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蛋白激酶B/Akt激活的机制与后果

Mechanisms and consequences of activation of protein kinase B/Akt.

作者信息

Downward J

机构信息

Imperial Cancer Research Fund, London, UK.

出版信息

Curr Opin Cell Biol. 1998 Apr;10(2):262-7. doi: 10.1016/s0955-0674(98)80149-x.

DOI:10.1016/s0955-0674(98)80149-x
PMID:9561851
Abstract

Protein kinase B (PKB)/Akt is a growth-factor-regulated serine/threonine kinase which contains a pleckstrin homology domain. Binding of phosphoinositide 3-OH kinase products to the pleckstrin homology domain results in translocation of PKB/Akt to the plasma membrane where it is activated by phosphorylation by upstream kinases including the phosphoinoside-dependent kinase 1 (PDK1). Activated PKB/Akt provides a survival signal that protects cells from apoptosis induced by various stresses, and also mediates a number of metabolic effects of insulin.

摘要

蛋白激酶B(PKB)/Akt是一种受生长因子调节的丝氨酸/苏氨酸激酶,含有一个普列克底物蛋白同源结构域。磷酸肌醇3-羟基激酶产物与普列克底物蛋白同源结构域的结合导致PKB/Akt转位至质膜,在质膜上它被包括磷酸肌醇依赖性激酶1(PDK1)在内的上游激酶磷酸化而激活。活化的PKB/Akt提供一种存活信号,保护细胞免受各种应激诱导的凋亡,并且还介导胰岛素的许多代谢效应。

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