PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 12598935-4 2003 Pretreatment with L-Arg (100 micromol/L) decreased significantly Ang II -activated PKC activity and PKC activity induced by phorbol 12-myristate 13-acetate (PMA) ( 10 micromol/L), a PKC activator. Tetradecanoylphorbol Acetate 124-155 angiotensinogen Rattus norvegicus 65-71 16680484-10 2006 Phorbol myristate acetate (PKC activator) mimicked in part the stimulatory effect of ANG II, but reduced Ca(+2) (i). Tetradecanoylphorbol Acetate 0-25 angiotensinogen Rattus norvegicus 85-91 15694920-6 2005 Pressure application of the PKC activator phorbol 12-myristate 13-acetate (PMA) onto angiotensin II-sensitive neurons in the AHA of Wistar rats increased their firing rate. Tetradecanoylphorbol Acetate 42-73 angiotensinogen Rattus norvegicus 85-99 15694920-6 2005 Pressure application of the PKC activator phorbol 12-myristate 13-acetate (PMA) onto angiotensin II-sensitive neurons in the AHA of Wistar rats increased their firing rate. Tetradecanoylphorbol Acetate 75-78 angiotensinogen Rattus norvegicus 85-99 15636703-7 2005 Angiotensin II and phorbol 12-myristate-13-acetate (PMA), the Rho-kinase agonist and PKC agonist, increased the calcium sensitivity, made the cumulative dose-response curve of Ca2+ shift to the left. Tetradecanoylphorbol Acetate 52-55 angiotensinogen Rattus norvegicus 0-14 12598935-4 2003 Pretreatment with L-Arg (100 micromol/L) decreased significantly Ang II -activated PKC activity and PKC activity induced by phorbol 12-myristate 13-acetate (PMA) ( 10 micromol/L), a PKC activator. Tetradecanoylphorbol Acetate 157-160 angiotensinogen Rattus norvegicus 65-71 10693967-4 2000 Stimulation of Na+,K(+)-ATPase activity by Ang II was dependent on protein kinase C (PKC) activation because PKC antagonists abolished the inducing effect of Ang II and the PKC activator phorbol 12-myristate 13-acetate enhanced transporter activity. Tetradecanoylphorbol Acetate 187-218 angiotensinogen Rattus norvegicus 43-49 12359735-5 2002 Moreover, the NO-induced degradation is reversed by the protein kinase C (PKC) activator, 12-O-tetradecanoylphorbol-13-acetate (TPA), and also by the physiological PKC activators platelet-derived growth factor-BB (PDGF), angiotensin II and ATP, resulting in a normalization of neutral ceramidase protein as well as activity. Tetradecanoylphorbol Acetate 128-131 angiotensinogen Rattus norvegicus 221-235 11179453-4 2001 Partial inhibition of the angiotensin II-induced calcium response was observed when cells were pretreated with dibutyryl cyclic AMP, tetradecanoyl phorbol acetate (TPA), vasopressin, or lysophosphatidic acid. Tetradecanoylphorbol Acetate 133-162 angiotensinogen Rattus norvegicus 26-40 11179453-4 2001 Partial inhibition of the angiotensin II-induced calcium response was observed when cells were pretreated with dibutyryl cyclic AMP, tetradecanoyl phorbol acetate (TPA), vasopressin, or lysophosphatidic acid. Tetradecanoylphorbol Acetate 164-167 angiotensinogen Rattus norvegicus 26-40 11108278-5 2000 High levels of glucose (i.e. 25 mM) and phorbol 12-myristate 13-acetate (PMA; 10(-7) M) increased the secretion of IR-rANG and cellular ANG messenger RNA as well as phosphorylation of p38 MAPK in IRPTCs. Tetradecanoylphorbol Acetate 40-71 angiotensinogen Rattus norvegicus 119-122 11108278-5 2000 High levels of glucose (i.e. 25 mM) and phorbol 12-myristate 13-acetate (PMA; 10(-7) M) increased the secretion of IR-rANG and cellular ANG messenger RNA as well as phosphorylation of p38 MAPK in IRPTCs. Tetradecanoylphorbol Acetate 73-76 angiotensinogen Rattus norvegicus 119-122 11078714-4 2000 Depletion of cellular PKC by overnight treatment with phorbol 12-myristate 13-acetate (PMA) similarly augmented ANG II-induced IP production. Tetradecanoylphorbol Acetate 54-85 angiotensinogen Rattus norvegicus 112-118 9307131-7 1997 Similar to the action of Ang II, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA, 100 nM) increased the firing rate from 0.76 +/- 0.3 Hz to 2.3 +/- 0.5 Hz (n = 6, P < 0.05) and increased the neuronal subthreshold activity. Tetradecanoylphorbol Acetate 70-101 angiotensinogen Rattus norvegicus 25-31 11775202-6 2000 Two agonists (angiotensin II and phenylephrine) coupled to Gq and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA) all inhibited Na(+)-Ca2+ exchange in late phase of sepsis. Tetradecanoylphorbol Acetate 96-127 angiotensinogen Rattus norvegicus 14-28 11775202-6 2000 Two agonists (angiotensin II and phenylephrine) coupled to Gq and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA) all inhibited Na(+)-Ca2+ exchange in late phase of sepsis. Tetradecanoylphorbol Acetate 129-132 angiotensinogen Rattus norvegicus 14-28 10537159-4 1999 Insulin inhibited the stimulatory effect of a high level of glucose (25 mM) and phorbol 12-myristate 