The regulation of Bax by c-Jun N-terminal protein kinase (JNK) is a prerequisite to the mitochondrial-induced apoptotic pathway
The regulation of Bax by c-Jun N-terminal protein kinase (JNK) is a prerequisite to the mitochondrial-induced apoptotic pathway
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DOI：
10.1016/j.febslet.2006.01.053
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发表时间：
2006-02-01
期刊：
影响因子：
3.5
通讯作者：
Tournier, C
中科院分区：
文献类型：
--
作者：
Papadakis, ES;Finegan, KG;Tournier, C
JNK 影响线粒体的信号传导机制对于启动细胞凋亡至关重要。在这里，我们表明，JNK 的缺失可以部分抵抗重金属镉的毒性作用。经历死亡的野生型和jnk-/-成纤维细胞均表现出胞质细胞色素c，但与野生型细胞不同，JNK缺陷的成纤维细胞不表现出增加的半胱天冬酶活性和DNA片段化。细胞凋亡的缺失与 Bax 激活的特定缺陷相关。我们得出的结论是，无论 Bid 和 Bim 是否激活，Bax 的 JNK 依赖性调节对于介导细胞色素 e 的凋亡释放至关重要。 (c) 2006 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
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.