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线粒体外膜通透性改变的机制。

Mechanisms of mitochondrial outer membrane permeabilization.

作者信息

James Dominic, Parone Philippe A, Terradillos Olivier, Lucken-Ardjomande Safa, Montessuit Sylvie, Martinou Jean-Claude

机构信息

Department of Cell Biology, University of Geneva, Quai Ernest-Ansermet 30, Geneva, Switzerland.

出版信息

Novartis Found Symp. 2007;287:170-6; discussion 176-82.

PMID:18074638
Abstract

In response to many apoptotic stimuli, Bcl-2 family pro-apoptotic members, such as Bax and Bak, are activated. This results in their oligomerization, permeabilization of the outer mitochondrial membrane, and release of many proteins that are normally confined in the mitochondrial inter-membrane space. Among these proteins are cytochrome c, Smac/DIABLO, OMI/HtrA2, AIF and endonuclease G. Mitochondrial outer membrane permeabilization (MOMP) is also associated with fragmentation of the mitochondrial network. The mechanisms that lead to the oligomerization of proapoptotic members of the Bcl-2 family and to MOMP are still unclear and the role of mitochondrial fission in these events remains elusive.

摘要

响应多种凋亡刺激时,Bcl-2家族促凋亡成员,如Bax和Bak,会被激活。这导致它们寡聚化、线粒体外膜通透性增加,并释放许多通常局限于线粒体膜间隙的蛋白质。这些蛋白质包括细胞色素c、Smac/DIABLO、OMI/HtrA2、AIF和核酸内切酶G。线粒体外膜通透性增加(MOMP)也与线粒体网络的碎片化有关。导致Bcl-2家族促凋亡成员寡聚化以及MOMP的机制仍不清楚,线粒体分裂在这些事件中的作用也仍然难以捉摸。

相似文献

1
Mechanisms of mitochondrial outer membrane permeabilization.线粒体外膜通透性改变的机制。
Novartis Found Symp. 2007;287:170-6; discussion 176-82.
2
Mitochondrial outer-membrane permeabilization and remodelling in apoptosis.细胞凋亡过程中的线粒体外膜通透性改变与重塑
Int J Biochem Cell Biol. 2009 Oct;41(10):1884-9. doi: 10.1016/j.biocel.2009.05.001. Epub 2009 May 9.
3
Bax is essential for Drp1-mediated mitochondrial fission but not for mitochondrial outer membrane permeabilization caused by photodynamic therapy.Bax 对于 Drp1 介导的线粒体裂变是必不可少的,但对于光动力疗法引起的线粒体外膜通透性增加则不是必需的。
J Cell Physiol. 2011 Feb;226(2):530-41. doi: 10.1002/jcp.22362.
4
Apoptosis-associated mitochondrial outer membrane permeabilization assays.凋亡相关的线粒体外膜通透性检测
Methods. 2008 Mar;44(3):229-34. doi: 10.1016/j.ymeth.2007.11.003.
5
Mitochondrial fragmentation in apoptosis.细胞凋亡中的线粒体碎片化
Trends Cell Biol. 2007 Jan;17(1):6-12. doi: 10.1016/j.tcb.2006.11.001. Epub 2006 Nov 20.
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The role of mitochondrial factors in apoptosis: a Russian roulette with more than one bullet.线粒体因子在细胞凋亡中的作用:一场不止一颗子弹的俄罗斯轮盘赌。
Cell Death Differ. 2002 Oct;9(10):1031-42. doi: 10.1038/sj.cdd.4401088.
7
Mitochondria in cell death.线粒体与细胞死亡。
Essays Biochem. 2010;47:99-114. doi: 10.1042/bse0470099.
8
Cell death regulation by the Bcl-2 protein family in the mitochondria.线粒体中Bcl-2蛋白家族对细胞死亡的调控
J Cell Physiol. 2003 May;195(2):158-67. doi: 10.1002/jcp.10254.
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At the gates of death.在死亡之门。
Cancer Cell. 2006 May;9(5):328-30. doi: 10.1016/j.ccr.2006.05.004.
10
A tale of two mitochondrial channels, MAC and PTP, in apoptosis.凋亡过程中两个线粒体通道——线粒体通透性转换孔(MAC)和线粒体通透性转换孔(PTP)的故事。 (注:这里MAC和PTP英文原文一样,推测可能有误,正常可能是不同英文缩写,比如Mitochondrial Outer Membrane Permeability Transition Pore线粒体膜通透性转换孔等,翻译按给定英文文本进行,但实际专业领域需准确英文缩写来精准理解)
Apoptosis. 2007 May;12(5):857-68. doi: 10.1007/s10495-007-0722-z.

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ORF005L from infectious spleen and kidney necrosis virus is located in the inner mitochondrial membrane and induces apoptosis.传染性脾肾坏死病毒的ORF005L位于线粒体内膜并诱导细胞凋亡。
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MCL-1ES induces MCL-1L-dependent BAX- and BAK-independent mitochondrial apoptosis.MCL-1ES 诱导 MCL-1L 依赖性 BAX 和 BAK 非依赖性线粒体凋亡。
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