetate 76-79 epidermal growth factor Mus musculus 0-3 8842529-5 1996 The release of [14C]-dihomo-gamma-linolenic acid (DHGLA), predominately bound to the 2-positions of phospholipids, was also stimulated by 8 h of TPA treatment but not by 24 h of EGF treatment. Tetradecanoylphorbol Acetate 145-148 epidermal growth factor Mus musculus 178-181 12654926-5 2003 TPA or IL-1alpha treatment resulted in rapid down-regulation of the EGF receptor in transgenic cells, indicative of transactivation. Tetradecanoylphorbol Acetate 0-3 epidermal growth factor Mus musculus 68-71 10365914-7 1999 Analysis of the IGF-1 receptor (IGF-1r) and epidermal growth factor (EGFr) in the epidermis of TPA-treated HK1.IGF-1 transgenic and non-transgenic mice revealed that both receptors were activated (hyperphosphorylated on tyrosine residues), and the level of activation was higher in transgenic mice. Tetradecanoylphorbol Acetate 95-98 epidermal growth factor Mus musculus 69-73 8635491-2 1996 Chronic treatment with low doses (0.1-0.5 nM) of phorbol 12-myristate 13-acetate (PMA) had no mitogenic action when given alone, but significantly enhanced epidermal growth factor (EGF)-induced growth. Tetradecanoylphorbol Acetate 49-80 epidermal growth factor Mus musculus 181-184 8635491-2 1996 Chronic treatment with low doses (0.1-0.5 nM) of phorbol 12-myristate 13-acetate (PMA) had no mitogenic action when given alone, but significantly enhanced epidermal growth factor (EGF)-induced growth. Tetradecanoylphorbol Acetate 82-85 epidermal growth factor Mus musculus 156-179 8635491-2 1996 Chronic treatment with low doses (0.1-0.5 nM) of phorbol 12-myristate 13-acetate (PMA) had no mitogenic action when given alone, but significantly enhanced epidermal growth factor (EGF)-induced growth. Tetradecanoylphorbol Acetate 82-85 epidermal growth factor Mus musculus 181-184 8635491-6 1996 Acute treatment with 10 ng/ml EGF or 20 nM PMA stimulated phospholipid-dependent PKC translocation from the cytosolic to the membrane fraction, and this effect was blocked by prior treatment for 7 days with 20 nM PMA. Tetradecanoylphorbol Acetate 213-216 epidermal growth factor Mus musculus 30-33 8635491-8 1996 Additional studies showed that treatment with 1-2 nM PMA caused an increase, whereas treatment with 5-100 nM PMA caused a dose-related decrease in EGF-dependent EGF-receptor (EGF-R) autophosphorylation, In summary, these findings suggest that submitogenic doses of PMA potentiate EGF-induced cell growth by enhancing EGF-R mitogenic signaling, whereas the mitogenic effects of high doses of PMA alone appear to be mediated through PKC- and EGF-independent mechanisms. Tetradecanoylphorbol Acetate 53-56 epidermal growth factor Mus musculus 147-150 8635491-8 1996 Additional studies showed that treatment with 1-2 nM PMA caused an increase, whereas treatment with 5-100 nM PMA caused a dose-related decrease in EGF-dependent EGF-receptor (EGF-R) autophosphorylation, In summary, these findings suggest that submitogenic doses of PMA potentiate EGF-induced cell growth by enhancing EGF-R mitogenic signaling, whereas the mitogenic effects of high doses of PMA alone appear to be mediated through PKC- and EGF-independent mechanisms. Tetradecanoylphorbol Acetate 53-56 epidermal growth factor Mus musculus 161-164 8635491-8 1996 Additional studies showed that treatment with 1-2 nM PMA caused an increase, whereas treatment with 5-100 nM PMA caused a dose-related decrease in EGF-dependent EGF-receptor (EGF-R) autophosphorylation, In summary, these findings suggest that submitogenic doses of PMA potentiate EGF-induced cell growth by enhancing EGF-R mitogenic signaling, whereas the mitogenic effects of high doses of PMA alone appear to be mediated through PKC- and EGF-independent mechanisms. Tetradecanoylphorbol Acetate 53-56 epidermal growth factor Mus musculus 431-443 2401043-5 1990 In contrast, TPA caused a rapid inhibition of EGF binding, primarily due to a loss of high-affinity receptors. Tetradecanoylphorbol Acetate 13-16 epidermal growth factor Mus musculus 46-49 7876145-5 1995 Down-regulation of PKC by prolonged treatment with 4 beta-phorbol 12-myristate 