Repression of HNF1α-mediated transcription by amino-terminal enhancer of split (AES)

Eun Hee Han, Amanda A. Gorman, Puja Singh, Young In Chi

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

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 languageEnglish (US)
Pages (from-to)14-20
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume468
Issue number1-2
DOIs
StatePublished - Dec 4 2015

Bibliographical note

Funding 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 .

Keywords

  • AES
  • Diabetes
  • Gene regulation
  • HNF1α
  • Homeodomain
  • Insulin secretion
  • POU transcription factor
  • Protein-protein interaction

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