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• W2014691444 endingPage "???" @default.
• W2014691444 startingPage "070915190224001" @default.
• W2014691444 abstract "Anthrax lethal toxin (LT) is cytotoxic to macrophages from certain inbred mouse strains. The gene controlling macrophage susceptibility to LT is Nalp1b. Nalp1b forms part of the inflammasome, a multiprotein complex involved in caspase-1 activation and release of interleukin (IL)-1β and IL-18. We confirm the role of caspase-1 in LT-mediated death by showing that caspase inhibitors differentially protected cells against LT, with the degree of protection corresponding to each compound's ability to inhibit caspase-1. Caspase-1 activation and cytokine processing and release were late events inhibited by elevated levels of KCl and sucrose, by potassium channel blockers, and by proteasome inhibitors, suggesting that inflammasome formation requires a protein-degradation event and occurs downstream of LT-mediated potassium efflux. In addition, IL-18 and IL-1β release was dependent on cell death, indicating that caspase-1-mediated cytotoxicity is independent of these cytokines. Finally, inducing NALP3-inflammasome formation in LT-resistant macrophages did not sensitize cells to LT, suggesting that general caspase-1 activation cannot account for sensitivity to LT and that a Nalp1b-mediated event is specifically required for death. Our data indicate that inflammasome formation is a contributing, but not initiating, event in LT-mediated cytotoxicity and that earlier LT-mediated events leading to ion fluxes are required for death." @default.
• W2014691444 created "2016-06-24" @default.
• W2014691444 creator A5004197275 @default.
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• W2014691444 date "2007-09-10" @default.
• W2014691444 modified "2023-10-18" @default.
• W2014691444 title "Anthrax lethal toxin-induced inflammasome formation and caspase-1 activation are late events dependent on ion fluxes and the proteasome" @default.
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• W2014691444 doi "https://doi.org/10.1111/j.1462-5822.2007.01044.x" @default.
• W2014691444 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2515708" @default.
• W2014691444 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17850338" @default.
• W2014691444 hasPublicationYear "2007" @default.
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