Regulation of glycogen synthase kinase 3 in human platelets: a possible role in platelet function?

被引：46

作者：

Barry, FA ^{[1
]}

Graham, GJ ^{[1
]}

Fry, MJ ^{[1
]}

Gibbins, JM ^{[1
]}

机构：

[1] Univ Reading, Sch Anim & Microbial Sci, Reading RG6 6AJ, Berks, England

来源：

FEBS LETTERS | 2003年 / 553卷 / 1-2期

关键词：

platelet; platelet activation; platelet aggregation; glycogen synthase kinase 3; phosphoinositide; 3-kinase; protein kinase B;

D O I：

10.1016/S0014-5793(03)01015-9

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：

In this study we show that both glycogen synthase kinase 3 (GSK3) isoforms, GSK3alpha and GSK3beta, are present in human platelets and are phosphorylated on Ser(21) and Ser(9), respectively, in platelets stimulated with collagen, convulxin and thrombin. Phosphorylation of GSK3alpha/beta was dependent on phosphoinositide 3-kinase (PI3K) activity and independent of platelet aggregation, and correlated with a decrease in GSK3 activity that was preserved by pre-incubating platelets with PI3K inhibitor LY294002. Three structurally distinct GSK3 inhibitors, lithium, SB415286 and TDZD-8, were found to inhibit platelet aggregation. This implicates GSK3 as a potential regulator of platelet function. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：173 / 178

页数：6

共 28 条

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