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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Thrap3 docks on phosphoserine 273 of PPAR gamma and controls diabetic gene programming

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Title
Thrap3 docks on phosphoserine 273 of PPAR gamma and controls diabetic gene programming
Author
Choi, Jang HyunChoi, Sun-SilKim, Eun SunJedrychowski, Mark P.Yang, Yong RyoulJang, Hyun-JunSuh, Pann-GhillBanks, Alexander S.Gygi, Steven P.Spiegelman, Bruce M.
Issue Date
2014-11
Publisher
COLD SPRING HARBOR LAB PRESS
Citation
GENES & DEVELOPMENT, v.28, no.21, pp.2361 - 2369
Abstract
Phosphorylation of peroxisome proliferator-activated receptor gamma (PPAR gamma) 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 PPAR gamma when it is phosphorylated at Ser273, and this interaction controls the diabetic gene programming mediated by the phosphorylation of PPAR gamma. Knockdown of Thrap3 restores most of the genes dysregulated by CDK5 action on PPAR gamma 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.
URI
https://scholarworks.unist.ac.kr/handle/201301/9364
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84908416698
DOI
10.1101/gad.249367.114
ISSN
0890-9369
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BIO_Journal Papers
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