The emerging mechanisms of isoform-specific PI3K signalling

被引：1399

作者：

Vanhaesebroeck, Bart ^{[1
]}

Guillermet-Guibert, Julie ^{[1
]}

Graupera, Mariona ^{[1
]}

Bilanges, Benoit ^{[1
]}

机构：

[1] Queen Mary Univ London, Ctr Cell Signalling, Inst Canc, London EC1M 6BQ, England

来源：

NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2010年 / 11卷 / 05期

基金：

英国医学研究理事会;

关键词：

II PHOSPHOINOSITIDE 3-KINASE; CANCER-SPECIFIC MUTATIONS; GROWTH-FACTOR RECEPTOR; LIPID KINASE-ACTIVITY; PHOSPHATIDYLINOSITOL; 3-KINASE; DISTINCT ROLES; CELL-MIGRATION; CAENORHABDITIS-ELEGANS; PHAGOSOME MATURATION; REGULATES AUTOPHAGY;

D O I：

10.1038/nrm2882

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Phosphoinositide 3-kinases (PI3Ks) function early in intracellular signal transduction pathways and affect many biological functions. A further level of complexity derives from the existence of eight PI3K isoforms, which are divided into class I, class II and class III PI3Ks. PI3K signalling has been implicated in metabolic control, immunity, angiogenesis and cardiovascular homeostasis, and is one of the most frequently deregulated pathways in cancer. PI3K inhibitors have recently entered clinical trials in oncology. A better understanding of how the different PI3K isoforms are regulated and control signalling could uncover their roles in pathology and reveal in which disease contexts their blockade could be most beneficial.

引用

页码：329 / 341

页数：13

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