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dc.contributor.authorPy, Bénédicte F.en_US
dc.contributor.authorJin, Mingzhien_US
dc.contributor.authorDesai, Bimal N.en_US
dc.contributor.authorPenumaka, Anirudhen_US
dc.contributor.authorZhu, Hongen_US
dc.contributor.authorKober, Maikeen_US
dc.contributor.authorDietrich, Alexanderen_US
dc.contributor.authorLipinski, Marta M.en_US
dc.contributor.authorHenry, Thomasen_US
dc.contributor.authorClapham, David E.en_US
dc.contributor.authorYuan, Junyingen_US
dc.date.accessioned2015-04-01T15:25:17Z
dc.date.issued2014en_US
dc.identifier.citationPy, B. F., M. Jin, B. N. Desai, A. Penumaka, H. Zhu, M. Kober, A. Dietrich, et al. 2014. “Caspase-11 Controls Interleukin-1β Release through Degradation of TRPC1.” Cell reports 6 (6): 1122-1128. doi:10.1016/j.celrep.2014.02.015. http://dx.doi.org/10.1016/j.celrep.2014.02.015.en
dc.identifier.issn2211-1247en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:14351050
dc.description.abstractSUMMARY Caspase-11 is a highly inducible caspase that controls both inflammatory responses and cell death. Caspase-11 controls interleukin 1β (IL-1β) secretion by potentiating caspase-1 activation and induces caspase-1-independent pyroptosis downstream of noncanonical NLRP3 inflammasome activators such as lipopolysaccharide (LPS) and Gram-negative bacteria. However, we still know very little about the downstream mechanism of caspase-11 in regulating inflammation because the known substrates of caspase-11 are only other caspases. Here, we identify the cationic channel subunit transient receptor potential channel 1 (TRPC1) as a substrate of caspase-11. TRPC1 deficiency increases the secretion of IL-1β without modulating caspase-1 cleavage or cell death in cultured macrophages. Consistently, trpc1−/− mice show higher IL-1β secretion in the sepsis model of intraperitoneal LPS injection. Altogether, our data suggest that caspase-11 modulates the cationic channel composition of the cell and thus regulates the unconventional secretion pathway in a manner independent of caspase-1.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1016/j.celrep.2014.02.015en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239700/pdf/en
dash.licenseLAAen_US
dc.titleCaspase-11 Controls Interleukin-1β Release through Degradation of TRPC1en
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalCell reportsen
dash.depositing.authorJin, Mingzhien_US
dc.date.available2015-04-01T15:25:17Z
dc.identifier.doi10.1016/j.celrep.2014.02.015*
dash.authorsorderedfalse
dash.contributor.affiliatedJin, Mingzhi
dash.contributor.affiliatedClapham, David
dash.contributor.affiliatedZhu, Hong
dash.contributor.affiliatedYuan, Junying


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