A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes

被引：380

作者：

Newton, K ^{[1
]}

Harris, AW ^{[1
]}

Bath, ML ^{[1
]}

Smith, KGC ^{[1
]}

Strasser, A ^{[1
]}

机构：

[1] Walter & Eliza Hall Inst Med Res, PO Royal Melbourne Hosp, Melbourne, Vic 3050, Australia

来源：

EMBO JOURNAL | 1998年 / 17卷 / 03期

关键词：

APO-1; apoptosis; CD95; FADD; MORT1; Fas; T lymphocytes;

D O I：

10.1093/emboj/17.3.706

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：

Members of the tumour necrosis factor receptor family that contain a death domain have pleiotropic activities. They induce apoptosis via interaction with intracellular FADD/MORT1 and trigger cell growth or differentiation via TRADD and TRAF molecules. The impact of FADD/MORT1-transduced signals on T lymphocyte development was investigated in transgenic mice expressing a dominant negative mutant protein, FADD-DN, Unexpectedly, FADD-DN enhanced negative selection of self-reactive thymic lymphocytes and inhibited T cell activation by increasing apoptosis, Thus signalling through FADD/MORT1 does not lead exclusively to cell death, but under certain circumstances can promote cell survival and proliferation.

引用

页码：706 / 718

页数：13

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