Deficiency in Bim, Bid and Bbc3 (Puma) do not prevent axonal injury induced death.
作者信息
Harder J M, Libby R T
出版信息
Cell Death Differ. 2013 Jan;20(1):182. doi: 10.1038/cdd.2012.119. Epub 2012 Sep 21.
Abstract
摘要
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Deficiency in Bim, Bid and Bbc3 (Puma) do not prevent axonal injury induced death.Bim、Bid和Bbc3（Puma）的缺乏并不能预防轴突损伤诱导的死亡。
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Bax regulates primary necrosis through mitochondrial dynamics.Bax 通过线粒体动力学调节原初坏死。
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Can the analysis of BH3-only protein knockout mice clarify the issue of 'direct versus indirect' activation of Bax and Bak?对仅含BH3结构域的蛋白质敲除小鼠的分析能否阐明Bax和Bak“直接激活与间接激活”的问题？
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BH3-only activator proteins Bid and Bim are dispensable for Bak/Bax-dependent thrombocyte apoptosis induced by Bcl-xL deficiency: molecular requisites for the mitochondrial pathway to apoptosis in platelets.BH3 仅激活蛋白 Bid 和 Bim 在 Bcl-xL 缺乏诱导的由 Bak/Bax 依赖性血小板凋亡中是可有可无的：血小板凋亡中线粒体途径的分子需求。
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In vivo contributions of BH3-only proteins to neuronal death following seizures, ischemia, and traumatic brain injury.在癫痫发作、缺血和创伤性脑损伤后，BH3 仅蛋白对神经元死亡的体内贡献。
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7
BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program.BID、BIM 和 PUMA 对于激活 Bax 和 Bak 依赖性细胞死亡程序是必不可少的。
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8
Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis.tBID、BIM 和 PUMA 依次激活 BAX 和 BAK，启动线粒体凋亡。
Mol Cell. 2009 Nov 13;36(3):487-99. doi: 10.1016/j.molcel.2009.09.030.
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Susceptibility to neurodegeneration in a glaucoma is modified by Bax gene dosage.青光眼患者对神经退行性变的易感性受Bax基因剂量的影响。
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Science. 2004 Feb 13;303(5660):1010-4. doi: 10.1126/science.1092734.
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