Phosphoinositide 3-kinase in disease: timing, location, and scaffolding

被引：169

作者：

Wymann, MP ^{[1
]}

Marone, R ^{[1
]}

机构：

[1] Univ Basel, Biomed Ctr, Dept Clin & Biol Sci, Inst Biochem & Genet, CH-4058 Basel, Switzerland

来源：

CURRENT OPINION IN CELL BIOLOGY | 2005年 / 17卷 / 02期

关键词：

D O I：

10.1016/j.ceb.2005.02.011

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

When PI3Ks are deregulated by aberrant surface receptors or modulators, accumulation of PtdIns(3,4,5)P-3 leads to increased cell growth, proliferation and contact-independent survival. The PI3K/PKB/TOR axis controls protein synthesis and growth, while PtdIns(3,4,5)P-3-mediated activation of Rho GTPases directs cell motility. PI3K activity has been linked to the formation of tumors, metastasis, chronic inflammation, allergy and cardiovascular disease. Although increased PtdIns(3,4,5)P-3 is a well-established cause of disease, it is seldom known which PI3K isoform is implied. Recent work has demonstrated that PI3K gamma contributes to the control of cAMP levels in the cardiac system, where the protein acts as a scaffold, but not as a lipid kinase.

引用

页码：141 / 149

页数：9

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