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Bcl-2 家族成员在线粒体形态发生中的新作用。

Emerging role for members of the Bcl-2 family in mitochondrial morphogenesis.

机构信息

Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin 2, Ireland.

出版信息

Mol Cell. 2009 Nov 13;36(3):355-63. doi: 10.1016/j.molcel.2009.10.011.

DOI:10.1016/j.molcel.2009.10.011
PMID:19917245
Abstract

Bcl-2 family proteins regulate apoptosis by controlling the release of mitochondrial cytochrome c via the Bax/Bak channel. However, recent studies have also implicated several members of this family in the regulation of mitochondrial fission/fusion dynamics. It has been debated whether the role of Bcl-2 proteins in mitochondrial morphogenesis is functionally distinct from their role in apoptosis, with some arguing that Bax/Bak-induced mitochondrial fission promotes apoptosis-associated cytochrome c release, while others suggest that these functions are separable. Here we review this emerging area and argue for a role for the Bcl-2 family as novel regulators of mitochondrial morphogenesis.

摘要

Bcl-2 家族蛋白通过 Bax/Bak 通道控制线粒体细胞色素 c 的释放来调节细胞凋亡。然而,最近的研究也表明该家族的几个成员参与了线粒体分裂/融合动力学的调节。Bcl-2 蛋白在线粒体形态发生中的作用是否与它们在细胞凋亡中的作用在功能上不同一直存在争议,一些人认为 Bax/Bak 诱导的线粒体分裂促进了与细胞凋亡相关的细胞色素 c 的释放,而另一些人则认为这些功能是可分离的。在这里,我们回顾了这一新兴领域,并提出了 Bcl-2 家族作为线粒体形态发生新的调节因子的作用。

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