PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20875097-8 2010 The bradykinin effect on resensitization was similar in the absence of extracellular Ca2+ or in the presence of the PKC activator PMA, but was inhibited by the protein phosphatase inhibitor okadaic acid and the PI3K inhibitor LY294002. Tetradecanoylphorbol Acetate 130-133 kininogen 1 Homo sapiens 4-14 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 kininogen 1 Homo sapiens 252-262 9893038-7 1998 Phorbol 12-myristate 13-acetate pretreatment diminished the ability of BK to stimulate IL-8 production. Tetradecanoylphorbol Acetate 0-31 kininogen 1 Homo sapiens 71-73 11419696-3 2001 The PLD activation induced by BK was blocked by pretreatment of A-431 cells with staurosporine, or by prolonged treatment with phorbol-12-myristate-13-acetate (PMA). Tetradecanoylphorbol Acetate 127-158 kininogen 1 Homo sapiens 30-32 11419696-3 2001 The PLD activation induced by BK was blocked by pretreatment of A-431 cells with staurosporine, or by prolonged treatment with phorbol-12-myristate-13-acetate (PMA). Tetradecanoylphorbol Acetate 160-163 kininogen 1 Homo sapiens 30-32 10444401-10 1999 Protein kinase C downregulation by phorbol 12-myristate 13-acetate and/or inhibitors to protein kinase C, p60(src) kinase, and MAPK kinase inhibited BK-induced MAPK tyrosine phosphorylation. Tetradecanoylphorbol Acetate 35-66 kininogen 1 Homo sapiens 149-151 9547352-1 1998 In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production. Tetradecanoylphorbol Acetate 76-107 kininogen 1 Homo sapiens 133-143 9547352-1 1998 In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production. Tetradecanoylphorbol Acetate 109-112 kininogen 1 Homo sapiens 133-143 8588976-6 1995 Chronic pretreatment with 400 nM TPA abolished PLD activation to subsequent treatment with either TPA and bradykinin. Tetradecanoylphorbol Acetate 33-36 kininogen 1 Homo sapiens 106-116 8769870-9 1996 The accumulation of total 3H-inositol (poly) phosphates in response to bradykinin or histamine was essentially abolished by prior treatment with 10-min PMA treatment (1 microM). Tetradecanoylphorbol Acetate 152-155 kininogen 1 Homo sapiens 71-81 8769870-10 1996 However, with 12-h exposure to PMA, the bradykinin response was restored to the level seen with no prior PMA exposure. Tetradecanoylphorbol Acetate 31-34 kininogen 1 Homo sapiens 40-50 8890934-5 1996 Activation of PKC with TPA diminished the number of BK receptors by 33% and proportionally decreased BK-mediated Ins(1,4,5)P3 formation by 28%. Tetradecanoylphorbol Acetate 23-26 kininogen 1 Homo sapiens 52-54 8890934-5 1996 Activation of PKC with TPA diminished the number of BK receptors by 33% and proportionally decreased BK-mediated Ins(1,4,5)P3 formation by 28%. Tetradecanoylphorbol Acetate 23-26 kininogen 1 Homo sapiens 101-103 9203625-8 1997 This reduction in PKC-alpha was sufficient to inhibit the reduction of bradykinin-induced calcium mobilization by TPA. Tetradecanoylphorbol Acetate 114-117 kininogen 1 Homo sapiens 71-81 8043027-1 1994 Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min. Tetradecanoylphorbol Acetate 139-175 kininogen 1 Homo sapiens 0-10 7473001-4 1995 Similar to BK, two phorbol esters, phorbol 12,13 dibutyrate (PDBu) and phorbol 12-myristate-13-acetate (PMA) which are known to stimulate protein kinase C (PKC), synergistically enhanced the TNF alpha induced IL-1 beta production in the gingival fibroblasts. Tetradecanoylphorbol Acetate 104-107 