Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-κB pathway
Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-κB pathway
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DOI：
10.1016/s1074-7613(00)80400-8
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发表时间：
1997-12-01
期刊：
影响因子：
32.4
通讯作者：
Hood, L
中科院分区：
文献类型：
--
作者：
Chaudhary, PM;Eby, M;Hood, L
死亡受体4（DR 4）是最近描述的细胞毒性配体TRAIL的受体，据报道其使用FADD非依赖性途径诱导细胞凋亡并且不激活NF-κ B途径。我们已经分离出肿瘤坏死因子受体（TNFR）家族的一个新成员，命名为DR 5，它与DR 4具有高度的序列同源性。然而，与以前的报道相反，DR 4和DR 5诱导的细胞凋亡都可以被显性负性FADD阻断，两种受体都可以通过TRADD依赖性途径激活NF-κ B B。最后，两种受体都可以与FADD、TRADD和RIP相互作用。因此，DR 5和DR 4都在其信号转导途径中使用FADD、TRADD和RIP，并且FADD是所有已知的含有死亡结构域的受体的细胞凋亡的共同介质。
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-kappa B 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-kappa B 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.