Synergy in activating class I PI3Ks

被引：169

作者：

Burke, John E. ^{[1
]}

Williams, Roger L. ^{[2
]}

机构：

[1] Univ Victoria, Dept Biochem & Microbiol, Victoria V8P 5C2, BC, Canada

[2] MRC, Mol Biol Lab, Cambridge CB2 0QH, England

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2015年 / 40卷 / 02期

基金：

加拿大自然科学与工程研究理事会;

关键词：

phosphoinositide; 3; kinases; lipid signaling; cancer; phosphoinositides; primary immunodeficiencies; lipid kinases; PHOSPHOINOSITIDE 3-KINASE ACTIVATION; PROTEIN-COUPLED RECEPTORS; G-BETA-GAMMA; PHOSPHATIDYLINOSITOL; 3-KINASE; B-CELL; HIGH-FREQUENCY; SELECTIVE INHIBITOR; P110-DELTA ISOFORMS; MEDIATED ACTIVATION; P110-ALPHA ISOFORM;

D O I：

10.1016/j.tibs.2014.12.003

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：

The class I phosphoinositide 3-kinases (PI3Ks) are lipid kinases that transduce a host of cellular signals and regulate a broad range of essential functions including growth, proliferation, and migration. As such, PI3Ks have pivotal roles in diseases such as cancer, diabetes, primary immune disorders, and inflammation. These enzymes are activated downstream of numerous activating stimuli including receptor tyrosine kinases, G protein-coupled receptors (GPCRs), and the Ras superfamily of small G proteins. A major challenge is to decipher how each PI3K isoform is able to successfully synergize these inputs into their intended signaling function. This article highlights recent progress in characterizing the molecular mechanisms of PI3K isoform-specific activation pathways, as well as novel roles for PI3Ks in human diseases, specifically cancer and immune diseases.

引用

页码：88 / 100

页数：13

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