HNF1α (Hepatocyte Nuclear Factor 1α) is one of the master regulators in pancreatic beta-cell development and function, and the mutations in Hnf1α are the most common monogenic causes of diabetes mellitus. As a member of the POU transcription factor family, HNF1α exerts its gene regulatory function through various molecular interactions; however, there is a paucity of knowledge in their functional complex formation. In this study, we identified the Groucho protein AES (Amino-terminal Enhancer of Split) as a HNF1α-specific physical binding partner and functional repressor of HNF1α-mediated transcription, which has a direct link to glucose-stimulated insulin secretion in beta-cells that is impaired in the HNF1α mutation-driven diabetes.
|Original language||English (US)|
|Number of pages||7|
|Journal||Biochemical and Biophysical Research Communications|
|State||Published - Dec 4 2015|
Bibliographical noteFunding Information:
We wish to thank Dr. Sabire Őzcan at the University of Kentucky for a kind gift of MIN6 cell cDNA library for yeast two-hybrid screenings and MIN6 cells for functional studies. This work was funded by the American Diabetes Association ( 7-08-CD-03 ) and the NIH Grant P20RR20171 from the COBRE program of the National Center for Research Resources .
- Gene regulation
- Insulin secretion
- POU transcription factor
- Protein-protein interaction