Structural basis of cell apoptosis and necrosis in TNFR signaling

被引：41
作者：
Huang, Jing [1 ,2 ,3 ]
Yu, Shaoning [3 ]
Ji, Chaoneng [1 ,2 ]
Li, Jixi [1 ,2 ]
机构：
[1] Fudan Univ, State Key Lab Genet Engn, Shanghai 200438, Peoples R China
[2] Fudan Univ, Sch Life Sci, Shanghai 200438, Peoples R China
[3] Fudan Univ, Dept Chem, Shanghai 200433, Peoples R China
来源：
APOPTOSIS | 2015年 / 20卷 / 02期
基金：
中国国家自然科学基金;
关键词：
TNFR; Apoptosis; Necrosis; RIP1; RIP3; MLKL; MIXED LINEAGE KINASE; DEATH-EFFECTOR DOMAIN; PROGRAMMED NECROSIS; CRYSTAL-STRUCTURE; KAPPA-B; COMPLEX; RECEPTOR; RIP3; PROTEIN; INFLAMMATION;
D O I：
10.1007/s10495-014-1061-5
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：
The tumor necrosis factor receptors (TNFRs) play essential roles in innate and adaptive immunity. Depending on conditions, TNFR induces multiple cell fates including cell survival, cell apoptosis, and cell programmed necrosis. Here, we review recent progress in structural studies of the TNFR signaling pathway. The structural basis for the high order signal complexes, including the DISC, ripoptosome, necrosome, and RIP3/MLKL complex, may provide novel insights for understanding the biophysical principles of cell signaling cascades.
引用
收藏
页码：210 / 215
页数：6
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