13-acetate also abolished EGF- and PDGF-stimulated phosphatidylbutanol formation. Tetradecanoylphorbol Acetate 51-89 epidermal growth factor Mus musculus 105-108 8038217-5 1994 Phorbol-myristate acetate (PMA) inhibited EGF-dependent protein tyrosine phosphorylation, and when compared to melittin or calcium ionophore A23187, only PMA potentiated the EGF-induced tyrosine phosphorylation of two proteins immunologically related to mitogen activated protein (MAP) kinases of 40 kDa and 44 kDa molecular mass. Tetradecanoylphorbol Acetate 0-25 epidermal growth factor Mus musculus 42-45 8038217-5 1994 Phorbol-myristate acetate (PMA) inhibited EGF-dependent protein tyrosine phosphorylation, and when compared to melittin or calcium ionophore A23187, only PMA potentiated the EGF-induced tyrosine phosphorylation of two proteins immunologically related to mitogen activated protein (MAP) kinases of 40 kDa and 44 kDa molecular mass. Tetradecanoylphorbol Acetate 0-25 epidermal growth factor Mus musculus 174-177 8038217-5 1994 Phorbol-myristate acetate (PMA) inhibited EGF-dependent protein tyrosine phosphorylation, and when compared to melittin or calcium ionophore A23187, only PMA potentiated the EGF-induced tyrosine phosphorylation of two proteins immunologically related to mitogen activated protein (MAP) kinases of 40 kDa and 44 kDa molecular mass. Tetradecanoylphorbol Acetate 27-30 epidermal growth factor Mus musculus 42-45 8038217-5 1994 Phorbol-myristate acetate (PMA) inhibited EGF-dependent protein tyrosine phosphorylation, and when compared to melittin or calcium ionophore A23187, only PMA potentiated the EGF-induced tyrosine phosphorylation of two proteins immunologically related to mitogen activated protein (MAP) kinases of 40 kDa and 44 kDa molecular mass. Tetradecanoylphorbol Acetate 154-157 epidermal growth factor Mus musculus 174-177 8246947-7 1993 In contrast, in Swiss 3T3 cells, inhibition of both p21ras activation and TPA-sensitive PKC, but not calcium influx, inhibited EGF-induced ERK2 phosphorylation. Tetradecanoylphorbol Acetate 74-77 epidermal growth factor Mus musculus 127-130 8581878-4 1995 Inhibition of protein kinase C activity by pretreatment with 1 microM chelerythrine chloride or by prolonged stimulation with 50 ng/ml tetradecanoyl phorbol acetate (TPA) partially diminished the induction of Egr-1 by EGF. Tetradecanoylphorbol Acetate 135-164 epidermal growth factor Mus musculus 218-221 8581878-4 1995 Inhibition of protein kinase C activity by pretreatment with 1 microM chelerythrine chloride or by prolonged stimulation with 50 ng/ml tetradecanoyl phorbol acetate (TPA) partially diminished the induction of Egr-1 by EGF. Tetradecanoylphorbol Acetate 166-169 epidermal growth factor Mus musculus 218-221 7744871-8 1995 The results indicate that the specific binding of ATF3/Jun and a previously uncharacterized factor account for signal-specific transcription in response to EGF or an activated Ha-ras gene in a cell type in which the cooperative action of an activated Ha-ras gene and 12-O-tetradecanoylphorbol-13-acetate cause tumor growth. Tetradecanoylphorbol Acetate 267-303 epidermal growth factor Mus musculus 156-159 8314805-2 1993 We report here that expression directed by a junB promoter/chloramphenicol acetyltransferase reporter construct (junB/CAT) is induced by fetal bovine serum, 12-O-tetradecanoylphorbol-13-acetate (TPA), epidermal growth factor (EGF), platelet-derived growth factor, and fibroblast growth factor in mouse fibroblast 3T6 cells. Tetradecanoylphorbol Acetate 195-198 epidermal growth factor Mus musculus 226-229 1554749-2 1992 While phorbol esters such as phorbol 12-myristate 13-acetate (PMA) are thought to induce the transcription of these genes by activating protein kinase C (PKC), the signal transduction pathway(s) mediating the effects of EGF and serum are still unclear. Tetradecanoylphorbol Acetate 62-65 epidermal growth factor Mus musculus 220-223 1803346-7 1991 In EGF-treated cells, staurosporine and TPA, but not H-7, decreased DNA synthesis. Tetradecanoylphorbol Acetate 40-43 epidermal growth factor Mus musculus 3-6 2401043-6 1990 The