PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2117049-6 1990 Quinacrine, a nonselective phospholipase A2 inhibitor, reduced the carbachol stimulation of adenylate cyclase activity, but this inhibition appeared to be competitive with a Ki of 0.2 microM. Carbachol 67-76 phospholipase A2 group IB Rattus norvegicus 27-43 2162060-7 1990 The carbachol inhibitory effect occurred under conditions that prevented activation of phospholipase A2, excluding a role of the arachidonic acid metabolism in this process. Carbachol 4-13 phospholipase A2 group IB Rattus norvegicus 87-103 3933882-0 1985 Stimulation by glucose and carbamylcholine of phospholipase A2 in pancreatic islets. Carbachol 27-42 phospholipase A2 group IB Rattus norvegicus 46-62 3879308-4 1985 Quinacrine, a phospholipase A2 inhibitor, methylene blue, a guanylate cyclase inhibitor and tetraethylammonium, a potassium permeability inhibitor, inhibited carbachol-induced relaxation and augmented the magnitude of norepinephrine-induced contraction only when endothelium was present. Carbachol 158-167 phospholipase A2 group IB Rattus norvegicus 14-30 3933882-5 1985 These results suggest that carbamylcholine and, to a lesser extent, glucose cause a Ca2+-dependent activation of phospholipase A2 in intact islet cells. Carbachol 27-42 phospholipase A2 group IB Rattus norvegicus 113-129 9117394-9 1996 Finally, the release of [3H]GABA evoked by the combined application of NMDA and carbachol (a treatment known to markedly stimulate arachidonic acid formation) was reduced by inhibitors of phospholipase A2 further indicating that endogenously formed arachidonic acid significantly facilitates the release of GABA in the striatum. Carbachol 80-89 phospholipase A2 group IB Rattus norvegicus 188-204 15814109-4 2005 Inhibitors of phospholipase A(2) (PLA(2)), COX and phospholipase C (PLC), calcium/calmodulin (CaM), NOS and soluble guanylate cyclase prevent the carbachol effect. Carbachol 146-155 phospholipase A2 group IB Rattus norvegicus 14-32 9726232-2 1998 In this study, we examined whether CCK-8 stimulates the Ca2+-independent form of PLA2 in isolated rat islets, in comparison with stimulation by the PLA2-activating cholinergic agonist carbachol. Carbachol 184-193 phospholipase A2 group IB Rattus norvegicus 148-152 9094163-3 1997 From enzymatic assays, PLA2 and diacylglycerol (DAG) lipase were activated by Cch and respectively inhibited by the PLA2 inhibitors, mepacrine and aristolochic acid, and by the DAG lipase inhibitor, RHC 80267. Carbachol 78-81 phospholipase A2 group IB Rattus norvegicus 23-27 9094163-3 1997 From enzymatic assays, PLA2 and diacylglycerol (DAG) lipase were activated by Cch and respectively inhibited by the PLA2 inhibitors, mepacrine and aristolochic acid, and by the DAG lipase inhibitor, RHC 80267. Carbachol 78-81 phospholipase A2 group IB Rattus norvegicus 116-120 9094163-8 1997 RHC 80267 and the PLA2 inhibitors separately and partially suppressed Cch-stimulated amylase secretion, with an additive effect observed when the DAG lipase and the PLA2 inhibitors were combined. Carbachol 70-73 phospholipase A2 group IB Rattus norvegicus 18-22 1636494-7 1992 The results of studies involving inhibitors of phospholipase A2 (PLA2) and phospholipase C (PLC) suggested that PLA2 is almost completely responsible for the Ca(2+)-dependent, carbachol-mediated AA liberation. Carbachol 176-185 phospholipase A2 group IB Rattus norvegicus 47-63 1636494-7 1992 The results of studies involving inhibitors of phospholipase A2 (PLA2) and phospholipase C (PLC) suggested that PLA2 is almost completely responsible for the Ca(2+)-dependent, carbachol-mediated AA liberation. Carbachol 176-185 phospholipase A2 group IB Rattus norvegicus 65-69 1636494-7 1992 The results of studies involving inhibitors of phospholipase A2 (PLA2) and phospholipase C (PLC) suggested that PLA2 is almost completely responsible for the Ca(2+)-dependent, carbachol-mediated AA liberation. Carbachol 176-185 phospholipase A2 group IB Rattus norvegicus 112-116 1910075-14 1991 Ca(2+)-dependent and carbachol-mediated AA liberation occurs mainly as the result of PLA2 action. Carbachol 21-30 phospholipase A2 group IB Rattus norvegicus 85-89 1848278-9 1991 Moreover, the inhibitory effect of 8-OH-DPAT on the carbachol response was blocked by 10 microM quinacrine (a phospholipase A2 inhibitor) but not by BW 755C (100 microM), a cyclooxygenase and lipoxygenase inhibitor. Carbachol 52-61 phospholipase A2 group IB Rattus norvegicus 110-126 1848278-10 1991 These results collectively suggest that 5-HT1A receptor activation inhibits carbachol-stimulated phosphoinositide turnover by stimulating a phospholipase A2 coupled to 5-HT1A receptors, leading to arachidonic acid release. Carbachol 76-85 phospholipase A2 group IB Rattus norvegicus 140-156 21153096-4 1996 From enzymatic assays, phospholipase A(2) and diacylglycerol lipase were activated by carbamylcholine and these activations were inhibited by the phospholipase A(2) inhibitors, mepacrine and aristolochic acid, and by the diacylglycerol lipase inhibitor RHC 80267. Carbachol 86-101 phospholipase A2 group IB Rattus norvegicus 23-67 1373616-1 1992 In intact rat pancreatic acini, the phospholipase A2 inhibitor mepacrine did not affect basal amylase release but dose-dependently inhibited the carbachol (IC50 65 microM) and CCK-8 (IC50 210 microM)-stimulated amylase release. Carbachol 145-154 phospholipase A2 group IB Rattus norvegicus 36-52 1373616-3 1992 From these results we conclude that carbachol, CCK-8 and GTPrS probably activate a phospholipase A2 closely coupled to exocytosis. Carbachol 36-45 phospholipase A2 group IB Rattus norvegicus 83-99