A NOVEL PHOSPHOINOSITIDE-3 KINASE-ACTIVITY IN MYELOID-DERIVED CELLS IS ACTIVATED BY G-PROTEIN BETA-GAMMA-SUBUNITS

被引：548

作者：

STEPHENS, L ^{[1
]}

SMRCKA, A ^{[1
]}

COOKE, FT ^{[1
]}

JACKSON, TR ^{[1
]}

STERNWEIS, PC ^{[1
]}

HAWKINS, PT ^{[1
]}

机构：

[1] UNIV TEXAS, SW MED CTR, DEPT PHARMACOL, DALLAS, TX 75235 USA

来源：

CELL | 1994年 / 77卷 / 01期

关键词：

D O I：

10.1016/0092-8674(94)90237-2

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：

Phosphoinositide 3 kinase (PI3K) is a key signaling enzyme implicated in receptor-stimulated mitogenesis, oxidative bursting in neutrophils, membrane ruffling, and glucose uptake. A PI3K has already been purified, cloned, and shown to be regulated by receptors that act via tyrosine kinase-dependent regulatory mechanisms. We report that an immunologically, pharmacologically, and chromatographically distinct form of PI3K activity present in neutrophils and U937 cells is specifically activated by G protein py subunits. This data suggests PI3Ks conform to the paradigm set by receptor regulation of phosphoinositidase Cs: different receptor transduction systems specifically regulate dedicated isoforms of effector protein.

引用

页码：83 / 93

页数：11

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