死亡受体5是肿瘤坏死因子受体（TNFR）家族的新成员，它与死亡受体4（DR4）可诱导依赖FADD的细胞凋亡并激活核因子κB（NF-κB）信号通路。

Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-kappaB pathway.

作者信息

Chaudhary P M, Eby M, Jasmin A, Bookwalter A, Murray J, Hood L

机构信息

Department of Molecular Biotechnology, University of Washington, Seattle 98195, USA.

出版信息

Immunity. 1997 Dec;7(6):821-30. doi: 10.1016/s1074-7613(00)80400-8.

DOI:10.1016/s1074-7613(00)80400-8

PMID:9430227

Abstract

Death receptor 4 (DR4) is a recently described receptor for the cytotoxic ligand TRAIL that reportedly uses a FADD-independent pathway to induce apoptosis and does not activate the NF-kappaB pathway. We have isolated a new member of the tumor necrosis factor receptor (TNFR) family, designated DR5, which bears a high degree of sequence homology to DR4. However, contrary to the previous reports, both DR4- and DR5-induced apoptosis can be blocked by dominant-negative FADD, and both receptors can activate NF-kappaB using a TRADD-dependent pathway. Finally, both receptors can interact with FADD, TRADD, and RIP. Thus, both DR5 and DR4 use FADD, TRADD, and RIP in their signal transduction pathways, and FADD is the common mediator of apoptosis by all known death domain-containing receptors.

摘要

死亡受体4（DR4）是最近发现的细胞毒性配体TRAIL的一种受体，据报道它利用一条不依赖FADD的途径诱导细胞凋亡，并且不激活核因子κB途径。我们分离出了肿瘤坏死因子受体（TNFR）家族的一个新成员，命名为DR5，它与DR4具有高度的序列同源性。然而，与先前的报道相反，DR4和DR5诱导的细胞凋亡均可被显性负性FADD阻断，并且两种受体都能利用依赖TRADD的途径激活核因子κB。最后，两种受体都能与FADD、TRADD和RIP相互作用。因此，DR5和DR4在其信号转导途径中均利用FADD、TRADD和RIP，并且FADD是所有已知含死亡结构域受体诱导细胞凋亡的共同介质。