The Differential Role of Hif1β/Arnt and the Hypoxic Response in Adipose Function, Fibrosis, and Inflammation

This publication has 50 references indexed in Scilit:

• Adipose Tissue-specific Inhibition of Hypoxia-inducible Factor 1α Induces Obesity and Glucose Intolerance by Impeding Energy Expenditure in Mice*
  Journal of Biological Chemistry, 2010
• Hypoxia-Inducible Factor 1α Induces Fibrosis and Insulin Resistance in White Adipose Tissue
  Molecular and Cellular Biology, 2009
• Ablation of ARNT/HIF1β in Liver Alters Gluconeogenesis, Lipogenic Gene Expression, and Serum Ketones
  Cell Metabolism, 2009
• Blockade of VEGFR2 and Not VEGFR1 Can Limit Diet-Induced Fat Tissue Expansion: Role of Local versus Bone Marrow-Derived Endothelial Cells
  PLOS ONE, 2009
• Hypoxia Decreases Insulin Signaling Pathways in Adipocytes
  Diabetes, 2009
• Regulation of gene expression by hypoxia: Integration of the HIF-transduced hypoxic signal at the hypoxia-responsive element
  Clinica Chimica Acta, 2008
• The Qo site of the mitochondrial complex III is required for the transduction of hypoxic signaling via reactive oxygen species production
  Journal of Cell Biology, 2007
• Inactivation of the Arylhydrocarbon Receptor Nuclear Translocator (Arnt) Suppresses von Hippel-Lindau Disease-Associated Vascular Tumors in Mice
  Molecular and Cellular Biology, 2005
• EPAS1 Promotes Adipose Differentiation in 3T3-L1 Cells
  Journal of Biological Chemistry, 2004
• Conditional Disruption of the Aryl Hydrocarbon Receptor Nuclear Translocator (Arnt) Gene Leads to Loss of Target Gene Induction by the Aryl Hydrocarbon Receptor and Hypoxia-Inducible Factor 1
  Molecular Endocrinology, 2000