13-acetate, an activator of protein kinase C) on the secretion of ANG and the expression of the ANG messenger RNA in IRPTC. Tetradecanoylphorbol Acetate 80-111 angiotensinogen Rattus norvegicus 167-170 10537159-4 1999 Insulin inhibited the stimulatory effect of a high level of glucose (25 mM) and phorbol 12-myristate 13-acetate, an activator of protein kinase C) on the secretion of ANG and the expression of the ANG messenger RNA in IRPTC. Tetradecanoylphorbol Acetate 80-111 angiotensinogen Rattus norvegicus 197-200 10209301-4 1999 Mesangial cells pretreated with PMA for 24 h to downregulate PKC demonstrated attenuated response to Ang II. Tetradecanoylphorbol Acetate 32-35 angiotensinogen Rattus norvegicus 101-107 10646512-5 2000 The inhibitory effects of Ang II on lipopolysaccharide-induced expression of iNOS mRNA and protein and nitrite accumulation were mimicked by the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 178-209 angiotensinogen Rattus norvegicus 26-32 10646512-6 2000 Down-regulation of PKC produced by long-term treatment of astroglia with phorbol 12-myristate 13-acetate abolished the inhibitory effect of Ang II on lipopolysaccharide-stimulated expression of iNOS mRNA and nitrite accumulation. Tetradecanoylphorbol Acetate 73-104 angiotensinogen Rattus norvegicus 140-146 9307131-7 1997 Similar to the action of Ang II, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA, 100 nM) increased the firing rate from 0.76 +/- 0.3 Hz to 2.3 +/- 0.5 Hz (n = 6, P < 0.05) and increased the neuronal subthreshold activity. Tetradecanoylphorbol Acetate 103-106 angiotensinogen Rattus norvegicus 25-31 9003008-9 1997 Moreover, the phorbol ester phorbol 12-myristate 13-acetate mimicked most of the effects of AngII in BAC and decreased both AT2-binding sites and mRNA on PC12W cells, indicating that the hormonal regulation of both AT1 and AT2 receptors is mediated through protein kinase C activation. Tetradecanoylphorbol Acetate 28-59 angiotensinogen Rattus norvegicus 92-97 8567051-6 1996 Acute activation (15 minutes) of PKC by phorbol 12-myristate 13-acetate (PMA) blocked responsiveness to both Ang II and AVP. Tetradecanoylphorbol Acetate 40-71 angiotensinogen Rattus norvegicus 109-115 8567051-6 1996 Acute activation (15 minutes) of PKC by phorbol 12-myristate 13-acetate (PMA) blocked responsiveness to both Ang II and AVP. Tetradecanoylphorbol Acetate 73-76 angiotensinogen Rattus norvegicus 109-115 7768986-6 1995 12-O-Tetradecanoylphorbol-13-acetate, a protein kinase C (PKC)-activating phorbol ester, significantly reduced the dexamethasone-induced enhancement of IP3 formation stimulated by vasopressin, angiotensin II or NaF 4 alpha-Phorbol-12, 13-didecanoate, a PKC-nonactivating phorbol ester, had little effect on the enhancement by dexamethasone. Tetradecanoylphorbol Acetate 0-36 angiotensinogen Rattus norvegicus 193-207 7943374-6 1994 Even after protein kinase C (PKC) activity was functionally depleted by treating VSMC with phorbol 12-myristate 13-acetate (10(-6) M) for 24 h, angiotensin II increased alpha 1-mRNA accumulation. Tetradecanoylphorbol Acetate 91-122 angiotensinogen Rattus norvegicus 144-158 7522595-4 1994 Phorbol 12-myristate 13-acetate pretreatment for 30 s caused an increase in the angiotensin II-induced rise in cytosolic calcium. Tetradecanoylphorbol Acetate 0-31 angiotensinogen Rattus norvegicus 80-94 7522595-5 1994 Although both captopril and verapamil reduced responses to angiotensin II to similar extents, only verapamil blocked the ability of phorbol 12-myristate 13-acetate to enhance responses to angiotensin II. Tetradecanoylphorbol Acetate 132-163 angiotensinogen Rattus norvegicus 188-202 8026583-1 1994 Addition of 12-O-tetradecanoylphorbol-13-acetate to RIE-1 rat intestinal epithelial cells stimulated a rapid (mean 3-fold) increase in the subsequent binding of 125I-labelled angiotensin II which was reversed or prevented when cellular protein kinase C was depleted. Tetradecanoylphorbol Acetate 12-48 angiotensinogen Rattus norvegicus 175-189 7987254-1 1994 Whereas direct activation of protein kinase C (PKC) by the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) increased the subsequent binding of 125I-labelled angiotensin II (125I-AII; 0.5 nM) to RIE-1 cells, ligand-mediated activation of the kinase via angiotensin II (AII), which activates the phosphoinositide (PI) pathway in these cells, had no effect. Tetradecanoylphorbol Acetate 74-111 angiotensinogen Rattus norvegicus 168-182 7987254-1 1994 Whereas direct activation of protein kinase C (PKC) by the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) increased the subsequent binding of 125I-labelled angiotensin II (125I-AII; 0.5 nM) to RIE-1 cells, ligand-mediated activation of the kinase via angiotensin II (AII), which activates the phosphoinositide (PI) pathway in these