NADPH oxidases are responsible for the failure of nitric oxide to inhibit migration of smooth muscle cells exposed to high glucose
- 1 December 2009
- journal article
- Published by Elsevier in Free Radical Biology & Medicine
- Vol. 47 (11) , 1578-1583
- https://doi.org/10.1016/j.freeradbiomed.2009.08.026
Abstract
No abstract availableKeywords
This publication has 24 references indexed in Scilit:
- Identification of Structural Elements in Nox1 and Nox4 Controlling Localization and ActivityAntioxidants and Redox Signaling, 2009
- Direct Interaction of the Novel Nox Proteins with p22phox Is Required for the Formation of a Functionally Active NADPH OxidaseJournal of Biological Chemistry, 2004
- Distinct Subcellular Localizations of Nox1 and Nox4 in Vascular Smooth Muscle CellsArteriosclerosis, Thrombosis, and Vascular Biology, 2004
- Nox4 as the Major Catalytic Component of an Endothelial NAD(P)H OxidaseCirculation, 2004
- NAD(P)H oxidase participates in the signaling events in high glucose-induced proliferation of vascular smooth muscle cellsLife Sciences, 2003
- Upregulation of Nox-Based NAD(P)H Oxidases in Restenosis After Carotid InjuryArteriosclerosis, Thrombosis, and Vascular Biology, 2002
- Upregulation of the vascular NAD(P)H-oxidase isoforms Nox1 and Nox4 by the renin-angiotensin system in vitro and in vivoFree Radical Biology & Medicine, 2001
- Novel gp91
phox
Homologues in Vascular Smooth Muscle CellsCirculation Research, 2001
- Interactions between NO and reactive oxygen species: pathophysiological importance in atherosclerosis, hypertension, diabetes and heart failureCardiovascular Research, 1999
- The phosphorylation targets of p47phox, a subunit of the respiratory burst oxidase. Functions of the individual target serines as evaluated by site-directed mutagenesis.Journal of Clinical Investigation, 1995