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dc.contributor.authorQian, Kun
dc.contributor.authorYu, Daozhan
dc.contributor.authorWang, Weiming
dc.contributor.authorJiang, Mengqi
dc.contributor.authorYang, Rongze
dc.contributor.authorBrown, Robert
dc.contributor.authorGong, Da-Wei
dc.date.accessioned2021-11-01T18:38:14Z
dc.date.available2021-11-01T18:38:14Z
dc.date.issued2021-10-20en_US
dc.identifier.urihttp://hdl.handle.net/10713/17028
dc.description.abstractPeroxisome proliferator-activated receptor-γ (PPARγ) is the master regulator of adipogenesis, but knowledge about how PPARγ is regulated at the protein level is very limited. We aimed to identify PPARγ-interacting proteins which modulate PPARγ’s protein levels and transactivating activities in human adipocytes. We expressed Flag-tagged PPARγ in human preadipocytes as bait to capture PPARγ-associated proteins, followed by mass spectroscopy and proteomics analysis, which identified serine/threonine kinase 38 (STK38) as a major PPARγ-associated protein. Protein pulldown studies confirmed this protein–protein interaction in transfected cells, and reporter assays demonstrated that STK38 enhanced PPARγ’s transactivating activities without requiring STK38’s kinase activity. In cell-based assays, STK38 increased PPARγ protein stability, extending PPARγ’s half-life from ~1.08 to 1.95 h. Notably, in human preadipocytes, the overexpression of STK38 enhanced adipogenesis, whereas knockdown impaired the process in a PPARγ-dependent manner. Thus, we discovered that STK38 is a novel PPARγ-cofactor promoting adipogenesis, likely through stabilization of PPARγ. © 2021 The Author(s).en_US
dc.description.urihttps://doi.org/10.1080/21623945.2021.1980257en_US
dc.language.isoenen_US
dc.publisherTaylor and Francis Inc.en_US
dc.relation.ispartofAdipocyteen_US
dc.subjectPPARγen_US
dc.subjectSTK38en_US
dc.subjectcofactors and adipocytesen_US
dc.titleSTK38 is a PPARγ-interacting protein promoting adipogenesisen_US
dc.typeArticleen_US
dc.identifier.doi10.1080/21623945.2021.1980257
dc.identifier.pmid34670478
dc.source.volume10
dc.source.issue1
dc.source.beginpage524
dc.source.endpage531
dc.source.countryUnited States


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