生物
信号转导
细胞凋亡
细胞生物学
交通2
肿瘤坏死因子α
受体
死亡域
程序性细胞死亡
癌症研究
遗传学
免疫学
作者
Olivier Micheau,Jürg Tschopp
出处
期刊:Cell
[Cell Press]
日期:2003-07-01
卷期号:114 (2): 181-190
被引量:2355
标识
DOI:10.1016/s0092-8674(03)00521-x
摘要
Apoptosis induced by TNF-receptor I (TNFR1) is thought to proceed via recruitment of the adaptor FADD and caspase-8 to the receptor complex. TNFR1 signaling is also known to activate the transcription factor NF-κB and promote survival. The mechanism by which this decision between cell death and survival is arbitrated is not clear. We report that TNFR1-induced apoptosis involves two sequential signaling complexes. The initial plasma membrane bound complex (complex I) consists of TNFR1, the adaptor TRADD, the kinase RIP1, and TRAF2 and rapidly signals activation of NF-κB. In a second step, TRADD and RIP1 associate with FADD and caspase-8, forming a cytoplasmic complex (complex II). When NF-κB is activated by complex I, complex II harbors the caspase-8 inhibitor FLIPL and the cell survives. Thus, TNFR1-mediated-signal transduction includes a checkpoint, resulting in cell death (via complex II) in instances where the initial signal (via complex I, NF-κB) fails to be activated.
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