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Title

Does chasing selected 'Fox' to the nucleus prevent diabetes?
Authors
Wang, Haiyan
Wollheim, Claes
Published in Trends in Molecular Medicine. 2005, vol. 11, no. 6, p. 262-5
Abstract Foxa2 (Hnf3beta) is a winged-helix/forkhead transcription factor that regulates gene expression in the liver, pancreatic islets and adipocytes. It is required for the maintenance of glucose and lipid homeostasis. Hyperinsulinemia-mediated inactivation of Foxa2 by nuclear exclusion has recently been implicated in the development of liver steatosis and insulin resistance in three animal models of diabetes. These abnormalities were cured by adenovirus-mediated expression of a constitutively active form of Foxa2 containing a mutated T156 phosphorylation site, which increases fatty acid oxidation and reduces its biosynthesis. Accordingly, the prevention of phosphorylation of Foxa2 was suggested as a pharmacological target for the treatment of obesity and diabetes.
Keywords Animals — Apoptosis — Binding Sites — Cell Nucleus/metabolism — DNA-Binding Proteins/metabolism/physiology — Diabetes Mellitus/drug therapy/prevention & control — Fatty Acids/metabolism — Forkhead Transcription Factors — Gene Expression Regulation — Genetic Predisposition to Disease — Glucose/metabolism — Hepatocyte Nuclear Factor 3-beta — Homeostasis — Humans — Hypoglycemia — Insulin Resistance — Islets of Langerhans — Lipid Metabolism — Liver/metabolism — Models, Biological — Mutation — Nuclear Proteins/metabolism — Obesity/drug therapy — Oxygen/metabolism — Phosphorylation — Transcription Factors/metabolism/physiology
Identifiers
PMID: 15949766
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Article (Published version) (98 Kb) - public document Free access
Structures
Faculté de médecine / Section de médecine fondamentale / Département de physiologie cellulaire et métabolisme
Citation
(ISO format) 		WANG, Haiyan, WOLLHEIM, Claes. Does chasing selected 'Fox' to the nucleus prevent diabetes?. In: Trends in Molecular Medicine, 2005, vol. 11, n° 6, p. 262-5. https://archive-ouverte.unige.ch/unige:47614

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Deposited on : 2015-03-06

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