Calcium-dependent activation of Pyk2 by hypoxia

被引：18

作者：

Beitner-Johnson, D ^{[1
]}

Ferguson, T ^{[1
]}

Rust, RT ^{[1
]}

Kobayashi, S ^{[1
]}

Millhorn, DE ^{[1
]}

机构：

[1] Univ Cincinnati, Coll Med, Dept Mol & Cellular Physiol, Cincinnati, OH 45267 USA

来源：

CELLULAR SIGNALLING | 2002年 / 14卷 / 02期

关键词：

oxygen sensing; protein tyrosine kinase; phosphorylation; MAP kinase; depolarization; pheochromocytoma;

D O I：

10.1016/S0898-6568(01)00253-4

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The Pyk2 tyrosine kinase can be activated by both calcium-dependent and calcium-independent mechanisms. Exposure to moderate hypoxia (5% O-2) induced a rapid and persistent tyrosine phosphorylation of Pyk2 in pleochromocytoma (PC12) cells. Hypoxia and KCl-depolarization increased the phosphotyrosine content of Pyk2 by twofold and fourfold, respectively. Both of these effects were abolished in the absence of extracellular calcium. There was a modest activation of MAPK in parallel with the onset of Pyk2 phosphorylation. However, there was no detectable activation of either JNK or c-src, two other known downstream targets of Pyk2. Thus, exposure to hypoxia may selectively target specific subsets of Pyk-2 signalling pathways. (C) 2002 Elsevier Science Inc. All rights reserved.

引用

页码：133 / 137

页数：5

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