PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10940738-6 2000 VIP and PACAP38 activation of ERK2 was blocked by the protein kinase A inhibitor H89, whereas the protein kinase C inhibitor GF109203X, or prior PMA-induced depletion of the protein kinases C, failed to inhibit VIP and PACAP38 activation of ERK2. Tetradecanoylphorbol Acetate 145-148 vasoactive intestinal peptide Rattus norvegicus 0-3 2474814-2 1989 Pretreatment of acini with TPA (10(-6) M) for 5 min at 37 degrees C potentiated their subsequent response to stimulation by VIP at a dose range of 10(-8)-10(-6) M in that the treated pancreatic acini released more amylase than could be accounted for by the additive effects of VIP or TPA acting individually. Tetradecanoylphorbol Acetate 27-30 vasoactive intestinal peptide Rattus norvegicus 124-127 2474814-2 1989 Pretreatment of acini with TPA (10(-6) M) for 5 min at 37 degrees C potentiated their subsequent response to stimulation by VIP at a dose range of 10(-8)-10(-6) M in that the treated pancreatic acini released more amylase than could be accounted for by the additive effects of VIP or TPA acting individually. Tetradecanoylphorbol Acetate 27-30 vasoactive intestinal peptide Rattus norvegicus 277-280 2474814-2 1989 Pretreatment of acini with TPA (10(-6) M) for 5 min at 37 degrees C potentiated their subsequent response to stimulation by VIP at a dose range of 10(-8)-10(-6) M in that the treated pancreatic acini released more amylase than could be accounted for by the additive effects of VIP or TPA acting individually. Tetradecanoylphorbol Acetate 284-287 vasoactive intestinal peptide Rattus norvegicus 124-127 2474814-3 1989 This potentiation effect of TPA was still evident when isobutyl methylxanthine was given together with VIP. Tetradecanoylphorbol Acetate 28-31 vasoactive intestinal peptide Rattus norvegicus 103-106 2474814-5 1989 The TPA preincubation was found also to potentiate VIP-stimulated net increases in intracellular cyclic AMP (cAMP) levels. Tetradecanoylphorbol Acetate 4-7 vasoactive intestinal peptide Rattus norvegicus 51-54 2474814-7 1989 This suggested that TPA potentiated the response of rat pancreatic acini to VIP by modulating the cAMP system. Tetradecanoylphorbol Acetate 20-23 vasoactive intestinal peptide Rattus norvegicus 76-79 2845113-3 1988 In contrast, PMA enhanced the cyclic AMP response to vasoactive intestinal peptide (VIP) and forskolin in cerebral cortical and diencephalic cells, whereas 4 alpha-PDD was inactive. Tetradecanoylphorbol Acetate 13-16 vasoactive intestinal peptide Rattus norvegicus 84-87 2825698-1 1987 Pretreatment of rat prostatic epithelial cells with the tumor-promoting phorbol ester 4 beta-phorbol 12-myristate 13-acetate resulted in a decrease of both the potency of vasoactive intestinal peptide (VIP) upon the stimulation of cyclic AMP accumulation and the affinity of the receptors of this peptide. Tetradecanoylphorbol Acetate 88-124 vasoactive intestinal peptide Rattus norvegicus 202-205 9815052-7 1998 12-O-tetradecanoylphorbol 13-acetate (TPA) also reduced the magnitude of the potentiation of amylase release caused by VIP plus CCK-8 or CCh, although TPA itself decreased neither VIP-stimulated adenylyl cyclase activity nor intracellular cAMP accumulation. Tetradecanoylphorbol Acetate 0-36 vasoactive intestinal peptide Rattus norvegicus 119-122 9815052-7 1998 12-O-tetradecanoylphorbol 13-acetate (TPA) also reduced the magnitude of the potentiation of amylase release caused by VIP plus CCK-8 or CCh, although TPA itself decreased neither VIP-stimulated adenylyl cyclase activity nor intracellular cAMP accumulation. Tetradecanoylphorbol Acetate 38-41 vasoactive intestinal peptide Rattus norvegicus 119-122 9815052-7 1998 12-O-tetradecanoylphorbol 13-acetate (TPA) also reduced the magnitude of the potentiation of amylase release caused by VIP plus CCK-8 or CCh, although TPA itself decreased neither VIP-stimulated adenylyl cyclase activity nor intracellular cAMP accumulation. Tetradecanoylphorbol Acetate 38-41 vasoactive intestinal peptide Rattus norvegicus 180-183 8708540-6 1996 Both PACAP- and VIP-stimulated cAMP accumulation were potentiated by 4 beta-phorbol 12-myristate 13-acetate, an activator of protein kinase C. Two PACAP antagonists, PACAP 6-27 (3 x 10(-6) M) and PACAP 6-38 (3 x 10(-6) M), blocked PACAP- and VIP-stimulated cAMP accumulation. Tetradecanoylphorbol Acetate 69-107 vasoactive intestinal peptide Rattus norvegicus 16-19 9307112-13 1997 The activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases the amplitude of the Ca2+ current, diminishes facilitation, and reduces the inhibition of this current by UK14304 and VIP. Tetradecanoylphorbol Acetate 46-77 vasoactive intestinal peptide Rattus norvegicus 212-215 9307112-13 1997 The activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases the amplitude of the Ca2+ current, diminishes facilitation, and reduces the inhibition of this current by