mechanism by which chrysarobin inhibited the binding of EGF to its receptor involved neither direct activation nor membrane translocation of epidermal protein kinase C, whereas the rapid decrease in EGF binding induced by TPA was consistent with its ability to activate protein kinase C. Structure-activity relationships for EGF binding inhibition by anthrones revealed that inhibition was inversely proportional to chain length at the C10-position, which correlated closely with oxidation rate and skin tumor-promoting activity. Tetradecanoylphorbol Acetate 226-229 epidermal growth factor Mus musculus 203-206 2401043-6 1990 The mechanism by which chrysarobin inhibited the binding of EGF to its receptor involved neither direct activation nor membrane translocation of epidermal protein kinase C, whereas the rapid decrease in EGF binding induced by TPA was consistent with its ability to activate protein kinase C. Structure-activity relationships for EGF binding inhibition by anthrones revealed that inhibition was inversely proportional to chain length at the C10-position, which correlated closely with oxidation rate and skin tumor-promoting activity. Tetradecanoylphorbol Acetate 226-229 epidermal growth factor Mus musculus 203-206 2298725-2 1990 Treatment with the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) also results in the transmodulation of the EGF receptor in many cell types. Tetradecanoylphorbol Acetate 35-71 epidermal growth factor Mus musculus 121-124 2298725-2 1990 Treatment with the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) also results in the transmodulation of the EGF receptor in many cell types. Tetradecanoylphorbol Acetate 73-76 epidermal growth factor Mus musculus 121-124 2298725-6 1990 264, 213-219) described the requirement for a sodium ion influx in the down-modulation of the EGF receptor stimulated by a non-TPA-type tumor promoter, palytoxin, in Swiss 3T3 cells. Tetradecanoylphorbol Acetate 127-130 epidermal growth factor Mus musculus 94-97 2298725-8 1990 Our results clearly show that the PDGF- and TPA-stimulated transmodulation of the EGF receptor does not require external sodium nor is the process affected by amiloride. Tetradecanoylphorbol Acetate 44-47 epidermal growth factor Mus musculus 82-85 2106323-4 1990 Treatment of cell cultures with phenobarbital or 3,4,3",4"-tetrachlorobiphenyl (enzyme inducers and tumor promoters in vivo) or with 12-O-tetradecanoylphorbol-13-acetate (the classical skin tumor promoter) further increased EGF-stimulated DNA synthesis. Tetradecanoylphorbol Acetate 133-169 epidermal growth factor Mus musculus 224-227 6419742-3 1983 Similarly, the stimulation of 2DG uptake by a tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) was prevented by EGTA, whereas the epidermal growth factor (EGF)-stimulated 2DG uptake was not affected by EGTA alone, but in the presence of both EGTA and A23187 which effectively depleted cellular Ca2+ content, EGF could no longer stimulate 2DG uptake. Tetradecanoylphorbol Acetate 61-97 epidermal growth factor Mus musculus 164-167 3136317-2 1988 Moreover, TPA-induced kinase C phosphorylation occurs mainly on Thr-654 of the EGF receptor, suggesting that the phosphorylation state of this residue regulates ligand-binding affinity and kinase activity of the EGF receptor. Tetradecanoylphorbol Acetate 10-13 epidermal growth factor Mus musculus 79-82 3136317-2 1988 Moreover, TPA-induced kinase C phosphorylation occurs mainly on Thr-654 of the EGF receptor, suggesting that the phosphorylation state of this residue regulates ligand-binding affinity and kinase activity of the EGF receptor. Tetradecanoylphorbol Acetate 10-13 epidermal growth factor Mus musculus 212-215 3136317-6 1988 The addition of TPA to NIH 3T3 cells expressing a wild-type human EGF receptor blocked the mitogenic capacity of EGF. Tetradecanoylphorbol Acetate 16-19 epidermal growth factor Mus musculus 66-69 3136317-8 1988 In the latter cells, EGF was able to stimulate DNA synthesis even in the presence of inhibitory concentrations of TPA. Tetradecanoylphorbol Acetate 114-117 epidermal growth factor Mus musculus 21-24 2601687-1 