PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23569086-5 2013 Moreover, stimulation of protein kinase C with phorbol-12-myristate-13-acetate mimicked the effect of AngII and increased Cl channel activity. Tetradecanoylphorbol Acetate 47-78 angiotensinogen Homo sapiens 102-107 15666830-1 2004 We have previously reported that the protein kinase C ligand 12-O-tetradecanoyphorbol-13-acetate (TPA) inhibited the angiotensin II (AII) stimulated CYP11B2 gene expression in the adrenocortical H295R cell line. Tetradecanoylphorbol Acetate 98-101 angiotensinogen Homo sapiens 117-131 16037256-3 2005 As presented here, the stimulation of cultured monocytes by phorbol-12-myristate-13-acetate (TPA), an activator of protein kinase C that can mimic the effects of high glucose, angiotensin II, and other physiological stimuli, leads to cellular ROS generation and concomitant formation of intracellular CML. Tetradecanoylphorbol Acetate 60-91 angiotensinogen Homo sapiens 176-190 16037256-3 2005 As presented here, the stimulation of cultured monocytes by phorbol-12-myristate-13-acetate (TPA), an activator of protein kinase C that can mimic the effects of high glucose, angiotensin II, and other physiological stimuli, leads to cellular ROS generation and concomitant formation of intracellular CML. Tetradecanoylphorbol Acetate 93-96 angiotensinogen Homo sapiens 176-190 15666830-7 2004 Taken together these results suggest that TPA inhibits the AII-dependent activation of CYP11B2 via the p44/42 MAPK signaling pathway leading to an increase of the level of nuclear JunB. Tetradecanoylphorbol Acetate 42-45 angiotensinogen Homo sapiens 59-62 18682265-4 2008 Considering that PMA prevents the inhibitory effect of Ado on Ang II-stimulated Na(+)-ATPase and PKC activities, it is likely that the PMA-induced effect, i.e. PKC activation, is downstream of the target for Ado-induced reversion of Ang II stimulation of Na(+)-ATPase activity. Tetradecanoylphorbol Acetate 17-20 angiotensinogen Homo sapiens 62-68 18682265-4 2008 Considering that PMA prevents the inhibitory effect of Ado on Ang II-stimulated Na(+)-ATPase and PKC activities, it is likely that the PMA-induced effect, i.e. PKC activation, is downstream of the target for Ado-induced reversion of Ang II stimulation of Na(+)-ATPase activity. Tetradecanoylphorbol Acetate 17-20 angiotensinogen Homo sapiens 233-239 18682265-4 2008 Considering that PMA prevents the inhibitory effect of Ado on Ang II-stimulated Na(+)-ATPase and PKC activities, it is likely that the PMA-induced effect, i.e. PKC activation, is downstream of the target for Ado-induced reversion of Ang II stimulation of Na(+)-ATPase activity. Tetradecanoylphorbol Acetate 135-138 angiotensinogen Homo sapiens 62-68 18682265-4 2008 Considering that PMA prevents the inhibitory effect of Ado on Ang II-stimulated Na(+)-ATPase and PKC activities, it is likely that the PMA-induced effect, i.e. PKC activation, is downstream of the target for Ado-induced reversion of Ang II stimulation of Na(+)-ATPase activity. Tetradecanoylphorbol Acetate 135-138 angiotensinogen Homo sapiens 233-239 15666830-1 2004 We have previously reported that the protein kinase C ligand 12-O-tetradecanoyphorbol-13-acetate (TPA) inhibited the angiotensin II (AII) stimulated CYP11B2 gene expression in the adrenocortical H295R cell line. Tetradecanoylphorbol Acetate 98-101 angiotensinogen Homo sapiens 133-136 12811831-5 2003 The Ang II-induced proliferation of breast cancer cells was reduced by (a) Go6976, an inhibitor of conventional PKC-alpha and -beta1, (b) AG1478, an inhibitor of the tyrosine kinase of the EGF receptor (EGFR), and (c) downregulation of 1,2-diacylglycerol-sensitive PKCs achieved by phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 282-313 angiotensinogen Homo sapiens 4-10 