紫外线辐射诱导的细胞凋亡是由CD-95（Fas/APO-1）的激活介导的。

Ultraviolet radiation-induced apoptosis is mediated by activation of CD-95 (Fas/APO-1).

作者信息

Rehemtulla A, Hamilton C A, Chinnaiyan A M, Dixit V M

机构信息

Department of Radiation Oncology, University of Michigan Medical Center, Ann Arbor, Michigan 48109, USA.

出版信息

J Biol Chem. 1997 Oct 10;272(41):25783-6. doi: 10.1074/jbc.272.41.25783.

DOI:10.1074/jbc.272.41.25783

PMID:9325306

Abstract

Exposure to ultraviolet light (UV) can induce apoptosis in mammalian cells. The mechanism by which UV radiation engages the suicide apparatus is unclear. Here we demonstrate that UV radiation can activate the Fas pathway via receptor aggregation and subsequent recruitment of the death adaptor molecule FADD/MORT1. UV radiation-induced apoptosis was inhibited by both a dominant negative version of FADD (FADD-DN) and the caspase inhibitor CrmA. Thus, activation of the Fas pathway represents a physiologic mechanism by which UV-damaged cells are eliminated.

摘要

暴露于紫外线（UV）可诱导哺乳动物细胞发生凋亡。紫外线辐射启动自杀机制的具体机制尚不清楚。在此我们证明，紫外线辐射可通过受体聚集以及随后募集死亡衔接分子FADD/MORT1来激活Fas途径。FADD的显性负性形式（FADD-DN）和半胱天冬酶抑制剂CrmA均可抑制紫外线辐射诱导的细胞凋亡。因此，Fas途径的激活代表了一种清除紫外线损伤细胞的生理机制。