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CD95(APO-1/Fas)介导的细胞凋亡机制。

Mechanisms of CD95 (APO-1/Fas)-mediated apoptosis.

作者信息

Peter M E, Krammer P H

机构信息

Tumor Immunology Program, German Cancer Research Center, Im NeuenheimerFeld 280, D-69120, Heidelberg, Germany.

出版信息

Curr Opin Immunol. 1998 Oct;10(5):545-51. doi: 10.1016/s0952-7915(98)80222-7.

DOI:10.1016/s0952-7915(98)80222-7
PMID:9794832
Abstract

This review covers recent advances of CD95 signaling. It focuses on CD95-interacting molecules, formation of the death inducing signaling complex and the role of caspases, particularly caspase-8, and their death substrates. We also discuss the relevance of mitochondria in the CD95-mediated apoptotic process and how viral proteins interfere with crucial steps of this signaling pathway.

摘要

本综述涵盖了CD95信号传导的最新进展。它聚焦于与CD95相互作用的分子、死亡诱导信号复合物的形成以及半胱天冬酶(尤其是半胱天冬酶-8)及其死亡底物的作用。我们还讨论了线粒体在CD95介导的凋亡过程中的相关性,以及病毒蛋白如何干扰该信号通路的关键步骤。

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Mechanisms of CD95 (APO-1/Fas)-mediated apoptosis.CD95(APO-1/Fas)介导的细胞凋亡机制。
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Caspase-2 is activated at the CD95 death-inducing signaling complex in the course of CD95-induced apoptosis.在CD95诱导的细胞凋亡过程中,半胱天冬酶-2在CD95死亡诱导信号复合物处被激活。
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Differential regulation and ATP requirement for caspase-8 and caspase-3 activation during CD95- and anticancer drug-induced apoptosis.CD95和抗癌药物诱导的细胞凋亡过程中caspase-8和caspase-3激活的差异调节及ATP需求
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TCR-mediated up-regulation of c-FLIPshort correlates with resistance toward CD95-mediated apoptosis by blocking death-inducing signaling complex activity.TCR介导的c-FLIPshort上调通过阻断死亡诱导信号复合物活性与对CD95介导的细胞凋亡的抗性相关。
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Two CD95 (APO-1/Fas) signaling pathways.两条CD95(APO-1/Fas)信号通路。
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B cell receptor cross-linking triggers a caspase-8-dependent apoptotic pathway that is independent of the death effector domain of Fas-associated death domain protein.B细胞受体交联触发一条依赖于半胱天冬酶-8的凋亡途径,该途径独立于Fas相关死亡结构域蛋白的死亡效应结构域。
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Caspase-10 is recruited to and activated at the native TRAIL and CD95 death-inducing signalling complexes in a FADD-dependent manner but can not functionally substitute caspase-8.半胱天冬酶-10以FADD依赖的方式被募集到天然肿瘤坏死因子相关凋亡诱导配体(TRAIL)和CD95死亡诱导信号复合物中并被激活,但不能在功能上替代半胱天冬酶-8。
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