{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bednash JS"],"funding":["NHLBI NIH HHS","National Heart, Lung, and Blood Institute"],"pagination":["109859"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10201604"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["79"],"pubmed_abstract":["The NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is a multimeric, cytoplasmic, protein complex that regulates maturation and secretion of interleukin (IL)-1β, a potent pro-inflammatory cytokine. Critical to host defense against pathogens, IL-1β amplifies early innate immune responses by activating transcription of numerous other cytokines and chemokines. Excessive IL-1β is associated with poor outcomes in inflammatory illnesses, such as sepsis and the acute respiratory distress syndrome (ARDS). Tight regulation of this signaling axis is vital, but little is known about mechanisms to limit excessive inflammasome activity. Here we identify the deubiquitinase STAM-binding protein (STAMBP) as a negative regulator of the NLRP3 inflammasome. In monocytes, knockout of STAM"],"journal":["Cellular signalling"],"pubmed_title":["The deubiquitinase STAMBP modulates cytokine secretion through the NLRP3 inflammasome."],"pmcid":["PMC10201604"],"funding_grant_id":["R01 HL081784","UH3 HL123502","P01 HL114453","R01 HL098174","R01 HL097376","R01 HL096376"],"pubmed_authors":["Londino JD","Patel N","Johns F","Bednash JS","Smail TR","Mallampalli RK"],"additional_accession":[]},"is_claimable":false,"name":"The deubiquitinase STAMBP modulates cytokine secretion through the NLRP3 inflammasome.","description":"The NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is a multimeric, cytoplasmic, protein complex that regulates maturation and secretion of interleukin (IL)-1β, a potent pro-inflammatory cytokine. Critical to host defense against pathogens, IL-1β amplifies early innate immune responses by activating transcription of numerous other cytokines and chemokines. Excessive IL-1β is associated with poor outcomes in inflammatory illnesses, such as sepsis and the acute respiratory distress syndrome (ARDS). Tight regulation of this signaling axis is vital, but little is known about mechanisms to limit excessive inflammasome activity. Here we identify the deubiquitinase STAM-binding protein (STAMBP) as a negative regulator of the NLRP3 inflammasome. In monocytes, knockout of STAM","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-06T19:15:40.929Z","creation":"2025-04-06T19:15:40.929Z"},"accession":"S-EPMC10201604","cross_references":{"pubmed":["33253913"],"doi":["10.1016/j.cellsig.2020.109859"]}}