RIP3: a molecular switch for necrosis and inflammation

被引:289
作者
Moriwaki, Kenta [1 ]
Chan, Francis Ka-Ming [1 ]
机构
[1] Univ Massachusetts, Sch Med, Dept Pathol, Immunol & Microbiol Program, Worcester, MA 01605 USA
基金
日本学术振兴会;
关键词
RIP1; MLKL; PGAM5; caspase; 8; FADD; inflammation; RECEPTOR-INTERACTING PROTEIN; MIXED LINEAGE KINASE; PROGRAMMED CELL-DEATH; DOMAIN-LIKE; APOPTOSIS; CASPASE-8; FADD; ACTIVATION; NECROPTOSIS; IDENTIFICATION;
D O I
10.1101/gad.223321.113
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.
引用
收藏
页码:1640 / 1649
页数:10
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