The regulation of Bax by c-Jun N-terminal protein kinase (JNK) is a prerequisite to the mitochondrial-induced apoptotic pathway

被引：80

作者：

Papadakis, ES ^{[1
]}

Finegan, KG ^{[1
]}

Wang, X ^{[1
]}

Robinson, AC ^{[1
]}

Guo, C ^{[1
]}

Kayahara, M ^{[1
]}

Tournier, C ^{[1
]}

机构：

[1] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England

来源：

FEBS LETTERS | 2006年 / 580卷 / 05期

基金：

英国医学研究理事会;

关键词：

c-Jun N-terminal protein kinase; apoptosis; stress; cytochrome c; Bcl-2; proteins;

D O I：

10.1016/j.febslet.2006.01.053

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：

The signaling mechanism by which JNK affects mitochondria is critical to initiate apoptosis. Here we show that the absence of JNK provides a partial resistance to the toxic effect of the heavy metal cadmium. Both wild type and jnk-/- fibroblasts undergoing death exhibit cytosolic cytochrome c but, unlike wild type cells, the JNK-deficient fibroblasts do not display increased caspase activity and DNA fragmentation. The absence of apoptotic death correlates with a specific defect in activation of Bax. We conclude that JNK-dependent regulation of Bax is essential to mediate the apoptotic release of cytochrome e regardless of Bid and Bim activation. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：1320 / 1326

页数：7

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