Gasdermins as evolutionarily conserved executors of inflammation and cell death.

Details

Serval ID
serval:BIB_19AC3AC64FEE
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Gasdermins as evolutionarily conserved executors of inflammation and cell death.
Journal
Nature cell biology
Author(s)
Chen K.W., Broz P.
ISSN
1476-4679 (Electronic)
ISSN-L
1465-7392
Publication state
Published
Issued date
09/2024
Peer-reviewed
Oui
Volume
26
Number
9
Pages
1394-1406
Language
english
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Abstract
The gasdermins are a family of pore-forming proteins that have recently emerged as executors of pyroptosis, a lytic form of cell death that is induced by the innate immune system to eradicate infected or malignant cells. Mammalian gasdermins comprise a cytotoxic N-terminal domain, a flexible linker and a C-terminal repressor domain. Proteolytic cleavage in the linker releases the cytotoxic domain, thereby allowing it to form β-barrel membrane pores. Formation of gasdermin pores in the plasma membrane eventually leads to a loss of the electrochemical gradient, cell death and membrane rupture. Here we review recent work that has expanded our understanding of gasdermin biology and function in mammals by revealing their activation mechanism, their regulation and their roles in autoimmunity, host defence and cancer. We further highlight fungal and bacterial gasdermin pore formation pointing to a conserved mechanism of cell death induction.
Keywords
Humans, Animals, Inflammation/metabolism, Inflammation/pathology, Inflammation/immunology, Pyroptosis, Cell Death, Phosphate-Binding Proteins/metabolism, Phosphate-Binding Proteins/genetics, Pore Forming Cytotoxic Proteins/metabolism, Pore Forming Cytotoxic Proteins/genetics, Neoplasms/pathology, Neoplasms/metabolism, Neoplasms/immunology, Neoplasms/genetics, Immunity, Innate, Evolution, Molecular, Gasdermins
Pubmed
Web of science
Create date
30/08/2024 15:38
Last modification date
21/09/2024 6:09
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