PI 3-kinase, Akt and cell survival

被引：649

作者：

Downward, J ^{[1
]}

机构：

[1] Canc Res UK, London Res Inst, London WC2A 3PX, England

来源：

SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY | 2004年 / 15卷 / 02期

关键词：

Akt; Bcl-2; Bax; FoxO; PKB; p53; p73;

D O I：

10.1016/j.semcdb.2004.01.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Phosphoinositide 3-OH kinase (PI 3-kinase) provides cells with a survival signal that allows them to withstand apoptotic stimuli. Many tumour cells display elevated levels of PI 3-kinase products as a result of deletion of the phosphatase PTEN, activation of Ras or expression of autocrine growth factors. As a result they are relatively resistant to apoptosis. The mechanisms for PI 3-kinase survival signalling are becoming clear. The principal mediator is Akt, a PI 3-kinase activated protein kinase. Akt has direct effects on the apoptosis machinery, for example targeting the pro-apoptotic Bcl-2 related protein, BAD. It also affects the transcriptional response to apoptotic stimuli, for example by acting on Forkhead factors and also influence the activity of the p53 family. In addition, novel connections between the metabolic effects of Akt and its control of survival have recently been made. (C) 2004 Elsevier Ltd. All rights reserved.

引用

页码：177 / 182

页数：6

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