cells, had no effect. Tetradecanoylphorbol Acetate 74-111 angiotensinogen Rattus norvegicus 263-277 7987254-1 1994 Whereas direct activation of protein kinase C (PKC) by the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) increased the subsequent binding of 125I-labelled angiotensin II (125I-AII; 0.5 nM) to RIE-1 cells, ligand-mediated activation of the kinase via angiotensin II (AII), which activates the phosphoinositide (PI) pathway in these cells, had no effect. Tetradecanoylphorbol Acetate 113-116 angiotensinogen Rattus norvegicus 168-182 7987254-1 1994 Whereas direct activation of protein kinase C (PKC) by the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) increased the subsequent binding of 125I-labelled angiotensin II (125I-AII; 0.5 nM) to RIE-1 cells, ligand-mediated activation of the kinase via angiotensin II (AII), which activates the phosphoinositide (PI) pathway in these cells, had no effect. Tetradecanoylphorbol Acetate 113-116 angiotensinogen Rattus norvegicus 263-277 8326007-5 1993 Tetradecanoylphorbol-acetate (10(-7) M) mimicked the effects of ANG II and ET-1 on induction of ppET-1 mRNA. Tetradecanoylphorbol Acetate 0-28 angiotensinogen Rattus norvegicus 64-70 7519561-3 1994 The maximal decrease (50 +/- 13% of control) occurred at 6 h, followed by a gradual return to the control level within 24 h. H-7 (30 microM), a relatively specific protein kinase C inhibitor, inhibited decrease in the expression of angiotensin II receptor mRNA induced by 6 h angiotensin II treatment, while 6 h stimulation by 0.3 microM phorbol 12-myristate 13-acetate also induced a decrease (35 +/- 8% of control) in the expression of angiotensin II receptor mRNA. Tetradecanoylphorbol Acetate 338-369 angiotensinogen Rattus norvegicus 232-246 1428115-7 1992 Phorbol 12-myristate 13-acetate-induced phosphorylation of pp42 indicates the possibility of an association between protein kinase C and the signal transduction pathway of angiotensin II-induced pp42 phosphorylation. Tetradecanoylphorbol Acetate 0-31 angiotensinogen Rattus norvegicus 172-186 8381612-6 1993 However, use of PMA to cause feedback inhibition of D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] formation blocked the effect of ANG II on agonist-stimulated cAMP formation, and the time course for this effect of PMA paralleled its inhibitory effect on Ins(1,4,5)P3 production. Tetradecanoylphorbol Acetate 16-19 angiotensinogen Rattus norvegicus 134-140 8381612-6 1993 However, use of PMA to cause feedback inhibition of D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] formation blocked the effect of ANG II on agonist-stimulated cAMP formation, and the time course for this effect of PMA paralleled its inhibitory effect on Ins(1,4,5)P3 production. Tetradecanoylphorbol Acetate 218-221 angiotensinogen Rattus norvegicus 134-140 1330500-12 1992 The stimulation of cAMP by AII was mimicked by 10-min incubation with phorbol 12-myristate 13-acetate (PMA), and prevented after cellular protein kinase-C (PKC) depletion by 4- or 6-h preincubation with PMA. Tetradecanoylphorbol Acetate 70-101 angiotensinogen Rattus norvegicus 27-30 1330500-12 1992 The stimulation of cAMP by AII was mimicked by 10-min incubation with phorbol 12-myristate 13-acetate (PMA), and prevented after cellular protein kinase-C (PKC) depletion by 4- or 6-h preincubation with PMA. Tetradecanoylphorbol Acetate 103-106 angiotensinogen Rattus norvegicus 27-30 1330500-12 1992 The stimulation of cAMP by AII was mimicked by 10-min incubation with phorbol 12-myristate 13-acetate (PMA), and prevented after cellular protein kinase-C (PKC) depletion by 4- or 6-h preincubation with PMA. Tetradecanoylphorbol Acetate 203-206 angiotensinogen Rattus norvegicus 27-30 7685444-6 1993 After pretreatment with PMA 10(-7) M, the maximum increase in [Ca2+]i induced by AII in hypertensive cells was limited to 108.0 +/- 6.2 nM (p < 0.05 as compared with normotensive cells), whereas the increase in [Ca2+]i in normotensive vSMC remained the same as before: 211.5 +/- 23.4 nM. Tetradecanoylphorbol Acetate 24-27 angiotensinogen Rattus norvegicus 81-84 1447224-4 1992 In response to TPA and AII, HB-EGF mRNA levels increased rapidly, peaked at 2 h, and returned to base line at 7 h. This effect of AII on HB-EGF induction was specific, as evidenced by the fact that it could be completely blocked by the AII antagonist saralasin. Tetradecanoylphorbol Acetate 15-18 angiotensinogen Rattus norvegicus 130-133 1447224-4 1992 In response to TPA and AII, HB-EGF mRNA levels increased rapidly, peaked at 2 h, and returned to base line at 7 h. This effect of AII on HB-EGF induction was specific, as evidenced by the fact that it could be completely blocked by the AII antagonist saralasin. Tetradecanoylphorbol Acetate 15-18 angiotensinogen Rattus norvegicus 130-133 1558167-11 