Conway B R, Laychock S G, Rubin R P
Department of Pharmacology and Toxicology, Medical College of Virginia, Richmond 23298.
Biochem Biophys Res Commun. 1991 Jul 31;178(2):780-5. doi: 10.1016/0006-291x(91)90176-8.
Carbachol (CCh) and epidermal growth factor (EGF) elicited a concentration-dependent increase in [32P]phosphatidyl-inositol-4-phosphate (PtdIns-4P) formation in homogenates derived from agonist-stimulated rat pancreatic acini. The combination of CCh and EGF produced a response which was not synergistic or additive. EGF, unlike CCh, failed to cause [32P]PtdIns-4,5P2 breakdown, suggesting different mechanisms involved in the stimulation of [32P]PtdIns-4P formation induced by EGF and CCh. We conclude that PtdIns kinase represents a key component of the signaling pathways utilized by EGF and CCh in exocrine pancreas.
卡巴胆碱（CCh）和表皮生长因子（EGF）可使来自激动剂刺激的大鼠胰腺腺泡的匀浆中[32P]磷脂酰肌醇-4-磷酸（PtdIns-4P）的生成呈浓度依赖性增加。CCh和EGF的联合作用产生的反应既无协同性也无加和性。与CCh不同，EGF未能引起[32P]PtdIns-4,5P2的分解，这表明EGF和CCh诱导[32P]PtdIns-4P生成的刺激机制不同。我们得出结论，磷脂酰肌醇激酶是EGF和CCh在外分泌胰腺中利用的信号通路的关键组成部分。
