SGK1: The Dark Side of PI3K Signaling

被引：82

作者：

Di Cristofano, Antonio ^{[1
]}

机构：

[1] Albert Einstein Coll Med, Bronx, NY 10467 USA

来源：

PROTEIN KINASES IN DEVELOPMENT AND DISEASE | 2017年 / 123卷

关键词：

AGC kinases; AKT; PDK1; PI3K; SGK1; GLUCOCORTICOID-INDUCIBLE KINASE; REGULATED PROTEIN-KINASE; TARGETED MICE LACKING; HOMOLOGY DOMAIN; SERUM; ACTIVATION; PHOSPHORYLATION; INSULIN; GROWTH; EXPRESSION;

D O I：

10.1016/bs.ctdb.2016.11.006

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Activation of the PI3K pathway is central to a variety of physiological and pathological processes. In these contexts, AKT is classically considered the de facto mediator of PI3K-dependent signaling. However, in recent years, accumulating data point to the existence of additional effectors of PI3K activity, parallel to and independent of AKT, that play critical and unique roles in mediating different developmental, homeostatic, and pathological processes. In this review, I summarize and discuss our current understanding of the function of the serine/threonine kinase SGK1 as a downstream effector of PI3K, and try to separate targets and pathways validated as uniquely SGK1-dependent from those shared with AKT. 2017 Elsevier Inc. All rights reserved.

引用

页码：49 / +

页数：8

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