1992 The levels of GDH mRNA are also increased by treating cells with adenosine 3",5"-cyclic monophosphate, epinephrine, triiodothyronine, or retinoic acid, whereas treatment with angiotensin II, vasopressin, phorbol 12-myristate 13-acetate, or cycloheximide did not produce an increase. Tetradecanoylphorbol Acetate 204-235 angiotensinogen Rattus norvegicus 175-189 1659379-2 1991 Short-term treatment of mesangial cells with phorbol 12-myristate 13-acetate (PMA) decreases angiotensin II-induced InsP3 formation, but potentiates hormone-stimulated arachidonic acid release and prostaglandin (PG) E2 synthesis. Tetradecanoylphorbol Acetate 45-76 angiotensinogen Rattus norvegicus 93-107 1655395-8 1991 12-O-Tetradecanolylphorbol 13-acetate (TPA), a stimulator of PKC was indeed able to increase intracellular cAMP; this effect was not additive with that of AII. Tetradecanoylphorbol Acetate 39-42 angiotensinogen Rattus norvegicus 155-158 1659379-2 1991 Short-term treatment of mesangial cells with phorbol 12-myristate 13-acetate (PMA) decreases angiotensin II-induced InsP3 formation, but potentiates hormone-stimulated arachidonic acid release and prostaglandin (PG) E2 synthesis. Tetradecanoylphorbol Acetate 78-81 angiotensinogen Rattus norvegicus 93-107 1846421-1 1991 Our previous studies have shown that angiotensin II (Ang II) has a dose-dependent biphasic effect on bicarbonate and sodium transport and 4-beta-phorbol-12-myristate-13-acetate can simulate the stimulatory effect of Ang II on Na+/H+ exchange in the proximal convoluted tubules (PCT) of the rat kidney. Tetradecanoylphorbol Acetate 138-176 angiotensinogen Rattus norvegicus 37-51 1872896-7 1991 TPA (12-O-tetradecanoylphorbol-13-acetate) also produced a significant (P less than 0.05) reduction of 32P-Pi uptake, suggesting that protein kinase C is involved in the transduction of ang II effects on intracellular Pi. Tetradecanoylphorbol Acetate 0-3 angiotensinogen Rattus norvegicus 186-192 1872896-7 1991 TPA (12-O-tetradecanoylphorbol-13-acetate) also produced a significant (P less than 0.05) reduction of 32P-Pi uptake, suggesting that protein kinase C is involved in the transduction of ang II effects on intracellular Pi. Tetradecanoylphorbol Acetate 5-41 angiotensinogen Rattus norvegicus 186-192 1830456-8 1991 Phorbol 12-myristate 13-acetate (PMA), 10(-6) and 10(-7) M, also decreased the amplitude of the Ca2+ transients similar to ANG II. Tetradecanoylphorbol Acetate 0-31 angiotensinogen Rattus norvegicus 123-129 1828153-7 1991 Ang II (10(9) - 10(-8) M) and a protein kinase C activator, phorbol 12-myristate 13-acetate (PMA, 10(-8) M) rapidly induced c-fos as well as c-Jun and Jun-B mRNA expression in RASM cells. Tetradecanoylphorbol Acetate 93-96 angiotensinogen Rattus norvegicus 0-6 1846421-1 1991 Our previous studies have shown that angiotensin II (Ang II) has a dose-dependent biphasic effect on bicarbonate and sodium transport and 4-beta-phorbol-12-myristate-13-acetate can simulate the stimulatory effect of Ang II on Na+/H+ exchange in the proximal convoluted tubules (PCT) of the rat kidney. Tetradecanoylphorbol Acetate 138-176 angiotensinogen Rattus norvegicus 53-59 1846421-1 1991 Our previous studies have shown that angiotensin II (Ang II) has a dose-dependent biphasic effect on bicarbonate and sodium transport and 4-beta-phorbol-12-myristate-13-acetate can simulate the stimulatory effect of Ang II on Na+/H+ exchange in the proximal convoluted tubules (PCT) of the rat kidney. Tetradecanoylphorbol Acetate 138-176 angiotensinogen Rattus norvegicus 216-222 2170389-5 1990 Addition of the protein kinase C inhibitor staurosporine or down-regulation of protein kinase C by prolonged incubation with phorbol 12-myristate 13-acetate partially reduced the effects of angiotensin II and alpha-thrombin and completely blunted the phorbol 12-myristate 13-acetate-induced stimulation of Na+/K+/Cl- cotransport but did not affect EGF-induced stimulation. Tetradecanoylphorbol Acetate 125-156 angiotensinogen Rattus norvegicus 190-204 2170389-5 1990 Addition of the protein kinase C inhibitor staurosporine or down-regulation of protein kinase C by prolonged incubation with phorbol 12-myristate 13-acetate partially reduced the effects of angiotensin II and alpha-thrombin and completely blunted the phorbol 12-myristate 13-acetate-induced stimulation of Na+/K+/Cl- cotransport but did not affect EGF-induced stimulation. Tetradecanoylphorbol Acetate 251-282 angiotensinogen Rattus norvegicus 190-204 2330986-5 1990 Pretreatment with PMA or with sphingosine each attenuated by approximately one-third the bicarbonate absorptive response usually observed following angiotensin II administration. Tetradecanoylphorbol Acetate 18-21 angiotensinogen Rattus norvegicus 148-162 2155825-3 1990 Long-term pretreatment with TPA also increased the