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Bcl-2家族成员对线粒体通透性的调控。

Control of mitochondrial permeability by Bcl-2 family members.

作者信息

Sharpe Juanita C, Arnoult Damien, Youle Richard J

机构信息

Biochemistry Section, Surgical Neurology Branch, NINDS, NIH, Bethesda, MD 20892, USA.

出版信息

Biochim Biophys Acta. 2004 Mar 1;1644(2-3):107-13. doi: 10.1016/j.bbamcr.2003.10.016.

DOI:10.1016/j.bbamcr.2003.10.016
PMID:14996495
Abstract

Programmed cell death (apoptosis) is regulated by the Bcl-2 family of proteins. Although it remains unclear how these family members control apoptosis, they clearly have the capacity to regulate the permeability of intracellular membranes to ions and proteins. Proapoptotic members of the Bcl-2 family, especially Bax and Bid, have been extensively analyzed for the ability to form channels in membranes and to regulate preexisting channels. Anti-apoptotic members of the family tend to have the opposing effects on membrane channel formation. The molecular mechanisms of the different models for the permeabilization of membranes by the Bcl-2 family members and the regulation of Bcl-2 family member subcellular localizations are discussed.

摘要

程序性细胞死亡(凋亡)受Bcl-2蛋白家族调控。尽管目前尚不清楚这些家族成员如何控制凋亡,但它们显然具有调节细胞内膜对离子和蛋白质通透性的能力。Bcl-2家族的促凋亡成员,尤其是Bax和Bid,已被广泛分析其在膜中形成通道以及调节已有通道的能力。该家族的抗凋亡成员往往对膜通道形成具有相反的作用。本文讨论了Bcl-2家族成员使膜通透化的不同模型的分子机制以及Bcl-2家族成员亚细胞定位的调控。

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Control of mitochondrial permeability by Bcl-2 family members.Bcl-2家族成员对线粒体通透性的调控。
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):107-13. doi: 10.1016/j.bbamcr.2003.10.016.
2
Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC.Bcl-2家族蛋白通过线粒体通道VDAC调节凋亡诱导因子细胞色素c的释放。
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Apoptosis. Key to the mitochondrial gate.细胞凋亡。线粒体之门的关键。
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Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity.仅含BH3结构域的促凋亡Bcl-2家族成员可诱导细胞色素c释放,但不会导致线粒体膜电位丧失,且不会直接调节电压依赖性阴离子通道活性。
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Bax and Bcl-xL independently regulate apoptotic changes of yeast mitochondria that require VDAC but not adenine nucleotide translocator.Bax和Bcl-xL独立调节酵母线粒体的凋亡变化,这种变化需要电压依赖性阴离子通道(VDAC),但不需要腺嘌呤核苷酸转位酶。
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VDAC2 inhibits BAK activation and mitochondrial apoptosis.电压依赖性阴离子通道蛋白2抑制BAK激活和线粒体凋亡。
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The voltage-dependent anion channel: an essential player in apoptosis.电压依赖性阴离子通道:细胞凋亡中的关键角色。
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Bax and Bak coalesce into novel mitochondria-associated clusters during apoptosis.在细胞凋亡过程中,Bax和Bak聚集成新的线粒体相关簇。
J Cell Biol. 2001 Jun 11;153(6):1265-76. doi: 10.1083/jcb.153.6.1265.

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