Hepatocyte Nuclear Factor-4α Is Essential for Glucose-stimulated Insulin Secretion by Pancreatic β-Cells-Reference-Cited by-同舟云学术

Hepatocyte Nuclear Factor-4α Is Essential for Glucose-stimulated Insulin Secretion by Pancreatic β-Cells

Published:2006-02 Issue:8 Volume:281 Page:5246-5257
ISSN:0021-9258
Container-title:Journal of Biological Chemistry
language:en
Short-container-title:Journal of Biological Chemistry

Author:

Miura Atsuko,Yamagata Kazuya,Kakei Masafumi,Hatakeyama Hiroyasu,Takahashi Noriko,Fukui Kenji,Nammo Takao,Yoneda Kazue,Inoue Yusuke,Sladek Frances M.,Magnuson Mark A.,Kasai Haruo,Miyagawa Junichiro,Gonzalez Frank J.,Shimomura Iichiro

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference45 articles.

1. Liver-enriched transcription factor HNF-4 is a novel member of the steroid hormone receptor superfamily.

2. Disruption of the HNF-4 gene, expressed in visceral endoderm, leads to cell death in embryonic ectoderm and impaired gastrulation of mouse embryos.

3. Nuclear Receptors and Genetic Diseases;Sladek,2001

4. Molecular Mechanisms and Clinical Pathophysiology of Maturity-Onset Diabetes of the Young

5. Mutations in the hepatocyte nuclear factor-4α gene in maturity-onset diabetes of the young (MODY1)

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