kininogen 1 Homo sapiens 11-13 7772573-6 1995 Pretreatment with phorbol-12-myristate-13-acetate (PMA), a protein kinase C (PKC) activator, significantly resulted in reduction of the descending shoulder of BK-induced increase in [Ca2+]i. Tetradecanoylphorbol Acetate 51-54 kininogen 1 Homo sapiens 159-161 7772573-8 1995 Furthermore, the BK-induced [45Ca] uptake was inhibited by EGTA and PMA. Tetradecanoylphorbol Acetate 68-71 kininogen 1 Homo sapiens 17-19 7772573-6 1995 Pretreatment with phorbol-12-myristate-13-acetate (PMA), a protein kinase C (PKC) activator, significantly resulted in reduction of the descending shoulder of BK-induced increase in [Ca2+]i. Tetradecanoylphorbol Acetate 18-49 kininogen 1 Homo sapiens 159-161 8043027-1 1994 Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min. Tetradecanoylphorbol Acetate 139-175 kininogen 1 Homo sapiens 12-14 8043027-1 1994 Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min. Tetradecanoylphorbol Acetate 177-180 kininogen 1 Homo sapiens 0-10 8043027-1 1994 Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min. Tetradecanoylphorbol Acetate 177-180 kininogen 1 Homo sapiens 12-14 8043027-6 1994 Although pre-treatment of SH-SY5Y cells with TPA enhanced BK-evoked [3H]NA release, the elevation of intracellular calcium [Ca2+]; was decreased by about 50%. Tetradecanoylphorbol Acetate 45-48 kininogen 1 Homo sapiens 58-60 8373725-6 1993 Bradykinin-stimulated release of arachidonic acid was prevented by down-regulating protein kinase C by pretreatment with phorbol 12-myristate 13-acetate and was unaffected by inhibitors of protein synthesis actinomycin D or cycloheximide. Tetradecanoylphorbol Acetate 121-152 kininogen 1 Homo sapiens 0-10 8408228-4 1993 Different from the stimulations with ATP and TPA, the effect of bradykinin of decreasing the high-affinity EGF binding was transient (a minimum binding at 2.5 min); the reduced EGF binding was, however, sustained for up to 30 min in the presence of calyculin A, a phosphoprotein phosphatase inhibitor. Tetradecanoylphorbol Acetate 45-48 kininogen 1 Homo sapiens 64-74 2037585-7 1991 Short pretreatment of the cells with phorbol 12-myristate 13-acetate (PMA) abolished the BK-induced breakdown of phosphoinositides, but did not affect the second-phase DGc level. Tetradecanoylphorbol Acetate 37-68 kininogen 1 Homo sapiens 89-91 2037585-7 1991 Short pretreatment of the cells with phorbol 12-myristate 13-acetate (PMA) abolished the BK-induced breakdown of phosphoinositides, but did not affect the second-phase DGc level. Tetradecanoylphorbol Acetate 70-73 kininogen 1 Homo sapiens 89-91 2037585-10 1991 In contrast, two inhibitors of PKC, staurosporin and 1-O-hexadecyl-2-O-methylglycerol, inhibited both BK- and PMA-induced DGc formation at 30 min, leaving the rapid response towards BK unaffected. Tetradecanoylphorbol Acetate 110-113 kininogen 1 Homo sapiens 182-184 2174449-7 1990 Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content. Tetradecanoylphorbol Acetate 54-57 kininogen 1 Homo sapiens 100-110 1703413-9 1991 Similarly, staurosporine, a relatively selective inhibitor of protein kinase C, and the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) an activator of this enzyme, both have pronounced effects on IgE-mediated histamine release from SMC but were completely inactive with regard to [DArg0-Hyp3-DPhe7]-bradykinin-stimulated release. Tetradecanoylphorbol Acetate 103-139 kininogen 1 Homo sapiens 310-320 1703413-9 1991 Similarly, staurosporine, a