PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8734475-5 1996 Prolonged exposure to TPA reduced the subsequent GH response to TPA equally in neonates and adults, but differentially affected the GH response to GHRH; TPA exposure reduced the GH response to GHRH in neonates, but not in adults. Tetradecanoylphorbol Acetate 22-25 growth hormone releasing hormone Rattus norvegicus 147-151 7649093-11 1995 The effect of GHRH on GHF-1 mRNA levels could be mimicked by direct activators of second messenger signaling systems such as forskolin (10(-5) M) or the phorbol ester tumor promoter tetradecanoyl phorbol acetate (TPA) (10(-6) M). Tetradecanoylphorbol Acetate 213-216 growth hormone releasing hormone Rattus norvegicus 14-18 1678698-6 1991 Potentiation by phorbol 12-myristate 13-acetate of forskolin-stimulated GHRH and SS release was observed. Tetradecanoylphorbol Acetate 16-47 growth hormone releasing hormone Rattus norvegicus 72-76 2535800-6 1989 In nonpretreated cultures, forskolin (1-100 microM) and the protein kinase C activator phorbol 12-myristate 13-acetate (10 nM-1 microM), stimulated basal GRF release in a dose-dependent fashion. Tetradecanoylphorbol Acetate 87-118 growth hormone releasing hormone Rattus norvegicus 154-157 2535800-7 1989 The Ca2+ channel blocker verapamil (100 microM) significantly inhibited the GRF response to both forskolin and phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 111-142 growth hormone releasing hormone Rattus norvegicus 76-79 3141549-2 1988 Pretreatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) for 3 h significantly suppressed the rGH release induced by GRF, but not that by 8-bromo-cAMP 20 h later; this suppressive effect of TPA was concentration-dependent from 8 to 160 nmol/l, and complete suppression was observed after pretreatment with 80-160 nmol TPA/l. Tetradecanoylphorbol Acetate 18-54 growth hormone releasing hormone Rattus norvegicus 121-124 3141549-2 1988 Pretreatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) for 3 h significantly suppressed the rGH release induced by GRF, but not that by 8-bromo-cAMP 20 h later; this suppressive effect of TPA was concentration-dependent from 8 to 160 nmol/l, and complete suppression was observed after pretreatment with 80-160 nmol TPA/l. Tetradecanoylphorbol Acetate 56-59 growth hormone releasing hormone Rattus norvegicus 121-124 3141549-3 1988 Production of cAMP by pituitary cells stimulated with GRF was similarly attenuated in TPA-pretreated cells. Tetradecanoylphorbol Acetate 86-89 growth hormone releasing hormone Rattus norvegicus 54-57 3141549-4 1988 The rGH responsiveness to GRF of these cells was fully recovered on prolonged culture (40 h), suggesting that the inhibitory effect of TPA is reversible. Tetradecanoylphorbol Acetate 135-138 growth hormone releasing hormone Rattus norvegicus 26-29 3141549-5 1988 In contrast, pretreatment with GRF (5 nmol/l) resulted in suppression of the rGH response to subsequent exposure to GRF (5 nmol/l) or 8-bromo-cAMP (10 mmol/l), but not to TPA. Tetradecanoylphorbol Acetate 171-174 growth hormone releasing hormone Rattus norvegicus 31-34 3141549-5 1988 In contrast, pretreatment with GRF (5 nmol/l) resulted in suppression of the rGH response to subsequent exposure to GRF (5 nmol/l) or 8-bromo-cAMP (10 mmol/l), but not to TPA. Tetradecanoylphorbol Acetate 171-174 growth hormone releasing hormone Rattus norvegicus 116-119 3141549-6 1988 These observations suggest that pretreatment with TPA modifies the rGH response to GRF at steps before the formation of cAMP. Tetradecanoylphorbol Acetate 50-53 growth hormone releasing hormone Rattus norvegicus 83-86 2896538-6 1987 Incubation in a low calcium medium that totally blocks GRF-stimulated GH release also inhibits TPA-stimulated GH release. Tetradecanoylphorbol Acetate 95-98 growth hormone releasing hormone Rattus norvegicus 55-58