UK14304 and VIP. Tetradecanoylphorbol Acetate 79-82 vasoactive intestinal peptide Rattus norvegicus 212-215 9075734-7 1997 Down-regulation of PKC activity by long term 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment (24 h) diminished, but did not abolish, the effect of SP on VIP-stimulated cAMP production. Tetradecanoylphorbol Acetate 83-86 vasoactive intestinal peptide Rattus norvegicus 158-161 9075734-9 1997 TPA, which translocates PKC alpha, beta, and delta in lactotrophs, had a synergistic effect on cAMP formation induced by VIP, but did also, unlike SP, display cAMP rising abilities when cells were not exposed to VIP and forskolin. Tetradecanoylphorbol Acetate 0-3 vasoactive intestinal peptide Rattus norvegicus 121-124 9075734-9 1997 TPA, which translocates PKC alpha, beta, and delta in lactotrophs, had a synergistic effect on cAMP formation induced by VIP, but did also, unlike SP, display cAMP rising abilities when cells were not exposed to VIP and forskolin. Tetradecanoylphorbol Acetate 0-3 vasoactive intestinal peptide Rattus norvegicus 212-215 8543566-6 1995 The addition of phorbol 12-myristate 13-acetate (PMA) or agents elevating the cyclic AMP content, such as vasoactive intestinal peptide (VIP) or an adenosine analog, also stimulated [3H]NA release. Tetradecanoylphorbol Acetate 16-47 vasoactive intestinal peptide Rattus norvegicus 137-140 8278627-7 1993 The study of the mechanism of action of this neuropeptide showed that protein kinase C (PKC) was activated in the presence of VIP concentrations from 10(-10) to 10(-8) M in a similar way to that found with a specific PKC activator such as phorbol myristate acetate (PMA, 50 ng/ml). Tetradecanoylphorbol Acetate 239-264 vasoactive intestinal peptide Rattus norvegicus 126-129 7768335-3 1995 The induction of the VIP mRNA was enhanced by the simultaneous treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 78-114 vasoactive intestinal peptide Rattus norvegicus 21-24 7768335-3 1995 The induction of the VIP mRNA was enhanced by the simultaneous treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 116-119 vasoactive intestinal peptide Rattus norvegicus 21-24 7768335-4 1995 PC12 cells stimulated with forskolin plus TPA released immunoreactive VIP. Tetradecanoylphorbol Acetate 42-45 vasoactive intestinal peptide Rattus norvegicus 70-73 8278627-7 1993 The study of the mechanism of action of this neuropeptide showed that protein kinase C (PKC) was activated in the presence of VIP concentrations from 10(-10) to 10(-8) M in a similar way to that found with a specific PKC activator such as phorbol myristate acetate (PMA, 50 ng/ml). Tetradecanoylphorbol Acetate 266-269 vasoactive intestinal peptide Rattus norvegicus 126-129 1846590-5 1991 Potentiation of the cAMP response to VIP can be produced in LD cells by treatment with agents that elevate intracellular Ca2+ (depolarizing concentrations of K+ or A23187) or an activator of protein kinase-C [14 beta-phorbol 12-myristate 13-acetate (PMA)]. Tetradecanoylphorbol Acetate 212-248 vasoactive intestinal peptide Rattus norvegicus 37-40 1846590-5 1991 Potentiation of the cAMP response to VIP can be produced in LD cells by treatment with agents that elevate intracellular Ca2+ (depolarizing concentrations of K+ or A23187) or an activator of protein kinase-C [14 beta-phorbol 12-myristate 13-acetate (PMA)]. Tetradecanoylphorbol Acetate 250-253 vasoactive intestinal peptide Rattus norvegicus 37-40 1846590-7 1991 In contrast, LL treatment augmented the PMA potentiation of VIP-stimulated cAMP response. Tetradecanoylphorbol Acetate 40-43 vasoactive intestinal peptide Rattus norvegicus 60-63 2174276-4 1990 The drug enhanced vasoactive intestinal polypeptide (VIP)-stimulated PRL-secretion, while thyroliberin (TRH)- and 12-0-tetradecanoyl phorbol-13-acetate (TPA)-elicited PRL egress were slightly reduced indicating a cAMP-mediated reduction of protein kinase C (PK-C) mediated PRL release. Tetradecanoylphorbol Acetate 153-156 vasoactive intestinal peptide Rattus norvegicus 53-56 7479387-2 1995 The treatment of cells with the PKC activator phorbol 12-myristate 13-acetate (PMA) resulted in an impairment of the stimulation of adenylyl cyclase activity in terms of both potency, as seen with both vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating peptide (PACAP-27), and efficacy, as seen with the beta-adrenergic agonist isoproterenol. Tetradecanoylphorbol Acetate 46-77 vasoactive intestinal peptide Rattus norvegicus 233-236 7479387-2 1995 The treatment of cells with the PKC activator phorbol 12-myristate 13-acetate (PMA) resulted in an impairment of the stimulation of adenylyl cyclase activity in terms of both potency, as seen with both vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating peptide (PACAP-27), and efficacy, as seen with the beta-adrenergic agonist isoproterenol. Tetradecanoylphorbol Acetate 79-82 vasoactive intestinal peptide Rattus norvegicus 233-236