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本文引用的文献

1
VDAC1 selectively transfers apoptotic Ca2+ signals to mitochondria.VDAC1 选择性地将凋亡 Ca2+信号传递到线粒体。
Cell Death Differ. 2012 Feb;19(2):267-73. doi: 10.1038/cdd.2011.92. Epub 2011 Jul 1.
2
Disruption of hexokinase II-mitochondrial binding blocks ischemic preconditioning and causes rapid cardiac necrosis.破坏己糖激酶 II 与线粒体的结合会阻断缺血预处理,并导致快速的心肌坏死。
Circ Res. 2011 May 13;108(10):1165-9. doi: 10.1161/CIRCRESAHA.111.244962. Epub 2011 Apr 28.
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Subcellular localization of hexokinases I and II directs the metabolic fate of glucose.己糖激酶 I 和 II 的亚细胞定位决定了葡萄糖的代谢命运。
PLoS One. 2011 Mar 9;6(3):e17674. doi: 10.1371/journal.pone.0017674.
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Simultaneous measurement of protein oxidation and S-nitrosylation during preconditioning and ischemia/reperfusion injury with resin-assisted capture.用树脂辅助捕获技术在预处理和缺血/再灌注损伤期间同时测量蛋白质氧化和 S-亚硝基化。
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Free tubulin modulates mitochondrial membrane potential in cancer cells.游离微管蛋白调节癌细胞中线粒体膜电位。
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Biphasic effect of nitric oxide on the cardiac voltage-dependent anion channel.一氧化氮对心脏电压依赖性阴离子通道的双相作用。
FEBS Lett. 2011 Jan 21;585(2):328-34. doi: 10.1016/j.febslet.2010.12.008. Epub 2010 Dec 13.
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Functional dynamics in the voltage-dependent anion channel.电压依赖性阴离子通道的功能动力学。
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Oligomerization of the mitochondrial protein voltage-dependent anion channel is coupled to the induction of apoptosis.线粒体蛋白电压依赖性阴离子通道的寡聚化与细胞凋亡的诱导相关联。
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电压依赖性阴离子通道是否调节心脏缺血再灌注损伤?

Does the voltage dependent anion channel modulate cardiac ischemia-reperfusion injury?

作者信息

Das Samarjit, Steenbergen Charles, Murphy Elizabeth

机构信息

Department of Pathology, Johns Hopkins Medical Institute and Systems Biology Center, NHLBI, NIH, Bethesda, MD, USA.

出版信息

Biochim Biophys Acta. 2012 Jun;1818(6):1451-6. doi: 10.1016/j.bbamem.2011.11.008. Epub 2011 Nov 11.

DOI:10.1016/j.bbamem.2011.11.008
PMID:22100866
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3382059/
Abstract

The voltage dependent anion channel (VDAC) provides exchange of metabolites, anions, and cations across the outer mitochondrial membrane. VDAC provides substrates and adenine nucleotides necessary for electron transport and therefore plays a key role in regulating mitochondrial bioenergetics. VDAC has also been suggested to regulate the response to cell death signaling. Emerging data show that VDAC is regulated by protein-protein interactions as well as by post-translational modifications. This review will focus on the regulation of VDAC and its potential role in regulating cell death in cardiac ischemia-reperfusion. This article is part of a Special Issue entitled: VDAC structure, function, and regulation of mitochondrial metabolism.

摘要

电压依赖性阴离子通道(VDAC)介导代谢物、阴离子和阳离子在线粒体外膜上的交换。VDAC为电子传递提供必要的底物和腺嘌呤核苷酸,因此在调节线粒体生物能量学中起关键作用。VDAC也被认为参与调节细胞对死亡信号的反应。新出现的数据表明,VDAC受蛋白质-蛋白质相互作用以及翻译后修饰的调控。本综述将聚焦于VDAC的调控及其在心脏缺血再灌注中调节细胞死亡的潜在作用。本文是名为“VDAC的结构、功能及线粒体代谢调控”的特刊的一部分。