{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He L"],"funding":["Ministry of Science and Technology of the People&apos;s Republic of China","National Natural Science Foundation of China"],"pagination":["e52036"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8406403"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(7)"],"pubmed_abstract":["Dysregulation of lipid metabolism could lead to the development of metabolic disorders. We report here that the F-box protein JFK promotes excessive lipid accumulation in adipose tissue and contributes to the development of metabolic syndrome. JFK transgenic mice develop spontaneous obesity, accompanied by dyslipidemia, hyperglycemia, and insulin resistance, phenotypes that are further exacerbated under high-fat diets. In contrast, Jfk knockout mice are lean and resistant to diet-induced metabolic malfunctions. Liver-specific reconstitution of JFK expression in Jfk knockout mice leads to hepatic lipid accumulation resembling human hepatic steatosis and nonalcoholic fatty liver disease. We show that JFK interacts with and destabilizes ING5 through assembly of the SCF complex. Integrative tr"],"journal":["EMBO reports"],"pubmed_title":["SCF<sup>JFK</sup> is functionally linked to obesity and metabolic syndrome."],"pmcid":["PMC8406403"],"funding_grant_id":["2016YFC1302304","31571340","82002992","81730079","81874158","81530073"],"pubmed_authors":["Wu J","Yang J","Shan L","He L","Yan R","Liu X","Yang X","Sun L","Yang Z","Xia L","Zhang Y","Liang J","Shang Y","Wang Y","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"SCF<sup>JFK</sup> is functionally linked to obesity and metabolic syndrome.","description":"Dysregulation of lipid metabolism could lead to the development of metabolic disorders. We report here that the F-box protein JFK promotes excessive lipid accumulation in adipose tissue and contributes to the development of metabolic syndrome. JFK transgenic mice develop spontaneous obesity, accompanied by dyslipidemia, hyperglycemia, and insulin resistance, phenotypes that are further exacerbated under high-fat diets. In contrast, Jfk knockout mice are lean and resistant to diet-induced metabolic malfunctions. Liver-specific reconstitution of JFK expression in Jfk knockout mice leads to hepatic lipid accumulation resembling human hepatic steatosis and nonalcoholic fatty liver disease. We show that JFK interacts with and destabilizes ING5 through assembly of the SCF complex. Integrative tr","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jul","modification":"2026-05-09T18:28:41.168Z","creation":"2022-07-23T19:07:32.716Z"},"accession":"S-EPMC8406403","cross_references":{"pubmed":["34114325"],"doi":["10.15252/embr.202052036"]}}