Calcineurin subunit B promotes TNF-alpha-induced apoptosis by binding to mitochondria and causing mitochondrial Ca2+ overload
Calcineurin subunit B promotes TNF-alpha-induced apoptosis by binding to mitochondria and causing mitochondrial Ca2+ overload
复制标题
钙调神经磷酸酶亚基 B 通过与线粒体结合并引起线粒体 Ca2 超载，促进 TNF-α 诱导的细胞凋亡
DOI：
10.1016/j.canlet.2012.01.042
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发表时间：
2012-08-28
期刊：
影响因子：
9.7
通讯作者：
Wei, Qun
中科院分区：
文献类型：
--
作者：
Cheng, Jinbo;Tang, Wei;Wei, Qun
以往的研究表明，过量的钙调神经磷酸酶亚基B（Cn B）与线粒体结合。在这里，CnB过表达增加CN活性的细胞和增强TNF-α诱导的细胞死亡的CN活性无关。CnB过表达增加细胞内Ca 2+浓度，增强caspase-3活性，降低Bcl-2表达，降低线粒体膜电位，而caspase-8或p53无变化。CnB绑定到分离的线粒体中的Ca 2+依赖性的方式，并刺激细胞色素c从线粒体的释放。总之，这些结果表明，CnB能够促进TNF-α诱导的细胞凋亡，可能是通过对线粒体功能的影响。(c)2012爱思唯尔爱尔兰有限公司保留所有权利。
Previous studies have shown that excess calcineurin subunit B (CnB) associates with mitochondria. Here, CnB overexpression increased CN activity in cells and enhanced TNF-alpha-induced cell death independent of CN activity. Overexpression of CnB increased intracellular Ca2+ concentration, enhanced caspase-3 activity, reduced Bcl-2 expression, and decreased mitochondrial membrane potential, with no change of caspase-8 or p53. CnB bound to isolated mitochondria in a Ca2+-dependent manner, and stimulated cytochrome c release from the mitochondria. Altogether, these results demonstrate that CnB is capable of promoting TNF-alpha-induced apoptosis, possibly through effects on mitochondrial functions. (c) 2012 Elsevier Ireland Ltd. All rights reserved.