{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang L"],"funding":["China Scholarship Council","The University of Texas MD Anderson Cancer Center","NIAID NIH HHS","NCI NIH HHS","National Institutes of Health"],"pagination":["109904"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12011377"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["37(4)"],"pubmed_abstract":["Inflammasomes are crucial for innate immunity against infections and, when deregulated, also contribute to inflammatory diseases. Here, we identify a critical function of the E3 ubiquitin ligase Peli1 in regulating the activation of NLRP3 inflammasome. Peli1 deficiency impairs induction of interleukin-1β (IL-1β) secretion by different NLRP3 inducers, but not by inducers of the Aim2, NLRP1, and NLRC4 inflammasomes. Peli1-deficient mice have alleviated peritonitis induction by alum and display increased resistance to lipopolysaccharide (LPS) endotoxin shock, coupled with decreased serum concentration of IL-1β. Peli1 is required for NLRP3-induced caspase-1 activation and IL-1β maturation. Mechanistically, Peli1 conjugates K63 ubiquitin chain to lysine 55 of the inflammasome adaptor apoptosis-"],"journal":["Cell reports"],"pubmed_title":["Peli1 facilitates NLRP3 inflammasome activation by mediating ASC ubiquitination."],"pmcid":["PMC12011377"],"funding_grant_id":["201906380080","P30 CA016672","AI057555","R01 AI057555","AI104519","R01 AI104519"],"pubmed_authors":["Ko CJ","Sun SC","Li Y","Jie Z","Xie X","Zhu L","Zhang L","Liu T","Zhou X","Cheng X","Gao T"],"additional_accession":[]},"is_claimable":false,"name":"Peli1 facilitates NLRP3 inflammasome activation by mediating ASC ubiquitination.","description":"Inflammasomes are crucial for innate immunity against infections and, when deregulated, also contribute to inflammatory diseases. Here, we identify a critical function of the E3 ubiquitin ligase Peli1 in regulating the activation of NLRP3 inflammasome. Peli1 deficiency impairs induction of interleukin-1β (IL-1β) secretion by different NLRP3 inducers, but not by inducers of the Aim2, NLRP1, and NLRC4 inflammasomes. Peli1-deficient mice have alleviated peritonitis induction by alum and display increased resistance to lipopolysaccharide (LPS) endotoxin shock, coupled with decreased serum concentration of IL-1β. Peli1 is required for NLRP3-induced caspase-1 activation and IL-1β maturation. Mechanistically, Peli1 conjugates K63 ubiquitin chain to lysine 55 of the inflammasome adaptor apoptosis-","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2026-06-01T13:05:39.445Z","creation":"2025-07-03T03:05:05.763Z"},"accession":"S-EPMC12011377","cross_references":{"pubmed":["34706239"],"doi":["10.1016/j.celrep.2021.109904"]}}