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

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• 作者：Irmler ; Martin ; Steiner ; Vé ; ronique ; Ruegg ; Curzio ; Wajant ; Harald ; Tschopp ; Jü ; rg
• 关键词：Apoptosis ; Fas ; Tumor necrosis factor ; NF-κ ; B ; Survival ; TNFR-associated factor
• 刊名：FEBS Letters
• 出版年：2000
• 出版时间：February 25, 2000
• 年：2000
• 卷：468
• 期：2-3
• 页码：129-133
• 全文大小：291 K

文摘

The activation of the transcription factor NF-κB often results in protection against apoptosis. In particular, pro-apoptotic tumor necrosis factor (TNF) signals are blocked by proteins that are induced by NF-κB such as TNFR-associated factor 1 (TRAF1). Here we show that TRAF1 is cleaved after Asp-163 when cells are induced to undergo apoptosis by Fas ligand (FasL). The C-terminal cleavage product blocks the induction of NF-κB 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.