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

Détails

ID Serval
serval:BIB_27CA2505F865
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation.
Périodique
European journal of immunology
Auteur(s)
Chen K.W., Demarco B., Broz P.
ISSN
1521-4141 (Electronic)
ISSN-L
0014-2980
Statut éditorial
Publié
Date de publication
14/08/2019
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: aheadofprint
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
Immunology, Immunology and Allergy, NLRP3, Pannexin-1, apoptosis, caspase-11, gasdermin, inflammasomes, Apoptosis, Caspase-11, Gasdermin, Inflammasomes
Pubmed
Création de la notice
15/08/2019 14:08
Dernière modification de la notice
27/12/2019 6:18
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