Necroptosis in development, inflammation and disease

被引:789
作者
Weinlich, Ricardo [1 ]
Oberst, Andrew [2 ]
Beere, Helen M. [3 ]
Green, Douglas R. [3 ]
机构
[1] Hosp Israelita Albert Einstein, BR-05652900 Sao Paulo, SP, Brazil
[2] Univ Washington, Dept Immunol, Seattle, WA 98109 USA
[3] St Jude Childrens Res Hosp, Dept Immunol, Memphis, TN 38105 USA
基金
美国国家卫生研究院;
关键词
NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; MIXED LINEAGE KINASE; DOMAIN-LIKE PROTEIN; NONAPOPTOTIC CELL-DEATH; TNF RECEPTOR 1; PROGRAMMED NECROSIS; NLRP3; INFLAMMASOME; RIP1; KINASE; PSEUDOKINASE MLKL;
D O I
10.1038/nrm.2016.149
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
In the early 2000s, receptor-interacting serine/threonine protein kinase 1 (RIPK1), a molecule already recognized as an important regulator of cell survival, inflammation and disease, was attributed an additional function: the regulation of a novel cell death pathway that came to be known as necroptosis. Subsequently, the related kinase RIPK3 and its substrate mixed-lineage kinase domain-like protein (MLKL) were also implicated in the necroptotic pathway, and links between this pathway and apoptosis were established. In this Timeline article, we outline the discoveries that have helped to identify the roles of RIPK1, RIPK3, MLKL and other regulators of necroptosis, and how they interact to determine cell fate.
引用
收藏
页码:127 / 136
页数:10
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