angiotensin II-induced mobilization of Ca2+ and the subsequent contraction of mesangial cells. Tetradecanoylphorbol Acetate 28-31 angiotensinogen Rattus norvegicus 51-65 2333947-5 1990 The PKC antagonist H-7 dose dependently inhibited phorbol 12-myristate 13-acetate (TPA)-stimulated increases in 125I-ANG II binding, whereas downregulation of PKC activity by chronic phorbol ester incubations of 24 and 48 h prevented TPA-stimulated increases in 125I-ANG II-specific binding. Tetradecanoylphorbol Acetate 50-81 angiotensinogen Rattus norvegicus 117-123 2333947-5 1990 The PKC antagonist H-7 dose dependently inhibited phorbol 12-myristate 13-acetate (TPA)-stimulated increases in 125I-ANG II binding, whereas downregulation of PKC activity by chronic phorbol ester incubations of 24 and 48 h prevented TPA-stimulated increases in 125I-ANG II-specific binding. Tetradecanoylphorbol Acetate 50-81 angiotensinogen Rattus norvegicus 267-273 2333947-5 1990 The PKC antagonist H-7 dose dependently inhibited phorbol 12-myristate 13-acetate (TPA)-stimulated increases in 125I-ANG II binding, whereas downregulation of PKC activity by chronic phorbol ester incubations of 24 and 48 h prevented TPA-stimulated increases in 125I-ANG II-specific binding. Tetradecanoylphorbol Acetate 83-86 angiotensinogen Rattus norvegicus 117-123 2333947-5 1990 The PKC antagonist H-7 dose dependently inhibited phorbol 12-myristate 13-acetate (TPA)-stimulated increases in 125I-ANG II binding, whereas downregulation of PKC activity by chronic phorbol ester incubations of 24 and 48 h prevented TPA-stimulated increases in 125I-ANG II-specific binding. Tetradecanoylphorbol Acetate 83-86 angiotensinogen Rattus norvegicus 267-273 2333947-7 1990 Temporally, the maximal stimulation of PKC translocation by mezerein, teleocidin A, and TPA preceded their ability to stimulate maximal 125I-ANG II-specific binding. Tetradecanoylphorbol Acetate 88-91 angiotensinogen Rattus norvegicus 141-147 2155825-0 1990 Potentiation of angiotensin II-stimulated phosphoinositide hydrolysis, calcium mobilization and contraction of renal mesangial cells upon down-regulation of protein kinase C. Long-term pretreatment of rat mesangial cells with 12-O-tetradecanoylphorbol 13-acetate (TPA) down-regulated protein kinase C activity and potentiated the angiotensin II-induced inositol trisphosphate (InsP3) formation. Tetradecanoylphorbol Acetate 226-262 angiotensinogen Rattus norvegicus 16-30 2154205-5 1990 Angiotensin II- and bradykinin-stimulated inositol phosphate accumulation in intact glomeruli was inhibited by phorbol myristate acetate, an activator of protein kinase C. Tetradecanoylphorbol Acetate 111-136 angiotensinogen Rattus norvegicus 0-14 2155825-0 1990 Potentiation of angiotensin II-stimulated phosphoinositide hydrolysis, calcium mobilization and contraction of renal mesangial cells upon down-regulation of protein kinase C. Long-term pretreatment of rat mesangial cells with 12-O-tetradecanoylphorbol 13-acetate (TPA) down-regulated protein kinase C activity and potentiated the angiotensin II-induced inositol trisphosphate (InsP3) formation. Tetradecanoylphorbol Acetate 264-267 angiotensinogen Rattus norvegicus 16-30 2601266-8 1989 Combined treatment with A23187 and TPA could mimic both the initial and sustained effect of Ang II in the presence of extracellular Ca, though either one of them failed to do so when used alone. Tetradecanoylphorbol Acetate 35-38 angiotensinogen Rattus norvegicus 92-98 8070351-4 1994 In VSMC, angiotensin-II, which induces PTHrP expression, also rapidly (30 min) desensitized the cAMP response and down-regulated (75-90%) receptor mRNA within 1 h. Treatment of cells with phorbol 12-myristate 13-acetate (0.1 microM) mimicked these effects, whereas neither PTHrP-(1-34)NH2, forskolin, nor (Bu)2cAMP altered receptor mRNA expression. Tetradecanoylphorbol Acetate 188-219 angiotensinogen Rattus norvegicus 9-23 2293979-5 1990 Incubation of the cells with 100 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in transient translocation of PKC activity to the membrane (15 min) which was followed by a 64% decrease in total cellular enzyme activity after 3 h. In PKC-depleted cells, the aldosterone response to ACTH was increased by 25% but AII-stimulated steroidogenesis was unchanged. Tetradecanoylphorbol Acetate 36-72 angiotensinogen Rattus norvegicus 319-322 2293979-5 1990 Incubation of the cells with 100 nM 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in transient translocation of PKC activity to the membrane (15 min) which was followed by a 64% decrease in total cellular enzyme activity after 3 h. In PKC-depleted cells, the aldosterone response to ACTH was increased by 25% but AII-stimulated steroidogenesis was unchanged. Tetradecanoylphorbol Acetate 74-77 angiotensinogen Rattus norvegicus 319-322 