AKT Signaling in Physiology and Disease

被引:116
作者
Vasudevan, Krishna M. [1 ,2 ,3 ]
Garraway, Levi A. [1 ,2 ,3 ,4 ]
机构
[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Canc Genome Discovery, Boston, MA 02115 USA
[3] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med, Boston, MA 02115 USA
[4] 7 Cambridge Ctr, Broad Inst, Cambridge, MA 02142 USA
来源
PHOSPHOINOSITIDE 3-KINASE IN HEALTH AND DISEASE, VOL 2 | 2011年 / 347卷
关键词
PROTEIN-KINASE-B; PROSTATE INTRAEPITHELIAL NEOPLASIA; PLECKSTRIN-HOMOLOGY DOMAIN; INHIBITS AKT/PKB ACTIVATION; SERINE-THREONINE KINASE; PHOSPHATIDYLINOSITOL; 3-KINASE; TYROSINE KINASE; PHOSPHOINOSITIDE; INSULIN-RESISTANCE; MOLECULAR-CLONING;
D O I
10.1007/82_2010_66
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The serine/threonine kinase AKT functions as a critical mediator of signaling downstream of PI3 kinase. Studies over the last two decades have firmly established the importance of AKT in the regulation of cell survival, proliferation, and insulin-dependent metabolic cell responses. AKT executes these diverse tasks through phosphorylation of numerous cellular substrates. Substantial progress has been made in understanding the regulation of AKT activity by upstream kinases and elucidating downstream mechanisms that mediate its myriad cellular effects. Here, we present an overview of AKT regulation and function in physiological and pathological settings. An emphasis is placed on the involvement of aberrant AKT signaling in human diseases ranging from diabetes to cancer and neurological diseases.
引用
收藏
页码:105 / 133
页数:29
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