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佛波酯而非胰岛素可促使大鼠脂肪细胞中的胞质蛋白激酶C耗竭。

Phorbol esters, but not insulin, promote depletion of cytosolic protein kinase C in rat adipocytes.

作者信息

Glynn B P, Colliton J W, McDermott J M, Witters L A

出版信息

Biochem Biophys Res Commun. 1986 Mar 28;135(3):1119-25. doi: 10.1016/0006-291x(86)91044-2.

Abstract

The tumor-promoting phorbol esters have insulinomimetic effects in several tissues. Employing two different assay systems, we have compared the effects of phorbol ester and insulin on the activity and intracellular distribution of the Ca++ and phospholipid dependent protein kinase (protein kinase C) in isolated rat adipocytes. Phorbol ester leads to a prompt depletion of kinase activity from the cytosolic fraction and appearance of activity in membrane extracts; neither of these effects is mimicked by insulin. These results, taken together with other data, emphasize important divergences between the actions of these agonists and suggest that changes in protein kinase C activity or intracellular distribution are not a necessary concomitant of the cascade of insulin action.

摘要

促肿瘤佛波酯在多种组织中具有类胰岛素作用。我们采用两种不同的检测系统,比较了佛波酯和胰岛素对分离的大鼠脂肪细胞中钙和磷脂依赖性蛋白激酶(蛋白激酶C)活性及细胞内分布的影响。佛波酯导致激酶活性迅速从胞质部分耗竭,并在膜提取物中出现活性;胰岛素不会模拟这两种作用。这些结果与其他数据一起,强调了这些激动剂作用之间的重要差异,并表明蛋白激酶C活性或细胞内分布的变化并非胰岛素作用级联反应的必然伴随现象。

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