Gasdermins as evolutionarily conserved executors of inflammation and cell death.

Détails

ID Serval
serval:BIB_19AC3AC64FEE
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Gasdermins as evolutionarily conserved executors of inflammation and cell death.
Périodique
Nature cell biology
Auteur⸱e⸱s
Chen K.W., Broz P.
ISSN
1476-4679 (Electronic)
ISSN-L
1465-7392
Statut éditorial
Publié
Date de publication
09/2024
Peer-reviewed
Oui
Volume
26
Numéro
9
Pages
1394-1406
Langue
anglais
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Résumé
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.
Mots-clé
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
Création de la notice
30/08/2024 15:38
Dernière modification de la notice
21/09/2024 6:09
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