11809859-4 2002 In C9 cells, phorbol-12-myristate-13-acetate (PMA) caused much greater phosphorylation of Pyk2 and ERK than the Ca(2+) ionophore ionomycin, and the effects of PMA and Ang II were abolished in PKC-depleted cells. Tetradecanoylphorbol Acetate 13-44 angiotensinogen Homo sapiens 167-173 12811831-5 2003 The Ang II-induced proliferation of breast cancer cells was reduced by (a) Go6976, an inhibitor of conventional PKC-alpha and -beta1, (b) AG1478, an inhibitor of the tyrosine kinase of the EGF receptor (EGFR), and (c) downregulation of 1,2-diacylglycerol-sensitive PKCs achieved by phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 315-318 angiotensinogen Homo sapiens 4-10 11809859-4 2002 In C9 cells, phorbol-12-myristate-13-acetate (PMA) caused much greater phosphorylation of Pyk2 and ERK than the Ca(2+) ionophore ionomycin, and the effects of PMA and Ang II were abolished in PKC-depleted cells. Tetradecanoylphorbol Acetate 46-49 angiotensinogen Homo sapiens 167-173 11411021-5 2001 RESULTS: Phorbol-12-myristate-13-acetate significantly upregulated the nephrin expression in A293 cells, while no change was found after treatment with additional stimulants for other main signalling pathways, e.g. okadaic acid, lysophosphatidic acid, bradykinin, angiotensin II (ANG II) and arginine vasopressin (AVP). Tetradecanoylphorbol Acetate 9-40 angiotensinogen Homo sapiens 264-278 11411021-5 2001 RESULTS: Phorbol-12-myristate-13-acetate significantly upregulated the nephrin expression in A293 cells, while no change was found after treatment with additional stimulants for other main signalling pathways, e.g. okadaic acid, lysophosphatidic acid, bradykinin, angiotensin II (ANG II) and arginine vasopressin (AVP). Tetradecanoylphorbol Acetate 9-40 angiotensinogen Homo sapiens 280-286 10692485-7 2000 In contrast, RGS2 mRNA was rapidly and dose dependently increased (395 +/- 24% peak, 45 min) by Ang II but returned to baseline level by 6 to 8 h. Phorbol-12-myristate-13-acetate, a PKC activator, robustly increased RGS2. Tetradecanoylphorbol Acetate 147-178 angiotensinogen Homo sapiens 96-102 10891386-7 2000 Ang II-induced ERK activation was inhibited by protein kinase C (PKC)-specific inhibitor GF109203X, while TRO was also able to block PKC activator phorbol 12 myristate 13-acetate (PMA)-induced ERK activation. Tetradecanoylphorbol Acetate 147-178 angiotensinogen Homo sapiens 0-6 10891386-7 2000 Ang II-induced ERK activation was inhibited by protein kinase C (PKC)-specific inhibitor GF109203X, while TRO was also able to block PKC activator phorbol 12 myristate 13-acetate (PMA)-induced ERK activation. Tetradecanoylphorbol Acetate 180-183 angiotensinogen Homo sapiens 0-6 8964847-15 1996 These effects of AII cotreatment on expression of P450c17 and P450scc were reproduced by cotreatment with TPA (10 nmol/L), suggesting the involvement of protein kinase C in these attenuative responses. Tetradecanoylphorbol Acetate 106-109 angiotensinogen Homo sapiens 17-20 9589661-8 1998 The action of AII was reproduced and indeed exceeded by the protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate (TPA; 10 nmol/L; 5.5-fold increase; P < 0.05). Tetradecanoylphorbol Acetate 87-123 angiotensinogen Homo sapiens 14-17 9589661-8 1998 The action of AII was reproduced and indeed exceeded by the protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate (TPA; 10 nmol/L; 5.5-fold increase; P < 0.05). Tetradecanoylphorbol Acetate 125-128 angiotensinogen Homo sapiens 14-17 8829112-4 1996 The PKC activator phorbol myristate acetate (PMA) dose-dependently inhibited both Ca2+ influx in resting cells and iCRAC, assessed by microfluorometry in fura-2-loaded monolayers, when added before or after 1 uM angiotensin II (AngII) (Ca2+ influx at 1 mM (Ca2+)e +278 +/- 56%/+80 +/- 8%, at 10 mM + 473 +/- 59%/+250 +/- 24% (Ca2+)e, -/+ PMA, respectively, P < 0.05). Tetradecanoylphorbol Acetate 18-43 angiotensinogen Homo sapiens 212-226 8829112-4 1996 The PKC activator phorbol myristate acetate (PMA) dose-dependently inhibited both Ca2+ influx in resting cells and iCRAC, assessed by microfluorometry in fura-2-loaded monolayers, when added before or after 1 uM angiotensin II (AngII) (Ca2+ influx at 1 mM (Ca2+)e +278 +/- 56%/+80 +/- 8%, at 10 mM + 473 +/- 59%/+250 +/- 24% (Ca2+)e, -/+ PMA, respectively, P < 0.05). Tetradecanoylphorbol Acetate 18-43 angiotensinogen Homo sapiens 228-233 8829112-4 1996 The PKC activator phorbol myristate acetate (PMA) dose-dependently inhibited both Ca2+ influx in resting cells and iCRAC, assessed by microfluorometry in fura-2-loaded monolayers, when added before or after 1 uM angiotensin II (AngII) (Ca2+ influx at 1 mM (Ca2+)e +278 +/- 56%/+80 +/- 8%, at 10 mM + 473 +/- 59%/+250 +/- 24% (Ca2+)e, -/+ PMA, respectively, P < 0.05). Tetradecanoylphorbol Acetate 45-48 angiotensinogen Homo sapiens 212-226 8829112-4 1996 The PKC activator phorbol myristate acetate (PMA) dose-dependently inhibited both Ca2+ influx in resting cells and iCRAC, assessed by microfluorometry in fura-2-loaded monolayers, when added before or after 1 uM angiotensin II (AngII) (Ca2+ influx at 1 mM (Ca2+)e +278 +/- 56%/+80 +/- 8%, at 10 mM + 473 +/- 59%/+250 +/- 24% (Ca2+)e, -/+ PMA, respectively, P < 0.05). Tetradecanoylphorbol Acetate 45-48 angiotensinogen Homo sapiens 228-233 24178685-7 1996 The inhibition of system B(0,+) by Ang II is mediated by protein kinase C (PKC) because it was mimicked by phorbol esters (phorbol 12-myristate 13-acetate) and was inhibited by staurosporine. Tetradecanoylphorbol Acetate 123-154 angiotensinogen Homo sapiens 35-41 10629421-3 1999 Following stimulation with the protein kinase stimulator phorbol 12-myristate 13-acetate (PMA, 1 microM) there was an 2.8-fold increase of L-012 chemiluminescence, whereas incubation with angiotensin II (100 nM) did not result in a measurable increase. Tetradecanoylphorbol Acetate 57-88 angiotensinogen Homo sapiens 188-202 10629421-3 1999 Following stimulation with the protein kinase stimulator phorbol 12-myristate 13-acetate (PMA, 1 microM) there was an 2.8-fold increase of L-012 chemiluminescence, whereas incubation with angiotensin II (100 nM) did not result in a measurable increase. Tetradecanoylphorbol Acetate 90-93 angiotensinogen Homo sapiens 188-202 10446131-8 1999 ATII induced extracellular-signal regulated kinase (p42/44 ERK) activity as did phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 80-111 angiotensinogen Homo sapiens 0-4 9648724-7 1998 Inhibition of protein kinase C by either calphostin C or phorbol 12-myristate 13-acetate downregulation inhibited the Ang II-induced tyrosine phosphorylation of p130Cas. Tetradecanoylphorbol Acetate 57-88 angiotensinogen Homo sapiens 118-124 8666999-2 1996 Angiotensin II-responsive elements are located within -54/+25-bp and -269/-55-bp promoter regions and were identified, respectively, as cyclic AMP (CRE)- and 12-O-tetradecanoylphorbol 13-acetate responsive element (TRE)-like sequences. Tetradecanoylphorbol Acetate 158-194 angiotensinogen Homo sapiens 0-14 8964847-8 1996 Whereas treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) reproduced the effect of AII on 3 beta-HSD expression, TPA failed to reproduce the effects of AII on P450c17 and P450scc and even resulted in a marked decrease in expression of P450c17. Tetradecanoylphorbol Acetate 61-64 angiotensinogen Homo sapiens 91-94 1636737-7 1992 Phorbol 12-myristate 13-acetate was also found to activate S6 kinase, and 24 h of pretreatment to deplete protein kinase C inhibited subsequent S6 kinase activation by a high concentration (10(-6) M) of angiotensin II. Tetradecanoylphorbol Acetate 0-31 angiotensinogen Homo sapiens 203-217 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 angiotensinogen Homo sapiens 369-383 8584237-3 1995 Pretreatment with 100 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) enhances the AII-evoked release of [3H]NA approximately two-fold. Tetradecanoylphorbol Acetate 25-61 angiotensinogen Homo sapiens 81-84 8584237-3 1995 Pretreatment with 100 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) enhances the AII-evoked release of [3H]NA approximately two-fold. Tetradecanoylphorbol Acetate 63-66 angiotensinogen Homo sapiens 81-84 8584237-4 1995 Removal of extracellular Ca2+ ([Ca2+]o) decreases 100 nM AII-evoked release of [3H]NA by over 50% both in the presence and absence of TPA. Tetradecanoylphorbol Acetate 134-137 angiotensinogen Homo sapiens 57-60 8584237-5 1995 AII increases intracellular Ca2+ ([Ca2+]i) in this cell line which is consistent with the AT1A receptor being coupled to phospholipase C. Pretreatment with 100 nM TPA for 8 min attenuated the effect of AII on [Ca2+]i. Tetradecanoylphorbol Acetate 163-166 angiotensinogen Homo sapiens 0-3 8584237-5 1995 AII increases intracellular Ca2+ ([Ca2+]i) in this cell line which is consistent with the AT1A receptor being coupled to phospholipase C. Pretreatment with 100 nM TPA for 8 min attenuated the effect of AII on [Ca2+]i. Tetradecanoylphorbol Acetate 163-166 angiotensinogen Homo sapiens 202-205 8253712-5 1993 Platelet-derived growth factor, alpha-thrombin, hydrogen peroxide, phorbol 12-myristate 13-acetate, and ionomycin also induced 3CH134 but to levels lower than angiotensin II. Tetradecanoylphorbol Acetate 67-98 angiotensinogen Homo sapiens 159-173 8253712-7 1993 Treatment with both phorbol 12-myristate 13-acetate and ionomycin induced 3CH134 mRNA to levels seen with angiotensin II, indicating that Ca2+ mobilization and protein kinase C activation can act synergistically to induce 3CH134. Tetradecanoylphorbol Acetate 20-51 angiotensinogen Homo sapiens 106-120 1514580-5 1992 Angiotensin II increased RNA content by 28% at 48 h but had no effect on growth up to 72 h. Growth stimulation and increased nuclear protein kinase C (PKC) activity were induced by contraction, NE, and PMA treatment and were inhibited by staurosporine (a PKC inhibitor), suggestive of a central role for PKC. Tetradecanoylphorbol Acetate 202-205 angiotensinogen Homo sapiens 0-14 1655385-8 1991 Depleting the cells of PKC by exposing them to PMA (1 microM) for 3 h caused a marked reduction in control and ANG II-stimulated Na+ influx and control pK (7.09 to 6.85, P less than 0.05). Tetradecanoylphorbol Acetate 47-50 angiotensinogen Homo sapiens 111-117 1651818-8 1991 To study the potential role of PKC in Ang II desensitization, the cells are treated with TPA for 24 hours, which downregulates PKC activity. Tetradecanoylphorbol Acetate 89-92 angiotensinogen Homo sapiens 38-44 2708448-7 1989 Nifedipine, verapamil, TPA, and pertussis toxin pretreatment were without effect on AII-induced increases in [Ca2+]i. PDGF and AII both stimulated increases in total inositol phosphate accumulation, although the one-half maximal concentration (ED50) for alterations in [Ca2+]i and phosphoinisitide hydrolysis differed by a factor of 10 for PDGF (3 X 10(-10) M for Ca2+ vs. 2.5 X 10(-9) M for phosphoinositide hydrolysis), but they were essentially identical for AII (7.5 X 10(-9) M for Ca2+ vs. 5.0 X 10(-9) M for phosphoinositide hydrolysis). Tetradecanoylphorbol Acetate 23-26 angiotensinogen Homo sapiens 127-130 1903932-8 1991 The protein kinase C activator phorbol myristate acetate also stimulated a large release of choline after a 5 min lag, which was unaffected by the Ca2+ ionophore ionomycin, but was additive with AngII