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- 저자 : Jedrychowski, Mark P. (검색결과 1 건)
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Thrap3 docks on phosphoserine 273 of PPARγ and controls diabetic gene programming
Choi, Jang Hyun,Choi, Sun-Sil,Kim, Eun Sun,Jedrychowski, Mark P.,Yang, Yong Ryoul,Jang, Hyun-Jun,Suh, Pann-Ghill,Banks, Alexander S.,Gygi, Steven P.,Spiegelman, Bruce M. Cold Spring Harbor Laboratory Press 2014 Genes & development Vol.28 No.21
<P>Phosphorylation of PPARγ at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimulates insulin resistance. Choi et al. find that Thrap3 (thyroid hormone receptor-associated protein 3) can directly interact with PPARγ when it is phosphorylated at Ser273, and this interaction controls the diabetic gene programing mediated by the phosphorylation of PPARγ. Reduced expression of Thrap3 in fat tissue by antisense oligonucleotides improves hyperglycemia and insulin resistance in high-fat-fed mice without affecting body weight.</P><P>Phosphorylation of peroxisome proliferator-activated receptor γ (PPARγ) at Ser273 by cyclin-dependent kinase 5 (CDK5) in adipose tissue stimulates insulin resistance, but the underlying molecular mechanisms are unclear. We show here that Thrap3 (thyroid hormone receptor-associated protein 3) can directly interact with PPARγ when it is phosphorylated at Ser273, and this interaction controls the diabetic gene programming mediated by the phosphorylation of PPARγ. Knockdown of Thrap3 restores most of the genes dysregulated by CDK5 action on PPARγ in cultured adipocytes. Importantly, reduced expression of Thrap3 in fat tissue by antisense oligonucleotides (ASOs) regulates a specific set of genes, including the key adipokines adiponectin and adipsin, and effectively improves hyperglycemia and insulin resistance in high-fat-fed mice without affecting body weight. These data indicate that Thrap3 plays a crucial role in controlling diabetic gene programming and may provide opportunities for the development of new therapeutics for obesity and type 2 diabetes.</P>
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