PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2473287-3 1989 The mRNA for ppET-1 was rapidly upregulated by O-tetradecanoylphorbol-13-acetate (TPA) (0.5 microM) and by ionomycin (5 microM) within 10 min of addition to the medium, but not by forskolin (50 microM). Tetradecanoylphorbol Acetate 82-85 endothelin 1 Homo sapiens 13-19 2670930-7 1989 Northern blot analysis in cultured endothelial cells from human umbilical veins shows that PPET-1 mRNA is in fact rapidly induced by the active phorbol ester 12-O-tetradecanoylphorbol 13-acetate within 10 min. Tetradecanoylphorbol Acetate 158-194 endothelin 1 Homo sapiens 91-97 2473287-4 1989 The rapid induction of ppET-1 mRNA by TPA or ionomycin occurred even in the presence of cycloheximide, indicating that the mRNA induction does not require de novo protein synthesis. Tetradecanoylphorbol Acetate 38-41 endothelin 1 Homo sapiens 23-29 9533826-6 1998 Phorbol esters (PMA), activators of PKC, also raised the immunoreactive levels of ET-1 and Big ET-1 while, staurosporine, a PKC inhibitor (20 nm), decreased ET-1 levels in TNF-alpha-stimulated cells. Tetradecanoylphorbol Acetate 16-19 endothelin 1 Homo sapiens 82-99 18257749-5 2008 In cells treated with NA or phorbol myristate acetate the amount of coimmunoprecipitated GRK2 and GRK3 increased ( approximately 2- to 3-fold), while treatment with ET-1 only augmented the amount of coimmunoprecipitated GRK2 ( approximately 2-fold). Tetradecanoylphorbol Acetate 28-53 endothelin 1 Homo sapiens 165-169 15115660-11 2004 The synergistic action of ET-1 with 8-bromo cAMP to enhance glucose transport was inhibited by GF109203X, a selective protein kinase C (PKC) inhibitor, and was mimicked by 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA), a PKC activator. Tetradecanoylphorbol Acetate 220-223 endothelin 1 Homo sapiens 26-30 9870082-4 1998 In another set of experiments cells were treated with ET-1 and BQ485, an ET-A receptor antagonist, or with phorbol 12-myristate-13 acetate (PMA), an activator of protein kinase C. RESULTS: ET-1 reduced both basal and human chorionic gonadotropin-induced progesterone production at all examined times, similarly PMA inhibited basal progesterone synthesis. Tetradecanoylphorbol Acetate 107-138 endothelin 1 Homo sapiens 189-193 9683456-6 1998 The phorbol ester phorbol 12-myristate 13-acetate (PMA) inhibited ET-1 production. Tetradecanoylphorbol Acetate 18-49 endothelin 1 Homo sapiens 66-70 9683456-6 1998 The phorbol ester phorbol 12-myristate 13-acetate (PMA) inhibited ET-1 production. Tetradecanoylphorbol Acetate 51-54 endothelin 1 Homo sapiens 66-70 9683456-7 1998 Downregulation of protein kinase C (PKC) with PMA (1 microM) preincubation potentiated OSM-induced ET-1 production. Tetradecanoylphorbol Acetate 46-49 endothelin 1 Homo sapiens 99-103 23657563-8 2013 To ascertain the role of NF-kappaB activation in the altered expression of ET-1 and eNOS, we treated HUVECs with phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 113-144 endothelin 1 Homo sapiens 75-88 23657563-8 2013 To ascertain the role of NF-kappaB activation in the altered expression of ET-1 and eNOS, we treated HUVECs with phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 146-149 endothelin 1 Homo sapiens 75-88 19302552-9 2009 Association of phospho-ERK 1/2 to alpha(1B)-adrenoceptors increased not only in response to agonist but also in response to agents that increase alpha(1B)-adrenoceptor and ERK1/2 phosphorylation [such as endothelin-1, phorbol 12-myristate-13-acetate (PMA) and epidermal growth factor (EGF)]; not surprisingly, PD98059 decreased this effect. Tetradecanoylphorbol Acetate 218-249 endothelin 1 Homo sapiens 204-216 9806262-7 1998 Luteal cells were then incubated for 24 h with phorbol 12-myristate-13 acetate (PMA) (100 ng/ml), an activator of protein kinase C. Inhibition of progesterone synthesis by PMA was similar to that induced by ET-1 alone. Tetradecanoylphorbol Acetate 80-83 endothelin 1 Homo sapiens 207-211 9533826-6 1998 Phorbol esters (PMA), activators of PKC, also raised the immunoreactive levels of ET-1 and Big ET-1 while, staurosporine, a PKC inhibitor (20 nm), decreased ET-1 levels in TNF-alpha-stimulated cells. Tetradecanoylphorbol Acetate 16-19 endothelin 1 Homo sapiens 82-86 8643084-3 1996 Both the inhibition of intracellular Ca2+ response by phospholipase C inhibitor U73122 and the down-regulation of protein kinase C (PKC) by pretreatment with phorbol 12-myristate-13-acetate (PMA) partially blocked the ET-1-induced mitogenic responses. Tetradecanoylphorbol Acetate 158-189 endothelin 1 Homo sapiens 218-222 9089652-6 1997 Activation of PKC by 2-O-tetradecanoyl phorbol 