Diphosphorylation of extracellular signal-regulated kinases and c-Jun N-terminal protein kinases in brain ischemic tolerance in rat

被引：50

作者：

Gu, ZL

Jiang, Q

Zhang, GY ^{[1
]}

Cui, ZC

Zhu, ZM

机构：

[1] Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Peoples R China

[2] Dalian Med Univ, Dept Biochem, Dalian 116027, Peoples R China

来源：

BRAIN RESEARCH | 2000年 / 860卷 / 1-2期

关键词：

extracellular signal-regulated kinase; c-Jun N-terminal protein kinase; phosphorylation; ischemic tolerance; brain;

D O I：

10.1016/S0006-8993(00)02006-0

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal protein kinases (JNKs) activation in brain ischemic tolerance were examined by Western immunoblot. ERK but not JNK diphosphorylation (activation) were increased after preconditioning ischemia. The increased JNK1 but not ERK diphosphorylation after lethal ischemia was eliminated by pretreatment with preconditioning ischemia. The results suggest that the elimination of JNK1 activation after lethal ischemia by preconditioning ischemia may be one of the important protective mechanisms in ischemic tolerance, and ERKs activation may be involved in the induction of the protective responses. (C) 2000 Elsevier Science B.V. All rights reserved.

引用

页码：157 / 160

页数：4

共 16 条

[1] The dual specificity mitogen-activated protein kinase phosphatase-1 and -2 are induced by the p42/p44(MAPK) cascade [J].