{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lawrence DW"],"funding":["BLRD VA","U.S. Department of Veterans Affairs"],"pagination":["e0222802"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6754162"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(9)"],"pubmed_abstract":["Recent studies have begun to elucidate a role for E3 ubiquitin ligases as important mediators of the innate immune response. Our previous work defined a role for the ubiquitin ligase natural killer lytic-associated molecule (NKLAM/RNF19b) in mouse and human innate immunity. Here, we present novel data describing a role for NKLAM in regulating the immune response to Sendai virus (SeV), a murine model of paramyxoviral pneumonia. NKLAM expression was significantly upregulated by SeV infection. SeV-infected mice that are deficient in NKLAM demonstrated significantly less weight loss than wild type mice. In vivo, Sendai virus replication was attenuated in NKLAM-/- mice. Autophagic flux and the expression of autophagy markers LC3 and p62/SQSTM1 were also less in NKLAM-/- mice. Using flow cytomet"],"journal":["PloS one"],"pubmed_title":["Mice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model."],"pmcid":["PMC6754162"],"funding_grant_id":["I01 BX000705","1 IO1BX000705"],"pubmed_authors":["Kornbluth J","Lawrence DW","Shornick LP"],"additional_accession":[]},"is_claimable":false,"name":"Mice deficient in NKLAM have attenuated inflammatory cytokine production in a Sendai virus pneumonia model.","description":"Recent studies have begun to elucidate a role for E3 ubiquitin ligases as important mediators of the innate immune response. Our previous work defined a role for the ubiquitin ligase natural killer lytic-associated molecule (NKLAM/RNF19b) in mouse and human innate immunity. Here, we present novel data describing a role for NKLAM in regulating the immune response to Sendai virus (SeV), a murine model of paramyxoviral pneumonia. NKLAM expression was significantly upregulated by SeV infection. SeV-infected mice that are deficient in NKLAM demonstrated significantly less weight loss than wild type mice. In vivo, Sendai virus replication was attenuated in NKLAM-/- mice. Autophagic flux and the expression of autophagy markers LC3 and p62/SQSTM1 were also less in NKLAM-/- mice. Using flow cytomet","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019","modification":"2026-05-06T22:34:43.343Z","creation":"2019-10-11T07:08:38Z"},"accession":"S-EPMC6754162","cross_references":{"pubmed":["31539400"],"doi":["10.1371/journal.pone.0222802"]}}