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Reactive Oxygen Species Activate the HIF-1α Promoter Via a Functional NFκB Site

Arteriosclerosis Thrombosis and Vascular Biology · 2007 · Vol. 27(4) · pp. 755–761

Steve Bonello✉(University of Namur)Christian ZähringerRachida S. BelAiba(University of Namur)Talija Djordjevic(University of Namur)John Hess(University of Namur)Carine Michiels(University of Namur)Thomas Kietzmann(University of Namur)Agnes Görlach

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Abstract

These findings show for the first time to our knowledge that reactive oxygen species directly link HIF-1alpha and NF-kappaB, implicating an important pathophysiological role of this novel pathway in disorders associated with elevated levels of reactive oxygen species.

Cancer, Hypoxia, and Metabolism Eicosanoids and Hypertension Pharmacology Cancer-related molecular mechanisms researchReactive oxygen speciesTranscription factorActivator (genetics)NADPH oxidaseChromatin immunoprecipitationMolecular biologyNOX4BiologyNF-κBNFKB1

MeSH terms

Binding SitesCells, CulturedGene Expression RegulationHumansHydrogen PeroxidePromoter Regions, GeneticPulmonary ArteryRNA, MessengerThrombinTranscription, GeneticNF-kappa BReactive Oxygen SpeciesPlasminogen Activator Inhibitor 1Myocytes, Smooth MuscleHypoxia-Inducible Factor 1, alpha Subunit

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618

FWCI

12.83

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