p90-RSK and Akt may promote rapid phosphorylation/inactivation of glycogen synthase kinase 3 in chemoattractant-stimulated neutrophils

被引：28

作者：

De Mesquita, DD ^{[1
]}

Zhan, Q ^{[1
]}

Crossley, L ^{[1
]}

Badwey, JA ^{[1
]}

机构：

[1] Harvard Univ, Sch Med,Brigham & Womens Hosp, Dept Anesthesiol Perioperat & Pain Med, Ctr Expt Therapeut & Reperfus Injury, Boston, MA 02115 USA

来源：

FEBS LETTERS | 2001年 / 502卷 / 03期

关键词：

neutrophil; cell signaling; chemoattractant; p90-RSK; glycogen synthase kinase 3;

D O I：

10.1016/S0014-5793(01)02669-2

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：

Stimulation of neutrophils with the chemoattractant fMet-Leu-Phe (fMLP) triggers phosphorylation/inactivation of the alpha- and beta -isoforms of glycogen synthase kinase 3 (GSK-3) with phosphorylation of the a-isoform predominating. These reactions were monitored with a phosphospecific antibody that only recognized the alpha- or beta -isoforms of GSK-3 when these proteins were phosphorylated on serine residues 21 and 9, respectively. Inhibitor studies indicated that phosphorylation of GSK-3 alpha may be catalyzed by the combined action of p90-RSK and Akt and may represent a new strategy by which G protein-coupled receptors inactivate GSK-3. Inactivation of GSK-3 may be one of the mechanisms that delay apoptosis in fMLP-stimulated neutrophils. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

引用

页码：84 / 88

页数：5

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