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The cytosolic domain of Bcl-2 forms small pores in model mitochondrial outer membrane after acidic pH-induced membrane association.在酸性pH诱导膜结合后，Bcl-2的胞质结构域在模型线粒体外膜上形成小孔。
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2009 Feb;26(1):130-7.
2
Bax activation initiates the assembly of a multimeric catalyst that facilitates Bax pore formation in mitochondrial outer membranes.Bax 的激活启动了多聚体催化剂的组装，促进了 Bax 在线粒体外膜中的孔形成。
PLoS Biol. 2012;10(9):e1001394. doi: 10.1371/journal.pbio.1001394. Epub 2012 Sep 25.
3
BAX insertion, oligomerization, and outer membrane permeabilization in brain mitochondria: role of permeability transition and SH-redox regulation.脑线粒体中BAX的插入、寡聚化及外膜通透性改变：通透性转换和SH-氧化还原调节的作用
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4
The cytosolic domain of Bcl-2 oligomerizes to form pores in model mitochondrial outer membrane at acidic pH.Bcl-2的胞质结构域在酸性pH值下寡聚化，在模型线粒体外膜上形成孔道。
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2009 Jun;26(3):631-7.
5
Lipids modulate the BH3-independent membrane targeting and activation of BAX and Bcl-xL.脂质调节 BAX 和 Bcl-xL 的 BH3 非依赖性膜靶向和激活。
Proc Natl Acad Sci U S A. 2021 Sep 14;118(37). doi: 10.1073/pnas.2025834118.
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Oligomerization of membrane-bound Bcl-2 is involved in its pore formation induced by tBid.膜结合的 Bcl-2 寡聚化参与了 tBid 诱导的其孔形成。
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Distinct lipid effects on tBid and Bim activation of membrane permeabilization by pro-apoptotic Bax.不同脂质对促凋亡蛋白Bax激活tBid和Bim诱导膜通透性改变的影响。
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Mechanistic differences in the membrane activity of Bax and Bcl-xL correlate with their opposing roles in apoptosis.Bax 和 Bcl-xL 在膜活性方面的机制差异与其在细胞凋亡中的相反作用有关。
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Mitochondrial outer membrane proteins assist Bid in Bax-mediated lipidic pore formation.线粒体外膜蛋白协助Bid参与Bax介导的脂质孔形成。
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Kaji-Ichigoside F1 and Rosamultin Protect Vascular Endothelial Cells against Hypoxia-Induced Apoptosis via the PI3K/AKT or ERK1/2 Signaling Pathway.栀子苷 F1 和瑞香素通过 PI3K/AKT 或 ERK1/2 信号通路保护血管内皮细胞免受缺氧诱导的细胞凋亡。
Oxid Med Cell Longev. 2020 Apr 12;2020:6837982. doi: 10.1155/2020/6837982. eCollection 2020.
2
The Bax BH3 peptide H2-H3 promotes apoptosis by inhibiting Bcl-2's pore-forming and anti-Bax activities in the membrane.Bax BH3肽H2-H3通过抑制Bcl-2在膜上的成孔活性和抗Bax活性来促进细胞凋亡。
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2009 Aug;26(4):829-35.
3
The cytosolic domain of Bcl-2 oligomerizes to form pores in model mitochondrial outer membrane at acidic pH.Bcl-2的胞质结构域在酸性pH值下寡聚化，在模型线粒体外膜上形成孔道。
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2009 Jun;26(3):631-7.

