Repression of HNF1α-mediated transcription by amino-terminal enhancer of split (AES). Biochem Biophys Res Commun 2015 Dec 4-11;468(1-2):14-20
Date
11/10/2015Pubmed ID
26549228DOI
10.1016/j.bbrc.2015.11.007Scopus ID
2-s2.0-84947714418 (requires institutional sign-in at Scopus site) 4 CitationsAbstract
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.
Author List
Han EH, Gorman AA, Singh P, Chi YIAuthor
Young-In Chi PhD Assistant Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCell Line
Co-Repressor Proteins
Glucose
HeLa Cells
Hepatocyte Nuclear Factor 1-alpha
Humans
Insulin
Insulin-Secreting Cells
Mice
Mutation
Protein Interaction Domains and Motifs
Protein Interaction Maps
Repressor Proteins
Transcription, Genetic
Transcriptional Activation
