PKC AND THE SECRETION AND BIOSYNTHESIS OF NEUROPEPTIDES IN ATT-20 CELLS

蛋白质磷酸化增强是细胞内 这些事件总是发生在膜受体激活之后。 蛋白激酶C（Protein Kinase C，PKC）是近年来发现的一种独特的酶 磷酸化特定的蛋白质，其功能保持不变， 要有决心。 PKC需要磷脂和甘油二酯 (DAG)最大的活动。 DAG是以下物质的水解产物： 膜多磷酸肌醇（PI）分解， 在膜受体占据之后，并且是最初的 信号转导中的事件。 PI期间FAG的释放 营业额大大刺激PKC活性超过观察到的 在静止的细胞中。 已知的共致癌物或肿瘤促进剂， 12-0-十四酰基佛波醇13-乙酸酯（TPA）特异性地增加 膜PKC活性。 与此同时， 膜PKC活性是细胞溶质PKC活性的降低， 这表明PKC从胞浆到胞浆的转位 膜是重要的细胞内事件。 TPA处理AtT-20细胞导致剂量相关性增加 在BE分泌和PKC从胞质到胞质的转位中， 膜部分。 最刺激的浓度 TPA在1 min内使PKC活性增加2倍， 将AtT-20细胞与乙醇（0.1- 100%）预孵育。 0.6%）持续24小时，导致剂量相关的2-5倍降低， 胞浆PKC活性和膜PKC减少50% 0.4%乙醇的活性。 仅乙醇预处理24小时 轻微降低了最大刺激的能力， 浓度的TPA诱导PKC易位。

Enhanced protein phosphorylation is one of the intracellular events which invariably follows membrane receptor activation. Recently identified Protein Kinase C (PKC) is a unique enzyme which phosphorylates specific proteins, whose functions remain to be determine. PKC requires a phospholipid and a diacylglycerol (DAG) for maximal activity. DAG is the hydrolytic product of membrane polyphosphoinositide (PI) breakdown, which occurs following membrane receptor occupancy, and is one of the initial events in signal transduction. The release of FAG during PI turnover substantially stimulates PKC activity over that observed in quiescent cells. The known co-carcinogen or tumor promoter, 12-0-tetradecanoylphorbol 13-acetate (TPA) specifically increases membrane PKC activity. Associated with this increased membrane PKC activity is a reduction of cytosolic PKC activity, which suggest that translocation of PKC from the cytosol to the membrane is an important intracellular event. TPA treatment of AtT-20 cells resulted in a dose-related increase in BE secretion and translocation of PKC from the cytosolic to the membrane fraction. A maximally-stimulating concentration of TPA enhanced PKC activity 2-fold within 1 min and 5-fold within 3 min. Preincubation of AtT-20 cells with ethanol (0.1- 0.6%) for 24 hours resulted in a dose-related 2-5 fold reduction in cytosolic PKC activity and a 50% reduction in membrane PKC activity at .0.4% ethanol. Ethanol pretreatment for 24 hours only marginally reduced the ability of a maximal stimulatory concentration of TPA to induce translocation of PKC.