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

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

doi:10.1016/j.bbrc.2015.11.007

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

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

Hormel Institute

Research output: Contribution to journal › Article › peer-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 language	English (US)
Pages (from-to)	14-20
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	468
Issue number	1-2
DOIs	https://doi.org/10.1016/j.bbrc.2015.11.007
State	Published - 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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title = "Repression of HNF1α-mediated transcription by amino-terminal enhancer of split (AES)",

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.",

keywords = "AES, Diabetes, Gene regulation, HNF1α, Homeodomain, Insulin secretion, POU transcription factor, Protein-protein interaction",

author = "Han, {Eun Hee} and Gorman, {Amanda A.} and Puja Singh and Chi, {Young In}",

note = "Funding Information: We wish to thank Dr. Sabire {\H O}zcan 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 . ",

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doi = "10.1016/j.bbrc.2015.11.007",

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AU - Gorman, Amanda A.

AU - Singh, Puja

AU - Chi, Young In

N1 - 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 .

PY - 2015/12/4

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N2 - 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.

AB - 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.

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KW - Gene regulation

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KW - Insulin secretion

KW - POU transcription factor

KW - Protein-protein interaction

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

Abstract

Bibliographical note

Keywords

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