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Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c (see comments)

机译：Bcl-2延长了Bax诱导的细胞色素c释放后的细胞存活（见评论）

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摘要

Following exposure of cells to stimuli that trigger programmed cell death (apoptosis), cytochrome c is rapidly released from mitochondria into the cytoplasm where it activates proteolytic molecules known as caspases that specifically cleave the amino-acid sequence DEVD and are crucial for the execution of apoptosis. The protein Bcl-2 interferes with this activation of caspases by preventing the release of cytochrome c. Here we study these molecular interactions during apoptosis induced by the protein Bax, a pro-apoptotic homologue of Bcl-2. We show that in cells transiently transfected with bax, Bax localizes to mitochondria and induces the release of cytochrome c, activation of caspase-3, membrane blebbing, nuclear fragmentation, and cell death. Caspase inhibitors do not affect Bax-induced cytochrome c release but block caspase-3 activation and nuclear fragmentation. Unexpectedly, Bcl-2 also fails to prevent Bax-induced cytochrome c release, although it co-localizes with Bax to mitochondria. Cells overexpressing both Bcl-2 and Bax show no signs of caspase activation and survive with significant amounts of cytochrome c in the cytoplasm. These findings indicate that Bcl-2 can interfere with Bax killing downstream of and independently of cytochrome c release.
机译：将细胞暴露于触发程序性细胞死亡（细胞凋亡）的刺激后，细胞色素c从线粒体迅速释放到细胞质中，在其中激活被称为caspases的蛋白水解分子，这种蛋白分解特定的氨基酸序列DEVD，对于执行凋亡至关重要。 Bcl-2蛋白通过阻止细胞色素c的释放来干扰胱天蛋白酶的激活。在这里，我们研究了由蛋白Bax诱导的凋亡过程中的这些分子相互作用，Bax是Bcl-2的促凋亡同源物。我们显示在用bax瞬时转染的细胞中，Bax定位于线粒体并诱导细胞色素c的释放，caspase-3的激活，膜起泡，核碎裂和细胞死亡。 Caspase抑制剂不影响Bax诱导的细胞色素C释放，但可以阻止caspase-3活化和核碎裂。出乎意料的是，Bcl-2也不能阻止Bax诱导的细胞色素c释放，尽管它​​与Bax共定位于线粒体。过度表达Bcl-2和Bax的细胞均未显示caspase活化的迹象，并且在细胞质中有大量的细胞色素c存活。这些发现表明，Bcl-2可以干扰Bax在细胞色素c释放下游的杀死，并且独立于细胞色素c的释放。

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