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既要生存也要面临死亡:Fas 介导的细胞凋亡中的调控机制

Live and let die: regulatory mechanisms in Fas-mediated apoptosis.

作者信息

Curtin James F, Cotter Thomas G

机构信息

Tumour Biology Laboratory, Department of Biochemistry, Biosciences Research Institute, University College Cork, College Road, Cork, Ireland.

出版信息

Cell Signal. 2003 Nov;15(11):983-92. doi: 10.1016/s0898-6568(03)00093-7.

DOI:10.1016/s0898-6568(03)00093-7
PMID:14499341
Abstract

Activation of Fas receptor by Fas ligand causes caspase 8 activation and apoptosis in cells and is an important mechanism by which normal tissue homeostasis and function are maintained. Activation of caspase 8 is preceded by the formation of a death-inducing signalling complex (DISC), and a number of redundant mechanisms regulate DISC formation in vivo. Fas receptor is widely expressed in tissues, and dysfunction of the regulatory mechanisms in Fas receptor signalling has been reported in several diseases including autoimmune disease and cancer. This review aims to identify and discuss the various mechanisms employed by cells to alter their sensitivity to Fas-mediated apoptosis by regulating DISC formation. We also discuss a number of defects identified with Fas receptor signalling and the associated pathologies.

摘要

Fas配体激活Fas受体可导致细胞中半胱天冬酶8激活及细胞凋亡,这是维持正常组织稳态和功能的重要机制。半胱天冬酶8的激活先于死亡诱导信号复合物(DISC)的形成,多种冗余机制在体内调节DISC的形成。Fas受体在组织中广泛表达,在包括自身免疫性疾病和癌症在内的多种疾病中,均报道了Fas受体信号传导调节机制的功能障碍。本综述旨在识别和讨论细胞通过调节DISC形成来改变其对Fas介导的细胞凋亡敏感性所采用的各种机制。我们还讨论了Fas受体信号传导中发现的一些缺陷及相关病理情况。

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