1989 12-O-tetradecanoylphorbol-13-acetate (TPA) induced ornithine decarboxylase (ODC) and suppressed 125I-epidermal growth factor (EGF) binding in primary cultured mouse epidermal cells. Tetradecanoylphorbol Acetate 0-36 epidermal growth factor Mus musculus 96-124 2601687-1 1989 12-O-tetradecanoylphorbol-13-acetate (TPA) induced ornithine decarboxylase (ODC) and suppressed 125I-epidermal growth factor (EGF) binding in primary cultured mouse epidermal cells. Tetradecanoylphorbol Acetate 0-36 epidermal growth factor Mus musculus 126-129 2601687-1 1989 12-O-tetradecanoylphorbol-13-acetate (TPA) induced ornithine decarboxylase (ODC) and suppressed 125I-epidermal growth factor (EGF) binding in primary cultured mouse epidermal cells. Tetradecanoylphorbol Acetate 38-41 epidermal growth factor Mus musculus 96-124 2601687-1 1989 12-O-tetradecanoylphorbol-13-acetate (TPA) induced ornithine decarboxylase (ODC) and suppressed 125I-epidermal growth factor (EGF) binding in primary cultured mouse epidermal cells. Tetradecanoylphorbol Acetate 38-41 epidermal growth factor Mus musculus 126-129 2601687-2 1989 TPA (30 nM)-caused ODC induction was almost completely blocked by 30 microM H-7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine], a well known protein kinase C inhibitor, but the same concentration of H-7 failed to restore the 125I-EGF binding suppressed by TPA (10 nM). Tetradecanoylphorbol Acetate 0-3 epidermal growth factor Mus musculus 232-235 2601687-3 1989 On the other hand, sphingosine, another protein kinase C inhibitor, blocked not only TPA-caused ODC induction but also TPA-caused suppression of 125I-EGF binding. Tetradecanoylphorbol Acetate 119-122 epidermal growth factor Mus musculus 150-153 2481744-8 1989 In contrast, 12-O-tetradencanoylphorbol-13-acetate (TPA), which is known to downregulate EGF receptors by blocking their protein tyrosine kinase, produced dissimilar end results. Tetradecanoylphorbol Acetate 52-55 epidermal growth factor Mus musculus 89-92 2613862-4 1989 EGF also stimulated phosphorylation of an Mr 80,000 protein whose pI, phosphopeptide map, and phosphoamino acid pattern were identical to those of an Mr 80,000 protein phosphorylated in response to phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 198-229 epidermal growth factor Mus musculus 0-3 3264402-7 1988 Similar to its effect on wild-type receptors, phorbol 12-myristate 13-acetate abolished the mutant-receptor high-affinity binding sites for EGF. Tetradecanoylphorbol Acetate 46-77 epidermal growth factor Mus musculus 140-143 6419742-3 1983 Similarly, the stimulation of 2DG uptake by a tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) was prevented by EGTA, whereas the epidermal growth factor (EGF)-stimulated 2DG uptake was not affected by EGTA alone, but in the presence of both EGTA and A23187 which effectively depleted cellular Ca2+ content, EGF could no longer stimulate 2DG uptake. Tetradecanoylphorbol Acetate 99-102 epidermal growth factor Mus musculus 317-320 6300862-0 1983 Tumor promoter 12-O-tetradecanoylphorbol 13-acetate, like epidermal growth factor, stimulates cell proliferation and inhibits differentiation of mouse mammary epithelial cells in culture. Tetradecanoylphorbol Acetate 15-51 epidermal growth factor Mus musculus 58-81 6302699-6 1983 A potent tumor promoter, 12-O-tetradecanoylphorbol 13-acetate, acted synergistically with EGF in terms of stimulation of DNA synthesis but not in terms of inhibition of casein synthesis when the two agents were added at a suboptimal concentration. Tetradecanoylphorbol Acetate 25-61 epidermal growth factor Mus musculus 90-93 6300862-1 1983 12-O-Tetradecanoylphorbol 13-acetate (TPA) is a potent tumor promoter and shares several biological activities of epidermal growth factor (EGF). Tetradecanoylphorbol Acetate 0-36 epidermal growth factor Mus musculus 114-137 6300862-1 1983 12-O-Tetradecanoylphorbol 13-acetate (TPA) is a potent tumor promoter and shares several biological activities of epidermal growth factor (EGF). Tetradecanoylphorbol Acetate 38-41 epidermal growth factor Mus musculus 114-137 6284358-0 1982 Phorbol diester and