2293979-6 1990 In contrast, in cells in which PKC was translocated to the membrane by a 15 min preincubation with TPA, aldosterone response to AII was enhanced by 40%, while the response to ACTH was reduced by 30%; under these conditions membrane PKC levels rapidly returned to basal. Tetradecanoylphorbol Acetate 99-102 angiotensinogen Rattus norvegicus 128-131 2293979-7 1990 However, the changes in aldosterone response were still evident when addition of AII or ACTH was delayed for up to 30 min after removal of TPA, indicating a persistent modification in the cell membrane secondary to PKC activation. Tetradecanoylphorbol Acetate 139-142 angiotensinogen Rattus norvegicus 81-84 2293979-11 1990 However, the fact that aldosterone responses to AII are potentiated during TPA-induced PKC translocation to the membrane suggests that AII and phorbol esters do not share the same mechanism of action in the regulation of steroidogenesis. Tetradecanoylphorbol Acetate 75-78 angiotensinogen Rattus norvegicus 48-51 2293979-11 1990 However, the fact that aldosterone responses to AII are potentiated during TPA-induced PKC translocation to the membrane suggests that AII and phorbol esters do not share the same mechanism of action in the regulation of steroidogenesis. Tetradecanoylphorbol Acetate 75-78 angiotensinogen Rattus norvegicus 135-138 2554890-2 1989 Short-term (10 min) pretreatment of SMC with 12-O-tetradecanoylphorbol 13-acetate (TPA; 100 nM) decreases the angiotensin II-induced InsP3 formation. Tetradecanoylphorbol Acetate 45-81 angiotensinogen Rattus norvegicus 110-124 2554890-2 1989 Short-term (10 min) pretreatment of SMC with 12-O-tetradecanoylphorbol 13-acetate (TPA; 100 nM) decreases the angiotensin II-induced InsP3 formation. Tetradecanoylphorbol Acetate 83-86 angiotensinogen Rattus norvegicus 110-124 2554890-7 1989 In parallel with this potentiation of angiotensin II-induced generation of InsP3 by TPA, a down-regulation of protein kinase C activity is observed. Tetradecanoylphorbol Acetate 84-87 angiotensinogen Rattus norvegicus 38-52 2655581-8 1989 In the presence of 10 nM-PMA, the sensitivity of cultured smooth-muscle cells towards Ang II was increased, and maximal values of Ang II-induced prostacyclin production were enhanced by about 60%. Tetradecanoylphorbol Acetate 25-28 angiotensinogen Rattus norvegicus 86-92 2655581-8 1989 In the presence of 10 nM-PMA, the sensitivity of cultured smooth-muscle cells towards Ang II was increased, and maximal values of Ang II-induced prostacyclin production were enhanced by about 60%. Tetradecanoylphorbol Acetate 25-28 angiotensinogen Rattus norvegicus 130-136 2448059-8 1988 Angiotensin II enhances the phosphorylation state of the same set of proteins as observed with TPA. Tetradecanoylphorbol Acetate 95-98 angiotensinogen Rattus norvegicus 0-14 2843541-12 1988 The 18-h TPA pretreatment diminished by 30-50% the induction of receptor protein synthesis by epinephrine or angiotensin II. Tetradecanoylphorbol Acetate 9-12 angiotensinogen Rattus norvegicus 109-123 3264151-1 1988 The inhibitory effect of phorbol-12-myristate-13-acetate (PMA) on the Ca2+-mobilization mechanisms by arginine vasopressin (AVP) and angiotensin II (AII) was analysed in rat vascular smooth muscle cells (VSMC) in culture. Tetradecanoylphorbol Acetate 25-56 angiotensinogen Rattus norvegicus 133-147 3264151-1 1988 The inhibitory effect of phorbol-12-myristate-13-acetate (PMA) on the Ca2+-mobilization mechanisms by arginine vasopressin (AVP) and angiotensin II (AII) was analysed in rat vascular smooth muscle cells (VSMC) in culture. Tetradecanoylphorbol Acetate 25-56 angiotensinogen Rattus norvegicus 149-152 3264151-1 1988 The inhibitory effect of phorbol-12-myristate-13-acetate (PMA) on the Ca2+-mobilization mechanisms by arginine vasopressin (AVP) and angiotensin II (AII) was analysed in rat vascular smooth muscle cells (VSMC) in culture. Tetradecanoylphorbol Acetate 58-61 angiotensinogen Rattus norvegicus 133-147 2836390-8 1988 Long-term pretreatment with PMA greatly reduced the contribution of agonist-induced desensitization to the angiotensin II response; in contrast, the extent of desensitization occurring during incubation of WB cells with epinephrine was unaltered by long-term treatment with PMA suggesting that an additional mechanism may be involved in alpha 1-adrenergic receptor desensitization. Tetradecanoylphorbol Acetate 28-31 angiotensinogen Rattus norvegicus 107-121 3281943-8 1988 12-O-tetradecanoyl phorbol 13-acetate (TPA) also induced beta-actin mRNA, decreased angiotensinogen mRNA, and caused an increase in [3H]methyl thymidine incorporation. Tetradecanoylphorbol Acetate 0-37 angiotensinogen Rattus norvegicus 84-99 3281943-8 1988 12-O-tetradecanoyl phorbol 13-acetate (TPA) also induced beta-actin mRNA, decreased angiotensinogen