PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9815052-1 1998 Exocrine pancreatic secretion stimulated by vasoactive intestinal polypeptide (VIP), which acts through the adenylyl cyclase-cAMP pathway, is potentiated by stimulation with other secretagogues such as CCK and carbachol (CCh). Carbachol 210-219 cholecystokinin Rattus norvegicus 202-205 9815052-1 1998 Exocrine pancreatic secretion stimulated by vasoactive intestinal polypeptide (VIP), which acts through the adenylyl cyclase-cAMP pathway, is potentiated by stimulation with other secretagogues such as CCK and carbachol (CCh). Carbachol 221-224 cholecystokinin Rattus norvegicus 202-205 9038886-7 1997 An opposite order of sensitivity was found for inhibition of PLC activity by anti-PLC-beta 3 antibody (carbachol > bombesin > CCK-8). Carbachol 103-112 cholecystokinin Rattus norvegicus 132-135 8897836-3 1996 In contrast, at higher supermaximal concentrations of agonists (> 300 pM CCK, > 1 microM CCh), which induce a large "peak-and-plateau" intracellular Ca2+ signal, all cells in the acinus appeared to increase Ca2+ concentration ([Ca2+]) in synchrony. Carbachol 95-98 cholecystokinin Rattus norvegicus 76-79 7529994-1 1995 Desensitization of rat pancreatic acinar cells with 0.1 mM carbamoylcholine (Cch) or 0.5 nM caerulein (CAE), a cholecystokinin (CCK) agonist, altered the subsequent secretory responses to these two agonists. Carbachol 59-75 cholecystokinin Rattus norvegicus 111-126 7948036-2 1994 Binding of [125I]CCK-8 to the high affinity state of the receptor was measured as carbachol-inhibitable binding of [125I]CCK-8, whereas binding of [125I]CCK-8 to the low affinity state was measured as carbachol-resistant binding of [125I]CCK-8. Carbachol 82-91 cholecystokinin Rattus norvegicus 17-20 7524683-3 1994 Treating acini with carbachol abolished the high affinity state of the CCK receptor and converted approximately 25% of the low affinity receptors to the very low affinity state. Carbachol 20-29 cholecystokinin Rattus norvegicus 71-74 7524683-4 1994 Carbachol treatment was particularly useful in establishing the values of Kd for the high and low affinity states for different CCK receptor agonists and antagonists. Carbachol 0-9 cholecystokinin Rattus norvegicus 128-131 7948036-2 1994 Binding of [125I]CCK-8 to the high affinity state of the receptor was measured as carbachol-inhibitable binding of [125I]CCK-8, whereas binding of [125I]CCK-8 to the low affinity state was measured as carbachol-resistant binding of [125I]CCK-8. Carbachol 82-91 cholecystokinin Rattus norvegicus 121-124 7948036-2 1994 Binding of [125I]CCK-8 to the high affinity state of the receptor was measured as carbachol-inhibitable binding of [125I]CCK-8, whereas binding of [125I]CCK-8 to the low affinity state was measured as carbachol-resistant binding of [125I]CCK-8. Carbachol 82-91 cholecystokinin Rattus norvegicus 121-124 7948036-2 1994 Binding of [125I]CCK-8 to the high affinity state of the receptor was measured as carbachol-inhibitable binding of [125I]CCK-8, whereas binding of [125I]CCK-8 to the low affinity state was measured as carbachol-resistant binding of [125I]CCK-8. Carbachol 82-91 cholecystokinin Rattus norvegicus 121-124 7948036-2 1994 Binding of [125I]CCK-8 to the high affinity state of the receptor was measured as carbachol-inhibitable binding of [125I]CCK-8, whereas binding of [125I]CCK-8 to the low affinity state was measured as carbachol-resistant binding of [125I]CCK-8. Carbachol 201-210 cholecystokinin Rattus norvegicus 17-20 1702070-1 1990 Chornic exogenous administration of cholecystokinin octapeptide (CCK8) to rats led to a reduced sensitivity of pancreatic acinar cells to both CCK8 and carbachol stimulation without changes in affinity or number of CCK or muscarinic receptors. Carbachol 