本文引用的文献

1
Auto-activation of the apoptosis protein Bax increases mitochondrial membrane permeability and is inhibited by Bcl-2.凋亡蛋白Bax的自激活会增加线粒体膜通透性，并受到Bcl-2的抑制。
J Biol Chem. 2006 May 26;281(21):14764-75. doi: 10.1074/jbc.M602374200. Epub 2006 Mar 29.
2
BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly.仅含BH3结构域的蛋白质的BH3结构域通过直接和间接方式对Bax介导的线粒体膜通透性进行差异调节。
Mol Cell. 2005 Feb 18;17(4):525-35. doi: 10.1016/j.molcel.2005.02.003.
3
Impact of pH on Bax alpha conformation, oligomerisation and mitochondrial integration.pH对Baxα构象、寡聚化及线粒体整合的影响
FEBS Lett. 2004 Dec 3;578(1-2):41-6. doi: 10.1016/j.febslet.2004.10.080.
4
Bcl-2 homodimerization involves two distinct binding surfaces, a topographic arrangement that provides an effective mechanism for Bcl-2 to capture activated Bax.Bcl-2 同二聚化涉及两个不同的结合表面，这种拓扑排列为 Bcl-2 捕获活化的 Bax 提供了一种有效机制。
J Biol Chem. 2004 Oct 15;279(42):43920-8. doi: 10.1074/jbc.M406412200. Epub 2004 Aug 9.
5
Position and ionization state of Asp in the core of membrane-inserted alpha helices control both the equilibrium between transmembrane and nontransmembrane helix topography and transmembrane helix positioning.插入膜内的α螺旋核心中天冬氨酸（Asp）的位置和电离状态控制着跨膜螺旋与非跨膜螺旋构象之间的平衡以及跨膜螺旋的定位。
Biochemistry. 2004 Jul 13;43(27):8794-806. doi: 10.1021/bi049696p.
6
Bcl-2 family members: integrators of survival and death signals in physiology and pathology [corrected].Bcl-2家族成员：生理与病理过程中生存与死亡信号的整合者[已修正]
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):95-105. doi: 10.1016/j.bbamcr.2003.09.006.
7
Structural biology of the Bcl-2 family of proteins.Bcl-2蛋白家族的结构生物学
Biochim Biophys Acta. 2004 Mar 1;1644(2-3):83-94. doi: 10.1016/j.bbamcr.2003.08.012.
8
Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilization.凋亡诱导因子（AIF）和核酸内切酶G（EndoG）从线粒体释放需要在Bax/Bak介导的通透性改变下游激活半胱天冬酶。
EMBO J. 2003 Sep 1;22(17):4385-99. doi: 10.1093/emboj/cdg423.
9
The structure of Bcl-w reveals a role for the C-terminal residues in modulating biological activity.Bcl-w的结构揭示了C末端残基在调节生物活性方面的作用。
EMBO J. 2003 Apr 1;22(7):1497-507. doi: 10.1093/emboj/cdg144.
10
Characterization of the signal that directs Bcl-x(L), but not Bcl-2, to the mitochondrial outer membrane.引导Bcl-x(L)而非Bcl-2定位于线粒体外膜的信号的特征分析。
J Cell Biol. 2003 Jan 6;160(1):53-64. doi: 10.1083/jcb.200210084.

在酸性pH诱导膜结合后，Bcl-2的胞质结构域在模型线粒体外膜上形成小孔。

The cytosolic domain of Bcl-2 forms small pores in model mitochondrial outer membrane after acidic pH-induced membrane association.

作者信息

Peng Jun, Lapolla Suzanne M, Zhang Zhi, Lin Jialing

机构信息

Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, 940 Stanton L. Young Boulevard, Oklahoma City, OK 73190, USA.

出版信息

Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2009 Feb;26(1):130-7.

PMID:19334571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2844873/
Abstract

The permeability of mitochondrial outer membrane (MOM) is regulated by the proteins of the Bcl-2 family via their interactions at the membrane. While pro-apoptotic Bax protein promotes MOM permeabilization (MOMP) releasing cytochrome c after activation by BH3-only protein, anti-apoptotic Bcl-2 protein protects MOM. However both Bax and Bcl-2 can form pores in model membranes. Unlike Bax pore that has been extensively studied and reported to be directly linked to MOMP, Bcl-2 pore is much less known; thus we investigated the pore-forming property of recombinant Bcl-2 lacking the C-terminal transmembrane sequence (Bcl-2deltaTM) in liposomal membranes of MOM lipids. We found that: (1) Bcl-2 formed pores at acidic pH that induced the association of Bcl-2 with liposome; (2) Bcl-2 pore size was dependent on Bcl-2 concentration, suggesting that oligomerization is involved in Bcl-2 pore formation; (3) Unlike Bax pore that could release large molecules up to 2 mega-Da, Bcl-2 pore was smaller and could only release the molecules of a few kilo-Da. Therefore, Bcl-2 and Bax may form different size pores in MOM, and while the large pore formed by Bax may release cytochrome c during apoptosis, the small pore formed by Bcl-2 may maintain the normal MOM permeability.

摘要

线粒体外膜（MOM）的通透性由Bcl-2家族蛋白通过它们在膜上的相互作用来调节。促凋亡的Bax蛋白在仅含BH3结构域的蛋白激活后促进线粒体外膜通透性改变（MOMP）并释放细胞色素c，而抗凋亡的Bcl-2蛋白则保护线粒体外膜。然而，Bax和Bcl-2都能在模型膜中形成孔道。与已被广泛研究且报道与MOMP直接相关的Bax孔道不同，Bcl-2孔道鲜为人知；因此，我们研究了缺乏C端跨膜序列的重组Bcl-2（Bcl-2deltaTM）在MOM脂质体膜中的成孔特性。我们发现：（1）Bcl-2在酸性pH下形成孔道，这诱导了Bcl-2与脂质体的结合；（2）Bcl-2孔道大小取决于Bcl-2浓度，表明寡聚化参与了Bcl-2孔道的形成；（3）与能释放高达2兆道尔顿大分子的Bax孔道不同，Bcl-2孔道较小，只能释放几千道尔顿的分子。因此，Bcl-2和Bax可能在MOM中形成不同大小的孔道，并且在细胞凋亡过程中，由Bax形成的大孔道可能释放细胞色素c，而由Bcl-2形成的小孔道可能维持MOM的正常通透性。