mRNA, and caused an increase in [3H]methyl thymidine incorporation. Tetradecanoylphorbol Acetate 39-42 angiotensinogen Rattus norvegicus 84-99 2448059-10 1988 The remarkable similarity in mechanical, electrical, and protein phosphorylation responses of cultured neonatal myocytes following TPA or angiotensin II application indicate that protein kinase C may mediate the action of angiotensin II. Tetradecanoylphorbol Acetate 131-134 angiotensinogen Rattus norvegicus 222-236 3500949-9 1987 Phorbol 12-myristate 13-acetate attenuated the production of Ins(1,4,5)P3 generated by angiotensin II over the concentration range of 10(-10) to 10(-8) M; however, the Ca2+ signal was only inhibited at the 10(-10) M dose of angiotensin II. Tetradecanoylphorbol Acetate 0-31 angiotensinogen Rattus norvegicus 87-101 3500949-9 1987 Phorbol 12-myristate 13-acetate attenuated the production of Ins(1,4,5)P3 generated by angiotensin II over the concentration range of 10(-10) to 10(-8) M; however, the Ca2+ signal was only inhibited at the 10(-10) M dose of angiotensin II. Tetradecanoylphorbol Acetate 0-31 angiotensinogen Rattus norvegicus 224-238 2829820-4 1987 Furthermore, activation of protein kinase C by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and by 1-oleoyl-2-acetylglycerol (OAG) abolishes angiotensin II-induced formation of inositol trisphosphate (IP3) in mesangial cells [Pfeilschifter (1986) FEBS Lett. Tetradecanoylphorbol Acetate 65-101 angiotensinogen Rattus norvegicus 157-171 2829820-4 1987 Furthermore, activation of protein kinase C by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and by 1-oleoyl-2-acetylglycerol (OAG) abolishes angiotensin II-induced formation of inositol trisphosphate (IP3) in mesangial cells [Pfeilschifter (1986) FEBS Lett. Tetradecanoylphorbol Acetate 103-106 angiotensinogen Rattus norvegicus 157-171 2829820-11 1987 Angiotensin II augments the increase in IP3 formation induced by GTP gamma S. However, when mesangial cells were pretreated with TPA there was a dose-dependent inhibition of the synergistic action of angiotensin II on GTP gamma S-induced IP3 production. Tetradecanoylphorbol Acetate 129-132 angiotensinogen Rattus norvegicus 0-14 2829820-11 1987 Angiotensin II augments the increase in IP3 formation induced by GTP gamma S. However, when mesangial cells were pretreated with TPA there was a dose-dependent inhibition of the synergistic action of angiotensin II on GTP gamma S-induced IP3 production. Tetradecanoylphorbol Acetate 129-132 angiotensinogen Rattus norvegicus 200-214 25711724-2 2015 Because protein kinase C (PKC) mimetic phorbol myristate acetate (PMA) can destabilize natriuretic peptide clearance receptor (NPR-C) mRNA and angiotensin II activates several PKC isoforms in VSMCs, we hypothesized that angiotensin II treatment decreases NPR-C mRNA stability and exerts this effect through PKC. Tetradecanoylphorbol Acetate 39-64 angiotensinogen Rattus norvegicus 143-157 3031039-7 1987 Activation of the Na+/H+ antiport by subjecting VSMCs to phorbol 12-myristate 13-acetate (100 nM) prevented a subsequent effect of AII on the pHi profile. Tetradecanoylphorbol Acetate 57-88 angiotensinogen Rattus norvegicus 131-134 3089838-0 1986 Tumour promotor 12-O-tetradecanoylphorbol 13-acetate inhibits angiotensin II-induced inositol phosphate production and cytosolic Ca2+ rise in rat renal mesangial cells. Tetradecanoylphorbol Acetate 16-52 angiotensinogen Rattus norvegicus 62-76 3089838-1 1986 Preincubation of rat renal mesangial cells with 12-O-tetradecanoylphorbol 13-acetate (TPA) strongly inhibited the increases of inositol phosphates and of free cytosolic Ca2+ induced by angiotensin II (10(-7) M). Tetradecanoylphorbol Acetate 48-84 angiotensinogen Rattus norvegicus 185-199 3089838-1 1986 Preincubation of rat renal mesangial cells with 12-O-tetradecanoylphorbol 13-acetate (TPA) strongly inhibited the increases of inositol phosphates and of free cytosolic Ca2+ induced by angiotensin II (10(-7) M). Tetradecanoylphorbol Acetate 86-89 angiotensinogen Rattus norvegicus 185-199 2997197-4 1985 In addition, pretreatment of VSMC with either PMA (IC50 approximately 1 nM) or 1-oleoyl-2-acetylglycerol (IC50 approximately 7.5 microM) also markedly inhibits angiotensin II (1 nM)-stimulated increases in cytosolic free Ca2+, as measured with the calcium-sensitive fluorescent indicator quin 2, or 45Ca2+ efflux. Tetradecanoylphorbol Acetate 46-49 angiotensinogen Rattus norvegicus 160-174 3572405-4 1987 The active phorbol ester phorbol-12-myristate-13-acetate (TPA) caused time- and concentration-dependent increases in the specific binding of [125I]Ang II to its receptors in neuronal cultures of normotensive and spontaneously hypertensive rat brains. Tetradecanoylphorbol Acetate 25-56 angiotensinogen Rattus norvegicus 147-153 3572405-4 1987 The active