RIPK1 and RIPK3: critical regulators of inflammation and cell death

被引:271
作者
Newton, Kim [1 ]
机构
[1] Genentech Inc, Dept Physiol Chem, San Francisco, CA 94080 USA
关键词
RIPK1; RIPK3; apoptosis; necroptosis; MIXED LINEAGE KINASE; NF-KAPPA-B; DOMAIN-LIKE PROTEIN; PROGRAMMED NECROSIS; CASPASE-8; ACTIVATION; TNF; APOPTOSIS; NECROPTOSIS; MLKL; FADD;
D O I
10.1016/j.tcb.2015.01.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
RIPK1 and RIPK3 (receptor-interacting serine/threonine protein kinases 1/3) interact by virtue of their RIP homotypic interaction motifs to mediate a form of cell death called necroptosis, although mice lacking these kinases have very different phenotypes. RIPK1-deficient mice die soon after birth, whereas RIPK3-deficient mice are healthy. Necroptosis involves cell rupture and is triggered by tumor necrosis factor (TNF), Toll-like receptors (TLRs), or the T cell receptor (TCR) when pro-apoptotic caspase-8 is inhibited. Various mouse models of disease are ameliorated by RIPK3 deficiency, suggesting that necroptosis contributes to pathology. Genetic rescue experiments now reveal why RIPK3-deficient are viable but RIPK1-deficient mice are not. These and other experiments indicate unexpected complexity in the regulation of both apoptosis and necroptosis by RIPK1 and RIPK3.
引用
收藏
页码:347 / 353
页数:7
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