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Trends Cell Biol. 2017 Sep;27(9):673-684. doi: 10.1016/j.tcb.2017.05.005. Epub 2017 Jun 12.

Gasdermins: Effectors of Pyroptosis.

Author information

1
Department of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
2
Department of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, and Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: emiao@med.unc.edu.

Abstract

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.

KEYWORDS:

apoptosis; gasdermin; inflammasome; programmed cell death; pyroptosis

PMID:
28619472
PMCID:
PMC5565696
DOI:
10.1016/j.tcb.2017.05.005
[Indexed for MEDLINE]
Free PMC Article

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