当前位置: X-MOL 学术Trends Cell Biol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Gasdermins: Effectors of Pyroptosis
Trends in Cell Biology ( IF 19.0 ) Pub Date : 2017-06-12 , DOI: 10.1016/j.tcb.2017.05.005
Stephen B Kovacs 1 , Edward A Miao 1
Affiliation  

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.



中文翻译:

Gasdermins:细胞焦亡的效应子

细胞焦亡是一种由炎症小体引发的裂解性程序性细胞死亡,可检测细胞质污染或扰动。这会驱动 caspase-1 或 caspase-11/4/5 的激活,从而裂解gasdermin D,将其 N 端成孔结构域 (PFD) 与 C 端阻遏结构域 (RD) 分开。PFD 低聚在膜中形成大孔,导致膨胀和膜破裂。Gasdermin D 是 Gasdermin 家族的六个(人类)成员之一;其他几种 Gasdermin 也被证明会形成孔,在裂解后激活其 PFD,从而导致细胞焦亡。其中之一,gasdermin E,由 caspase-3 裂解激活。我们回顾了目前对细胞焦亡的理解以及目前对 Gasdermin 家族的了解。

更新日期:2017-06-12
down
wechat
bug