Caspase-induced inactivation of the anti-apoptotic TRAF1 during Fas ligand-mediated apoptosis

被引：59

作者：

Irmler, M

Steiner, V

Ruegg, C

Wajant, H

Tschopp, J

机构：

[1] Univ Lausanne, Inst Biochem, CH-1066 Epalinges, Switzerland

[2] Ctr Pluridisciplinaire Oncol, CH-1066 Epalinges, Switzerland

[3] Univ Stuttgart, Dept Cell Biol & Immunol, D-70569 Stuttgart, Germany

来源：

FEBS LETTERS | 2000年 / 468卷 / 2-3期

关键词：

apoptosis; fas; tumor necrosis factor; NF-kappa B; survival; TNFR-associated factor;

D O I：

10.1016/S0014-5793(00)01206-0

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The activation of the transcription factor NF-kappa B often results in protection against apoptosis, In particular, proapoptotic tumor necrosis factor (TNF) signals are blocked hy proteins that are induced by NF-kappa B such as TNFR-associated factor 1 (TRAF1). Here se show that TRAF1 is cleaved after Asp-163 wen cells are induced to undergo apoptosis by Fas ligand (FasL). The C-terminal cleavage product blocks the induction of NF-kappa B by TNF and therefore functions as a dominant negative (DN) form of TRAF1. Our results suggest that the generation of DN-TRAF1 is part of a pro-apoptotic amplification system to assure rapid cell death. (C) 2000 Federation of European Biochemical Societies.

引用

页码：129 / 133

页数：5

共 33 条

[1] 4-1BB and Ox40 are members of a tumor necrosis factor (TNF)-nerve growth factor receptor subfamily that bind TNF receptor-associated factors and activate nuclear factor κB [J].