{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["135(16)"],"submitter":["Cao L"],"pubmed_abstract":["Atherosclerosis arises from disrupted cholesterol metabolism, notably impaired macrophage cholesterol efflux leading to foam cell formation. Through single-cell and bulk RNA-Seq, we identified Listerin E3 ubiquitin protein ligase 1 (Listerin) as a regulator of macrophage cholesterol metabolism. Listerin expression increased during atherosclerosis progression in humans and rodents. Its deficiency suppressed cholesterol efflux, promoted foam cell formation, and exacerbated plaque features (macrophage infiltration, lipid deposition, necrotic cores) in macrophage-specific KO mice. Conversely, Listerin overexpression attenuated these atherosclerotic manifestations. Mechanistically, Listerin stabilizes ABCA1, a key cholesterol efflux mediator, by catalyzing K63-linked polyubiquitination at resid"],"journal":["The Journal of clinical investigation"],"pagination":["e186509"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12352907"],"repository":["biostudies-literature"],"pubmed_title":["E3 ubiquitin ligase Listerin regulates macrophage cholesterol efflux and atherosclerosis by targeting ABCA1."],"pmcid":["PMC12352907"],"pubmed_authors":["Cao L","Yu L","Zhang J","Qi W","Li Q","Zhang M","Hou Y","Gao C","Yang W","Liu Y","Zhang Z","Sui W","Zhang Y","Cao Y","Wang X","Li B","Zhang C","Ren R"],"additional_accession":[]},"is_claimable":false,"name":"E3 ubiquitin ligase Listerin regulates macrophage cholesterol efflux and atherosclerosis by targeting ABCA1.","description":"Atherosclerosis arises from disrupted cholesterol metabolism, notably impaired macrophage cholesterol efflux leading to foam cell formation. Through single-cell and bulk RNA-Seq, we identified Listerin E3 ubiquitin protein ligase 1 (Listerin) as a regulator of macrophage cholesterol metabolism. Listerin expression increased during atherosclerosis progression in humans and rodents. Its deficiency suppressed cholesterol efflux, promoted foam cell formation, and exacerbated plaque features (macrophage infiltration, lipid deposition, necrotic cores) in macrophage-specific KO mice. Conversely, Listerin overexpression attenuated these atherosclerotic manifestations. Mechanistically, Listerin stabilizes ABCA1, a key cholesterol efflux mediator, by catalyzing K63-linked polyubiquitination at resid","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-05-29T17:23:03.579Z","creation":"2026-04-08T05:36:26.746Z"},"accession":"S-EPMC12352907","cross_references":{"pubmed":["40526435"],"doi":["10.1172/JCI186509"]}}