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肿瘤坏死因子受体2和CD40通过TRAF2介导的核因子κB激活

TRAF2-mediated activation of NF-kappa B by TNF receptor 2 and CD40.

作者信息

Rothe M, Sarma V, Dixit V M, Goeddel D V

机构信息

Molecular Biology Department, Tularik, Inc., South San Francisco, CA 94080, USA.

出版信息

Science. 1995 Sep 8;269(5229):1424-7. doi: 10.1126/science.7544915.

DOI:10.1126/science.7544915
PMID:7544915
Abstract

TNF receptor-associated factor (TRAF) proteins are candidate signal transducers that associate with the cytoplasmic domains of members of the tumor necrosis factor (TNF) receptor superfamily. The role of TRAFs in the TNF-R2 and CD40 signal transduction pathways, which result in the activation of transcription factor NF-kappa B, was investigated. Overexpression of TRAF2, but not TRAF1 or TRAF3, was sufficient to induce NF-kappa B activation. A truncated derivative of TRAF2 lacking an amino-terminal RING finger domain was a dominant-negative inhibitor of NF-kappa B activation mediated by TNF-R2 and CD40. Thus, TRAF2 is a common mediator of TNF-R2 and CD40 signaling.

摘要

肿瘤坏死因子受体相关因子(TRAF)蛋白是候选信号转导分子,可与肿瘤坏死因子(TNF)受体超家族成员的胞质结构域结合。研究了TRAFs在导致转录因子NF-κB激活的TNF-R2和CD40信号转导通路中的作用。TRAF2的过表达足以诱导NF-κB激活,而TRAF1或TRAF3则不然。一种缺乏氨基末端RING指结构域的TRAF2截短衍生物是TNF-R2和CD40介导的NF-κB激活的显性负性抑制剂。因此,TRAF2是TNF-R2和CD40信号传导的共同介质。

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