Mitochondrial membrane permeabilisation by Bax/Bak
Mitochondrial membrane permeabilisation by Bax/Bak
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DOI：
10.1016/s0006-291x(03)00617-x
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发表时间：
2003-05-09
影响因子：
3.1
通讯作者：
Dive, C
中科院分区：
文献类型：
--
作者：
Esposti, MD;Dive, C
最近对同时缺失Bcl2家族多结构域促凋亡基因Bax和Bak的小鼠细胞的研究表明，这些蛋白中的一种或另一种是从线粒体释放细胞色素c等凋亡素所必需的。此外，除了BH-3外，只有Bid等该家族的蛋白被认为是关键的死亡诱导配体，通过与线粒体表面的Bax或Bak与促和抗凋亡的Bcl2家族蛋白相互作用而发挥作用。尽管人们的认识有所增加，但Bak和Bax是如何促进线粒体膜外膜(OMM)通透性的仍不清楚。我们认为，BAX和BAK可能不会以完全相同的方式运行，并评估当前模型的功能。我们还考虑了新出现的信息，即脂-蛋白相互作用可能对BAX和BAK的作用至关重要。(C)2003年埃尔塞维尔科学公司(美国)。版权所有。
Recent studies on cells derived from mice deficient in both multi-domain pro-apoptotic genes of the Bcl-2 family, Bax and Bak, suggest that one or other of these proteins are required for the release of apoptogens such as cytochrome c from mitochondria. In addition BH-3, only proteins of this family such as Bid are suggested to act as critical death inducing ligands via interactions with pro- and anti-apoptotic Bcl-2 family proteins with Bax or Bak at the mitochondrial surface. Despite this increase in knowledge it remains unclear precisely how Bak and Bax promote outer mitochondrial membrane (OMM) permeabilisation. We suggest that Bax and Bak may not operate in precisely the same manner and evaluate the current models for their function. We also consider the emerging information that lipid-protein interactions may be crucial to the actions of Bax and Bak. (C) 2003 Elsevier Science (USA). All rights reserved.