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Thyroid Hormone Receptor Interacting Protein 3 (Trip3) Is a Novel Coactivator of Hepatocyte Nuclear Factor-4

¹ Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan
² First Department of Internal Medicine, Osaka Medical College, Osaka, Japan
³ Second Department of Internal Medicine, Hyogo Medical College of Medicine, Hyogo, Japan

Mutations of the hepatocyte nuclear factor-4 (HNF-4) gene are associated with a subtype of maturity-onset diabetes of the young (MODY1) that is characterized by impaired insulin secretion in response to a glucose load. HNF-4, which is a transcription factor expressed in pancreatic ß-cells, plays an important role in regulating the expression of genes involved in glucose metabolism. Thus, cofactors that interact with HNF-4 and modify its transcriptional activity might also play an important role in regulating the metabolic pathways in pancreatic ß-cells, and the genes of such cofactors are plausible candidate genes for MODY. In the present study, we showed, using a yeast two-hybrid screening assay, that thyroid hormone receptor interacting protein 3 (Trip3) interacted with HNF-4, and their interaction was confirmed by the glutathione S-transferase pull-down assay. Human Trip3 cDNA contained an open reading frame for a protein of 155 amino acids, and the gene was expressed in both pancreatic islets and MIN6 cells. Cotransfection experiments indicated that Trip3 could enhance (two- to threefold) the transcription activity of HNF-4 in COS-7 cells and MIN6 cells. These results suggest that Trip3 is a coactivator of HNF-4. Mutation screening revealed that variation of the Trip3 gene is not a common cause of MODY/early-onset type 2 diabetes in Japanese individuals. Trip3 may play an important role in glucose metabolism by regulating the transcription activity of HNF-4.

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