phorbol ester phorbol-12-myristate-13-acetate (TPA) caused time- and concentration-dependent increases in the specific binding of [125I]Ang II to its receptors in neuronal cultures of normotensive and spontaneously hypertensive rat brains. Tetradecanoylphorbol Acetate 58-61 angiotensinogen Rattus norvegicus 147-153 3572405-5 1987 The stimulatory effect of TPA on Ang II receptors was apparent within 15 min and reached a maximum between 1 and 2 h. Ang II specific binding had returned to control levels by 24 h. Various phorbol esters increased [125I]Ang II binding in accordance with their order of potency in stimulating protein kinase C activity. Tetradecanoylphorbol Acetate 26-29 angiotensinogen Rattus norvegicus 33-39 3572405-5 1987 The stimulatory effect of TPA on Ang II receptors was apparent within 15 min and reached a maximum between 1 and 2 h. Ang II specific binding had returned to control levels by 24 h. Various phorbol esters increased [125I]Ang II binding in accordance with their order of potency in stimulating protein kinase C activity. Tetradecanoylphorbol Acetate 26-29 angiotensinogen Rattus norvegicus 118-124 3572405-5 1987 The stimulatory effect of TPA on Ang II receptors was apparent within 15 min and reached a maximum between 1 and 2 h. Ang II specific binding had returned to control levels by 24 h. Various phorbol esters increased [125I]Ang II binding in accordance with their order of potency in stimulating protein kinase C activity. Tetradecanoylphorbol Acetate 26-29 angiotensinogen Rattus norvegicus 118-124 3031037-10 1987 The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), stimulated Na+/H+ exchange in VSMC cultured for 24 h in serum-free medium, and the subsequent angiotensin II response was inhibited. Tetradecanoylphorbol Acetate 19-55 angiotensinogen Rattus norvegicus 157-171 3031037-10 1987 The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), stimulated Na+/H+ exchange in VSMC cultured for 24 h in serum-free medium, and the subsequent angiotensin II response was inhibited. Tetradecanoylphorbol Acetate 57-60 angiotensinogen Rattus norvegicus 157-171 3031037-12 1987 TPA caused no intracellular alkalinization of VSMC grown in serum, while the angiotensin II response was actually enhanced compared to VSMC deprived of serum for 24 h. We conclude that angiotensin II stimulates an amiloride-sensitive Na+/H+ exchange system in cultured VSMC which is mediated by protein kinase C-dependent and -independent mechanisms. Tetradecanoylphorbol Acetate 0-3 angiotensinogen Rattus norvegicus 185-199 3758157-1 1986 A possible role for protein kinase C during the tonic phase of arterial contraction was examined in rat aorta by observing the effects of the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), on angiotensin II (AII)-induced responses. Tetradecanoylphorbol Acetate 157-193 angiotensinogen Rattus norvegicus 204-218 3758157-1 1986 A possible role for protein kinase C during the tonic phase of arterial contraction was examined in rat aorta by observing the effects of the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), on angiotensin II (AII)-induced responses. Tetradecanoylphorbol Acetate 157-193 angiotensinogen Rattus norvegicus 220-223 25711724-2 2015 Because protein kinase C (PKC) mimetic phorbol myristate acetate (PMA) can destabilize natriuretic peptide clearance receptor (NPR-C) mRNA and angiotensin II activates several PKC isoforms in VSMCs, we hypothesized that angiotensin II treatment decreases NPR-C mRNA stability and exerts this effect through PKC. Tetradecanoylphorbol Acetate 39-64 angiotensinogen Rattus norvegicus 220-234 25711724-2 2015 Because protein kinase C (PKC) mimetic phorbol myristate acetate (PMA) can destabilize natriuretic peptide clearance receptor (NPR-C) mRNA and angiotensin II activates several PKC isoforms in VSMCs, we hypothesized that angiotensin II treatment decreases NPR-C mRNA stability and exerts this effect through PKC. Tetradecanoylphorbol Acetate 66-69 angiotensinogen Rattus norvegicus 143-157 25711724-2 2015 Because protein kinase C (PKC) mimetic phorbol myristate acetate (PMA) can destabilize natriuretic peptide clearance receptor (NPR-C) mRNA and angiotensin II activates several PKC isoforms in VSMCs, we hypothesized that angiotensin II treatment decreases NPR-C mRNA stability and exerts this effect through PKC. Tetradecanoylphorbol Acetate 66-69 angiotensinogen Rattus norvegicus 220-234 25711724-5 2015 However, this response to angiotensin II was undiminished by the PKC inhibitor chelerythrine, or by depletion of PKC by prior exposure of cells to PMA for 48 h. Inhibitors of tyrosine kinases, phospholipase C, or mitogen-activated protein kinase kinase also failed to reverse the angiotensin II effect. Tetradecanoylphorbol Acetate 147-150 angiotensinogen Rattus norvegicus 26-40