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- W4310366945 abstract "While numerous microbes and stress signals can activate caspase-1 in the canonical inflammasome, the related inflammatory caspases-4 and -5 in humans and caspase-11 in mice are only activated upon recognition of intracellular LPS derived from the outer membrane of Gram-negative bacteria, in the noncanonical inflammasome. Caspases-4, -5, and -11 proteolytically cleave the pore-forming gasdermin D, and the resulting lytic pore releases danger signals and causes pyroptotic cell death. In addition, the subsequent canonical NLRP3 inflammasome activation enables inflammatory cytokine release. While the noncanonical inflammasome is crucial for host defense against Gram-negative bacteria, it also contributes to severe systemic inflammation known as endotoxin shock. Here we summarize the recent developments about noncanonical inflammasome activation and regulation." @default.
- W4310366945 created "2022-12-09" @default.
- W4310366945 creator A5029005602 @default.
- W4310366945 creator A5053112398 @default.
- W4310366945 date "2023-01-01" @default.
- W4310366945 modified "2023-09-27" @default.
- W4310366945 title "Cellular signaling, molecular activation, and regulation of the noncanonical inflammasome" @default.
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- W4310366945 doi "https://doi.org/10.1016/b978-0-323-91802-2.00028-1" @default.
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