Gasdermins: Effectors of Pyroptosis.

Gasdermins: Effectors of Pyroptosis.
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加油动物:凋亡的效应因子。

DOI:
10.1016/j.tcb.2017.05.005
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发表时间:
2017-09
影响因子:
19
通讯作者:
Miao EA
Miao EA
中科院分区:
生物学1区
文献类型:
--
作者:
Kovacs SB;Miao EA

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细胞凋亡是一种由炎性小体引发的裂解性程序性细胞死亡,其检测细胞溶质污染或扰动。这驱动半胱天冬酶-1或半胱天冬酶-11/4/5的活化,其切割gasdermin D,将其N-末端孔形成结构域(PFD)与C-末端阻遏物结构域(RD)分离。PFD寡聚化以在膜中形成大孔,其驱动溶胀和膜破裂。Gasdermin D是Gasdermin家族的六个成员之一;其他几种Gasdermin也被证明在裂解后形成导致焦亡的孔,以激活它们的PFDs。其中之一,gasdermin E,被半胱天冬酶-3切割激活。我们回顾我们目前的理解,以及目前的知识gasdermin家庭的焦睑下垂。
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.
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