relatively selective inhibitor of protein kinase C, and the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) an activator of this enzyme, both have pronounced effects on IgE-mediated histamine release from SMC but were completely inactive with regard to [DArg0-Hyp3-DPhe7]-bradykinin-stimulated release. Tetradecanoylphorbol Acetate 141-144 kininogen 1 Homo sapiens 310-320 1708255-9 1991 The inactivation of bradykinin by intact neutrophils was decreased by phorbol 12-myristate 13-acetate, probably due to down-regulation by endocytosis of the neutral endopeptidase on the plasma membrane. Tetradecanoylphorbol Acetate 70-101 kininogen 1 Homo sapiens 20-30 1812285-5 1991 Furthermore, preincubation of endothelial cell with phorbol-12-myristate-13-acetate (PMA) abolished the stimulatory effect of bradykinin on the formation of 1,4,5-IP3 and 1,3,4,5-IP4, but did not affect the longlasting Ca(2+)-influx. Tetradecanoylphorbol Acetate 52-83 kininogen 1 Homo sapiens 126-136 1812285-5 1991 Furthermore, preincubation of endothelial cell with phorbol-12-myristate-13-acetate (PMA) abolished the stimulatory effect of bradykinin on the formation of 1,4,5-IP3 and 1,3,4,5-IP4, but did not affect the longlasting Ca(2+)-influx. Tetradecanoylphorbol Acetate 85-88 kininogen 1 Homo sapiens 126-136 2174449-7 1990 Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content. Tetradecanoylphorbol Acetate 54-57 kininogen 1 Homo sapiens 208-218 1963797-10 1990 Pretreatment for 10 min with TPA (but not the relatively inactive 4-methoxy TPA) or the non-phorbol protein kinase C stimulator mezerein potently inhibited bradykinin- and histamine-stimulated accumulation of total [3H]-inositol phosphate; inhibition of [3H]-inositol phosphate formation was also seen with 24 h TPA treatment. Tetradecanoylphorbol Acetate 29-32 kininogen 1 Homo sapiens 156-166 2643439-6 1989 Exposure of human umbilical vein endothelial cells to bradykinin, thrombin or interleukin-1 resulted in negligible release of either hexosaminidase or lactate dehydrogenase (LDH), in contrast to phorbol myristate acetate, which caused a parallel, dose-dependent release of both enzymes. Tetradecanoylphorbol Acetate 195-220 kininogen 1 Homo sapiens 54-64 3138977-9 1988 Treatment of the cells with 12-O-tetradecanoylphorbol 13-acetate completely abolishes the response to EGF and to sub-optimal doses of bradykinin, suggesting a negative-feedback function of protein kinase C. Pretreatment of the cells with pertussis toxin has no effect on inositol phosphate formation induced by either EGF or bradykinin. Tetradecanoylphorbol Acetate 28-64 kininogen 1 Homo sapiens 134-144 3138977-9 1988 Treatment of the cells with 12-O-tetradecanoylphorbol 13-acetate completely abolishes the response to EGF and to sub-optimal doses of bradykinin, suggesting a negative-feedback function of protein kinase C. Pretreatment of the cells with pertussis toxin has no effect on inositol phosphate formation induced by either EGF or bradykinin. Tetradecanoylphorbol Acetate 28-64 kininogen 1 Homo sapiens 325-335 2888113-6 1987 Phorbol 12-myristate 13-acetate enhanced bradykinin-stimulated PGE2 synthesis but inhibited bradykinin-stimulated InsP formation. Tetradecanoylphorbol Acetate 0-31 kininogen 1 Homo sapiens 41-51 2888113-6 1987 Phorbol 12-myristate 13-acetate enhanced bradykinin-stimulated PGE2 synthesis but inhibited bradykinin-stimulated InsP formation. Tetradecanoylphorbol Acetate 0-31 kininogen 1 Homo sapiens 92-102