13-acetate (TPA) also stimulated ET-1 secretion in MCF-7 cells. Tetradecanoylphorbol Acetate 59-62 endothelin 1 Homo sapiens 80-84 8764613-6 1996 Staurosporine, a protein kinase C (PKC) inhibitor, had no effect on Et-1-induced AA release but abolished that by phorbol 12-myristate 13-acetate, demonstrating that the Et-1 response was PKC independent. Tetradecanoylphorbol Acetate 114-145 endothelin 1 Homo sapiens 170-174 8643084-4 1996 Wortmannin, a phosphatidylinositol-3-kinase inhibitor, caused dose-dependent inhibition of the ET-1-induced mitogenic responses in both PMA-treated and -untreated cells. Tetradecanoylphorbol Acetate 136-139 endothelin 1 Homo sapiens 95-99 8745210-12 1996 In addition, the protein kinase C activator, phorbol 12-myristate 13-acetate, stimulated exchanger activity by 32%, raising the possibility that all three Gq agonists mediate their actions in part through the promotion of phospholipase C activity and the subsequent activation of protein kinase C. The contribution of Na+/Ca2+ exchange to the actions of phenylephrine, angiotensin II, and endothelin 1 is discussed. Tetradecanoylphorbol Acetate 45-76 endothelin 1 Homo sapiens 389-401 7498555-3 1995 Basal and phorbol ester (PMA)-stimulated ET-1 secretion were unaffected by ODQ, but stimulated secretion was increased by L-NNA. Tetradecanoylphorbol Acetate 25-28 endothelin 1 Homo sapiens 41-45 8632715-8 1996 Overnight pretreatment of the cardiac myocytes with 100 ng/ml pertussis toxin inhibited the ET-1 stimulated increase in MAPK activity by 50 - 70%, but did not alter stimulation by 100 nM phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 220-223 endothelin 1 Homo sapiens 92-96 8825394-7 1996 PMA-stimulated production of O2- increased when cells were preincubated with several doses of ET-1 (5 x 10(-13) to 2 x 10(-12) M), whereas ET-3 was without effect. Tetradecanoylphorbol Acetate 0-3 endothelin 1 Homo sapiens 94-98 7598740-9 1995 The PKC activator phorbol 12-myristate 13-acetate (0.4 microM) stimulated ET-1 release 1.4-fold (P < 0.01) and its effect was abolished by EGTA (5 mM). Tetradecanoylphorbol Acetate 18-49 endothelin 1 Homo sapiens 74-78 7810625-5 1994 The protein kinase C agonist phorbol 12-myristate 13-acetate (PMA) stimulated basal renin release and potentiated the effect of ET-1 on renin release. Tetradecanoylphorbol Acetate 29-60 endothelin 1 Homo sapiens 128-132 7810625-5 1994 The protein kinase C agonist phorbol 12-myristate 13-acetate (PMA) stimulated basal renin release and potentiated the effect of ET-1 on renin release. Tetradecanoylphorbol Acetate 62-65 endothelin 1 Homo sapiens 128-132 7810625-6 1994 However, PMA inhibited basal PRL release and also enhanced the inhibitory effect of ET-1. Tetradecanoylphorbol Acetate 9-12 endothelin 1 Homo sapiens 84-88 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 46-49 endothelin 1 Homo sapiens 18-22 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 endothelin 1 Homo sapiens 126-132 8257866-5 1993 The amount of immunoreactive (ir)-ET-1 secreted from the cells was also increased by TPA and was decreased by TSH. Tetradecanoylphorbol Acetate 85-88 endothelin 1 Homo sapiens 34-38 8347169-2 1993 The thrombin-induced expression of PPET-1 mRNA was markedly inhibited by calphostin C, a specific inhibitor of protein kinase C, and phorbol 12-myristate 13-acetate (TPA) induced the expression of PPET-1 mRNA dose-dependently, but 4 alpha-phorbol 12, 13-didecanoate, an inactive enantiomer of phorbol ester, had no effect on the expression of PPET-1 mRNA. Tetradecanoylphorbol Acetate 133-164 endothelin 1 Homo sapiens 35-41 8347169-2 1993 The thrombin-induced expression of PPET-1 mRNA was markedly inhibited by calphostin C, a specific inhibitor of protein kinase C, and phorbol 12-myristate 13-acetate (TPA) induced the expression of PPET-1 mRNA dose-dependently, but 4 alpha-phorbol 12, 13-didecanoate, an inactive enantiomer of phorbol ester, had no effect on the expression of PPET-1 mRNA. Tetradecanoylphorbol Acetate 133-164 endothelin 1 Homo sapiens 197-203 8347169-2 1993 The thrombin-induced expression of PPET-1 mRNA was markedly inhibited by calphostin C, a specific inhibitor of protein kinase C, and phorbol 12-myristate 13-acetate (TPA) induced the expression of PPET-1 mRNA dose-dependently, but 4 alpha-phorbol 12, 13-didecanoate, an inactive enantiomer of phorbol ester, had no effect on the expression of PPET-1 mRNA. Tetradecanoylphorbol Acetate 133-164 endothelin 1 Homo sapiens 197-203 1430083-4 1992 Phorbol myristate acetate, a protein kinase C activator, dose-dependently increased the release of ET-1-LI from the decidual cells, while a protein kinase