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- W2968698979 endingPage "177" @default.
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- W2968698979 abstract "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-/- 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." @default.
- W2968698979 created "2019-08-22" @default.
- W2968698979 creator A5010558157 @default.
- W2968698979 creator A5034864461 @default.
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- W2968698979 date "2019-08-29" @default.
- W2968698979 modified "2023-10-17" @default.
- W2968698979 title "Pannexin‐1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation" @default.
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- W2968698979 doi "https://doi.org/10.1002/eji.201948254" @default.
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