epidermal growth factor receptors in 12-O-tetradecanoylphorbol-13-acetate-resistant and -sensitive mouse epidermal cells. Tetradecanoylphorbol Acetate 57-93 epidermal growth factor Mus musculus 20-43 6288114-0 1982 Effect of retinoic acid and 12-O-tetradecanoyl phorbol-13-acetate on the binding of epidermal growth factor to its cellular receptors. Tetradecanoylphorbol Acetate 28-65 epidermal growth factor Mus musculus 84-107 6288114-5 1982 TPA inhibited binding of EGF to the cells by abolishing the binding to the high affinity sites, whereas retinoic acid, in the presence of TPA, enhanced it by increasing the number of the low affinity sites. Tetradecanoylphorbol Acetate 0-3 epidermal growth factor Mus musculus 25-28 6284358-7 1982 Lack of EGF receptors may account for TPA mitogen resistance in at least three of four resistant variants. Tetradecanoylphorbol Acetate 38-41 epidermal growth factor Mus musculus 8-11 6284358-8 1982 The TPA-induced EGF binding decrease occurs in both sensitive and resistant variants. Tetradecanoylphorbol Acetate 4-7 epidermal growth factor Mus musculus 16-19 16068160-1 1979 TPA (12-O-tetradecanoyl-phorbol-13-acetate) reversibly inhibits the binding of (125)I-labelled epidermal growth factor (EGF) to treated mouse and human cells, but does not affect the binding of various other ligands to their membrane receptors. Tetradecanoylphorbol Acetate 0-3 epidermal growth factor Mus musculus 95-118 16068160-1 1979 TPA (12-O-tetradecanoyl-phorbol-13-acetate) reversibly inhibits the binding of (125)I-labelled epidermal growth factor (EGF) to treated mouse and human cells, but does not affect the binding of various other ligands to their membrane receptors. Tetradecanoylphorbol Acetate 5-42 epidermal growth factor Mus musculus 120-123 16068160-1 1979 TPA (12-O-tetradecanoyl-phorbol-13-acetate) reversibly inhibits the binding of (125)I-labelled epidermal growth factor (EGF) to treated mouse and human cells, but does not affect the binding of various other ligands to their membrane receptors. Tetradecanoylphorbol Acetate 0-3 epidermal growth factor Mus musculus 120-123 16068160-1 1979 TPA (12-O-tetradecanoyl-phorbol-13-acetate) reversibly inhibits the binding of (125)I-labelled epidermal growth factor (EGF) to treated mouse and human cells, but does not affect the binding of various other ligands to their membrane receptors. Tetradecanoylphorbol Acetate 5-42 epidermal growth factor Mus musculus 95-118 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 epidermal growth factor Mus musculus 232-235 30219864-6 2019 Nonetheless, overexpression of WT-SMAD7 caused a susceptibility to 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperproliferation through activation of epidermal growth factor (EGF) signaling. Tetradecanoylphorbol Acetate 67-103 epidermal growth factor Mus musculus 163-186 30219864-6 2019 Nonetheless, overexpression of WT-SMAD7 caused a susceptibility to 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperproliferation through activation of epidermal growth factor (EGF) signaling. Tetradecanoylphorbol Acetate 67-103 epidermal growth factor Mus musculus 188-191 21400615-5 2011 In addition, 5"-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Tetradecanoylphorbol Acetate 69-72 epidermal growth factor Mus musculus 222-225 21400615-5 2011 In addition, 5"-NIO exerted strong inhibitory effects on the EGF- or TPA-induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA. Tetradecanoylphorbol Acetate 229-232 epidermal growth factor Mus musculus 61-64 18838072-6 2008 By comparing effects of signalling inhibitors (wortmannin, SH-6, TPA, Go6983, PP2, PD98059) on EGF- and PDGF-induced Erk1/2 activation and cell proliferation (3H-thymidine incorporation), we conclude that while the signal transduction pathways initiated by these growth factors are clearly markedly different, their effects on cell proliferation can be fully explained through their stimulation of Erk1/2 activation; thus Erk1/2 is a common, essential step for stimulation of proliferation in these cells. Tetradecanoylphorbol Acetate 65-68 epidermal growth factor Mus musculus 95-98