C inhibitor, H7, significantly attenuated the stimulatory effect of phorbol myristate acetate on ET-1-LI release. Tetradecanoylphorbol Acetate 0-25 endothelin 1 Homo sapiens 99-103 1430083-4 1992 Phorbol myristate acetate, a protein kinase C activator, dose-dependently increased the release of ET-1-LI from the decidual cells, while a protein kinase C inhibitor, H7, significantly attenuated the stimulatory effect of phorbol myristate acetate on ET-1-LI release. Tetradecanoylphorbol Acetate 0-25 endothelin 1 Homo sapiens 252-267 1430083-4 1992 Phorbol myristate acetate, a protein kinase C activator, dose-dependently increased the release of ET-1-LI from the decidual cells, while a protein kinase C inhibitor, H7, significantly attenuated the stimulatory effect of phorbol myristate acetate on ET-1-LI release. Tetradecanoylphorbol Acetate 223-248 endothelin 1 Homo sapiens 99-103 1430083-4 1992 Phorbol myristate acetate, a protein kinase C activator, dose-dependently increased the release of ET-1-LI from the decidual cells, while a protein kinase C inhibitor, H7, significantly attenuated the stimulatory effect of phorbol myristate acetate on ET-1-LI release. Tetradecanoylphorbol Acetate 223-248 endothelin 1 Homo sapiens 252-267 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 18-22 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 137-141 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 137-141 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 18-22 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 137-141 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 137-141 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 18-22 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 137-141 1446649-3 1992 The release of IR-ET-1 from control cells (no TPA) increased according to time for up to 72 h. In the presence of TPA, the release of IR-ET-1 from the cells was higher than the control level for up to 8 h, but was lower thereafter and reached a plateau after 48 h. TPA dose-dependently stimulated IR-ET-1 release during incubation for 4 h, but suppressed it after incubation for 72 h. Stimulation of PKC by diacylglycerol mimicked the early (4 h) action of TPA. Tetradecanoylphorbol Acetate 114-117 endothelin 1 Homo sapiens 137-141 1446649-4 1992 On the other hand, pretreatment of cells with TPA to downregulate PKC significantly suppressed basal and thrombin- or FCS-stimulated IR-ET-1 release. Tetradecanoylphorbol Acetate 46-49 endothelin 1 Homo sapiens 136-140 1865754-3 1991 In addition, a tumor-promoting phorbol ester, phorbol 12-myristate 13-acetate (PMA), inhibited the serum-induced ET-1 production and stimulated PGI2 synthesis in a concentration- and time-dependent manner. Tetradecanoylphorbol Acetate 46-77 endothelin 1 Homo sapiens 113-117 1571476-7 1992 Phorbol myristate acetate, which activates PKC and the Ca2+ ionophore A23187, stimulated the release of ir-endothelin-1 and ir-big endothelin-1 in a dose-dependent way, respectively. Tetradecanoylphorbol Acetate 0-25 endothelin 1 Homo sapiens 107-119 1571476-7 1992 Phorbol myristate acetate, which activates PKC and the Ca2+ ionophore A23187, stimulated the release of ir-endothelin-1 and ir-big endothelin-1 in a dose-dependent way, respectively. Tetradecanoylphorbol Acetate 0-25 endothelin 1 Homo sapiens 131-143 1865754-3 1991 In addition, a tumor-promoting phorbol ester, phorbol 12-myristate 13-acetate (PMA), inhibited the serum-induced ET-1 production and stimulated PGI2 synthesis in a concentration- and time-dependent manner. Tetradecanoylphorbol Acetate 79-82 endothelin 1 Homo sapiens 113-117 1701822-6 1990 The secretion of endothelin 1, but not of endothelin 3, from macrophages could be stimulated 6-10-fold by lipopolysaccharide or phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 128-153 endothelin 1 Homo sapiens 17-29 1701822-6 1990 The secretion of endothelin 1, but not of endothelin 3, from macrophages could be stimulated 6-10-fold by lipopolysaccharide or phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 155-158 endothelin 1 Homo sapiens 17-29 1701822-7 1990 Northern blot analysis of total macrophage RNA using an endothelin 1 cDNA probe revealed induction of endothelin mRNA in PMA-treated macrophages. Tetradecanoylphorbol Acetate 121-124 endothelin 1 Homo sapiens 56-68 2176245-3 1990 The results demonstrated that there were three distinct mRNAs for ET and that TPA-responsive element, mRNA stabilizing sequence, motifs for binding site of nuclear factor 1 and acute phase reactant regulatory elements were recognized in preproform ET-1 gene. Tetradecanoylphorbol Acetate 78-81 endothelin 1 Homo sapiens 248-252