152-161 cholecystokinin Rattus norvegicus 65-68 1722647-0 1991 Carbachol acts through protein kinase C to modulate cholecystokinin receptors on pancreatic acini. Carbachol 0-9 cholecystokinin Rattus norvegicus 52-67 1722647-4 1991 Preincubation with 0.1 mM carbachol for 60 min reduced the CCK octapeptide (CCK-8; 100 pM)-stimulated amylase release by 43 +/- 5%. Carbachol 26-35 cholecystokinin Rattus norvegicus 59-62 1722647-4 1991 Preincubation with 0.1 mM carbachol for 60 min reduced the CCK octapeptide (CCK-8; 100 pM)-stimulated amylase release by 43 +/- 5%. Carbachol 26-35 cholecystokinin Rattus norvegicus 76-79 1722647-7 1991 Preincubation of acini with 12-O-tetradecanoylphorbol 12,13-acetate (TPA, 1 microM), an activator of protein kinase C (PKC), decreased subsequent CCK-8-stimulated amylase release, and total binding of 125I-BH-CCK-8 to a similar extent as with pretreatment with CCh. Carbachol 261-264 cholecystokinin Rattus norvegicus 146-149 1722647-8 1991 The inhibitory effect of TPA or CCh on CCK-8-stimulated amylase release was reversed by simultaneous preincubation with H-7, an inhibitor of PKC. Carbachol 32-35 cholecystokinin Rattus norvegicus 39-42 1722647-10 1991 After CCh or TPA preincubation, CCK-8-stimulated production of [3H]inositol phosphates was inhibited by at least 49%. Carbachol 6-9 cholecystokinin Rattus norvegicus 32-35 6791509-6 1981 Carbachol mimicked both the stimulatory and inhibitory effects of CCK, whereas the Ca2+ ionophore A23187 mimicked only the inhibitory effects. Carbachol 0-9 cholecystokinin Rattus norvegicus 66-69 3101510-0 1987 Carbachol regulates cholecystokinin receptor on pancreatic acinar cells. Carbachol 0-9 cholecystokinin Rattus norvegicus 20-35 3101510-1 1987 We have examined the effect of carbamylcholine on the binding of cholecystokinin (CCK) to dispersed acini from rat pancreas. Carbachol 31-46 cholecystokinin Rattus norvegicus 65-80 3101510-1 1987 We have examined the effect of carbamylcholine on the binding of cholecystokinin (CCK) to dispersed acini from rat pancreas. Carbachol 31-46 cholecystokinin Rattus norvegicus 82-85 3101510-3 1987 Simultaneous addition of carbamylcholine inhibited binding of CCK to acini due to an apparent loss of high affinity CCK binding sites. Carbachol 25-40 cholecystokinin Rattus norvegicus 62-65 4047976-5 1985 The acetylcholine agonist carbachol, injected directly into the NTS region, effectively mimicked the actions of intraperitoneally administered CCK on feeding and exploration. Carbachol 26-35 cholecystokinin Rattus norvegicus 143-146 2450276-4 1988 Upon stimulation with carbamylcholine (CCh) or cholecystokinin (CCK), [Ca2+]i increased within seconds by 4- to 8-fold. Carbachol 22-37 cholecystokinin Rattus norvegicus 64-67 3101510-3 1987 Simultaneous addition of carbamylcholine inhibited binding of CCK to acini due to an apparent loss of high affinity CCK binding sites. Carbachol 25-40 cholecystokinin Rattus norvegicus 116-119 3101510-8 1987 These findings, at least in part, account for the inhibition of the CCK-induced stimulation of amylase secretion by carbamylcholine. Carbachol 116-131 cholecystokinin Rattus norvegicus 68-71 21527320-5 2011 When recording carbachol-evoked inhibitory postsynaptic currents (IPSCs) which presumably originate from CB1 expressing cholecystokinin (CCK) interneurons, we found that depolarization-induced suppression of inhibition (DSI) was impaired by the stress. Carbachol 15-24 cholecystokinin Rattus norvegicus 137-140 29270134-2 2017 Our previous in vitro studies with molecular approaches on AR42J cell showed that protein kinase D (PKD/PKD1) activation was required in NF-kappaB activation induced by cholecystokinin 8 (CCK) or carbachol (CCh) in pancreatic acinar cells. Carbachol 207-210 cholecystokinin Rattus norvegicus 188-191