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Does chasing selected 'Fox' to the nucleus prevent diabetes?

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 AnimalsApoptosisBinding SitesCell Nucleus/metabolismDNA-Binding Proteins/metabolism/physiologyDiabetes Mellitus/drug therapy/prevention & controlFatty Acids/metabolismForkhead Transcription FactorsGene Expression RegulationGenetic Predisposition to DiseaseGlucose/metabolismHepatocyte Nuclear Factor 3-betaHomeostasisHumansHypoglycemiaInsulin ResistanceIslets of LangerhansLipid MetabolismLiver/metabolismModels, BiologicalMutationNuclear Proteins/metabolismObesity/drug therapyOxygen/metabolismPhosphorylationTranscription Factors/metabolism/physiology
PMID: 15949766
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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. doi: 10.1016/j.molmed.2005.04.003 https://archive-ouverte.unige.ch/unige:47614

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Deposited on : 2015-03-06

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