Gasdermins: Effectors of Pyroptosis

被引：1618

作者：

Kovacs, Stephen B. ^{[1
,2
]}

Miao, Edward A. ^{[1
,2
]}

机构：

[1] Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA

[2] Univ N Carolina, Ctr Gastrointestinal Biol & Dis, Chapel Hill, NC 27599 USA

来源：

TRENDS IN CELL BIOLOGY | 2017年 / 27卷 / 09期

关键词：

NONSYNDROMIC HEARING IMPAIRMENT; GENETIC-VARIANTS; HAIR FOLLICLE; CELL-DEATH; GASTROINTESTINAL-TRACT; RHEUMATOID-ARTHRITIS; SUSCEPTIBILITY LOCI; DFNA5; GENE; INFLAMMASOME; MUTATION;

D O I：

10.1016/j.tcb.2017.05.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Pyroptosis is a form of lytic programmed cell death initiated by inflammasomes, which detect cytosolic contamination or perturbation. This drives activation of caspase-1 or caspase-11/4/5, which cleave gasdermin D, separating its N-terminal pore-forming domain (PFD) from the C-terminal repressor domain (RD). The PFD oligomerizes to form large pores in the membrane that drive swelling and membrane rupture. Gasdermin D is one of six (in humans) gasdermin family members; several other gasdermins have also been shown to form pores that cause pyroptosis after cleavage to activate their PFDs. One of these, gasdermin E, is activated by caspase-3 cleavage. We review our current understanding of pyroptosis as well as current knowledge of the gasdermin family.

引用

页码：673 / 684

页数：12

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