stimulation. Tetradecanoylphorbol Acetate 31-56 angiotensinogen Homo sapiens 195-200 1700277-7 1990 TPA plus A23187 transiently increased CAT activity before repressing it, reflecting the complex actions of angiotensin II in vivo. Tetradecanoylphorbol Acetate 0-3 angiotensinogen Homo sapiens 107-121 2708448-7 1989 Nifedipine, verapamil, TPA, and pertussis toxin pretreatment were without effect on AII-induced increases in [Ca2+]i. PDGF and AII both stimulated increases in total inositol phosphate accumulation, although the one-half maximal concentration (ED50) for alterations in [Ca2+]i and phosphoinisitide hydrolysis differed by a factor of 10 for PDGF (3 X 10(-10) M for Ca2+ vs. 2.5 X 10(-9) M for phosphoinositide hydrolysis), but they were essentially identical for AII (7.5 X 10(-9) M for Ca2+ vs. 5.0 X 10(-9) M for phosphoinositide hydrolysis). Tetradecanoylphorbol Acetate 23-26 angiotensinogen Homo sapiens 127-130 2538464-6 1989 When the Ca2+ transient was induced with 0.1 microM angiotensin II, the PMA pretreatment markedly suppressed it and reduced also the rate of 45Ca2+ efflux from cells slightly. Tetradecanoylphorbol Acetate 72-75 angiotensinogen Homo sapiens 52-66 30536349-2 2018 MATERIALS AND METHODS: THP-1 cells were adopted for research, and phorbol-12-myristate-13-acetate (PMA) was utilized to induce THP-1 cells to be transformed into macrophages, with Ang II as a stimulating factor and telmisartan as a therapeutic drug. Tetradecanoylphorbol Acetate 66-97 angiotensinogen Homo sapiens 180-186 2426266-10 1986 Treatment of hepatocytes with PMA likewise inhibits the ability of vasopressin, angiotensin II, and alpha 1-adrenergic agonists to increase IP3 and mobilize Ca2+ (Lynch, C. J., Charest, R., Bocckino, S. B., Exton, J. H., and Blackmore, P. F. (1985) J. Biol. Tetradecanoylphorbol Acetate 30-33 angiotensinogen Homo sapiens 80-94 3163921-2 1988 12-O-Tetradecanoyl phorbol -13-acetate (TPA, 10(-7) M), which stimulates protein kinase C activity in soluble fractions of glomerular homogenates, suppressed angiotensin II actions on inositol phosphate production and PGE2. Tetradecanoylphorbol Acetate 0-38 angiotensinogen Homo sapiens 158-172 3163921-2 1988 12-O-Tetradecanoyl phorbol -13-acetate (TPA, 10(-7) M), which stimulates protein kinase C activity in soluble fractions of glomerular homogenates, suppressed angiotensin II actions on inositol phosphate production and PGE2. Tetradecanoylphorbol Acetate 40-43 angiotensinogen Homo sapiens 158-172 3163921-4 1988 1-(5-Isoquinolinyl)-2-methylpiperazine (H-7), which inhibits protein kinase C activity in soluble fractions of glomerular homogenates, prevented TPA induced suppression of angiotensin II actions on inositol phosphate production and PGE2. Tetradecanoylphorbol Acetate 145-148 angiotensinogen Homo sapiens 172-186 3099777-6 1986 The combined addition of TPA and the Ca2+ ionophore, A23187, which, like angiotensin II, evokes a sustained increase in aldosterone production, reproduced the temporal patterns of protein phosphorylation seen after angiotensin II action. Tetradecanoylphorbol Acetate 25-28 angiotensinogen Homo sapiens 73-87 3099777-6 1986 The combined addition of TPA and the Ca2+ ionophore, A23187, which, like angiotensin II, evokes a sustained increase in aldosterone production, reproduced the temporal patterns of protein phosphorylation seen after angiotensin II action. Tetradecanoylphorbol Acetate 25-28 angiotensinogen Homo sapiens 215-229 30536349-2 2018 MATERIALS AND METHODS: THP-1 cells were adopted for research, and phorbol-12-myristate-13-acetate (PMA) was utilized to induce THP-1 cells to be transformed into macrophages, with Ang II as a stimulating factor and telmisartan as a therapeutic drug. Tetradecanoylphorbol Acetate 99-102 angiotensinogen Homo sapiens 180-186