Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation.

Détails

Ressource 1Télécharger: Chen_main_manuscript_accepted.pdf (882.30 [Ko])
Etat: Public
Version: Author's accepted manuscript
Licence: Non spécifiée
ID Serval
serval:BIB_27CA2505F865
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation.
Périodique
European journal of immunology
Auteur⸱e⸱s
Chen K.W., Demarco B., Broz P.
ISSN
1521-4141 (Electronic)
ISSN-L
0014-2980
Statut éditorial
Publié
Date de publication
02/2020
Peer-reviewed
Oui
Volume
50
Numéro
2
Pages
170-177
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Inflammasomes are multimeric protein complex that assemble in the cytosol upon microbial infection or cellular stress. Upon activation, inflammasomes drive the maturation of proinflammatory cytokines, IL-1β and IL-18, and also activate the pore-forming protein, gasdermin D to initiate a form of lytic cell death known as "pyroptosis". Pannexin-1 is channel-forming glycoprotein that promotes membrane permeability and ATP release during apoptosis; and was implicated in canonical NLRP3 or noncanonical inflammasome activation. Here, by utilizing three different pannexin-1 channel inhibitors and two lines of Panx1 <sup>-/-</sup> macrophages, we provide genetic and pharmacological evidence that pannexin-1 is dispensable for canonical or noncanonical inflammasome activation. In contrast, we demonstrate that pannexin-1 cleavage and resulting channel activity during apoptosis promotes NLRP3 inflammasome activation.
Mots-clé
Adenosine Triphosphate/metabolism, Animals, Apoptosis/physiology, Apoptosis Regulatory Proteins/metabolism, Caspases/metabolism, Cell Line, Cell Membrane Permeability/physiology, Connexins/metabolism, Inflammasomes/metabolism, Interleukin-18/metabolism, Macrophages/metabolism, Mice, Mice, Inbred C57BL, NLR Family, Pyrin Domain-Containing 3 Protein/metabolism, Nerve Tissue Proteins/metabolism, Signal Transduction/physiology, Apoptosis, Caspase-11, Gasdermin, Inflammasomes, NLRP3, Pannexin-1
Pubmed
Web of science
Création de la notice
15/08/2019 14:08
Dernière modification de la notice
12/11/2020 7:08
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