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NOX1 — NOX4

Text-mined interactions from Literome

Sorescu et al., Circ Res 2004 : Together, these results suggest that BMP4 produced in ECs by OS stimulates ROS release from the nox1 dependent NADPH oxidase leading to inflammation, a critical early atherogenic step
Ellmark et al., Cardiovasc Res 2005 : Under resting conditions, NADPH oxidase activity in VSMCs is largely dependent upon Nox4 expression
Valente et al., Free Radic Biol Med 2007 : NOX1 NADPH oxidase regulation by the NOXA1 SH3 domain
Choi et al., J Biol Chem 2008 : Ang II enhanced the activity of both Nox1 and Nox2 supported by either adaptor pair, with more effective activation of Nox1 in the presence of NOXO1 and NOXA1 and of Nox2 in the presence of p47(phox) and p67(phox)
Han et al., Hypertension 2008 : We have demonstrated for the first time that disruption of LRs results in NADPH oxidase activation that is abolished by antioxidants and silencing of Nox2 or Nox4
Chose et al., J Cardiovasc Pharmacol 2008 : Distinct role of nox1 , nox2, and p47phox in unstimulated versus angiotensin II-induced NADPH oxidase activity in human venous smooth muscle cells
Dammanahalli et al., Endocrinology 2008 : ET1 significantly attenuated NADPH oxidase activity and cell proliferation, which could be abolished by silence of Nox1 gene, suggesting that ET1 induced inhibition of NADPH oxidase activity was mediated by Nox1
Meng et al., Cardiovasc Res 2008 : Over-expression of Nox4 increased NADPH oxidase activity, which was not influenced by inactivation of Rac1
Chéret et al., J Neurosci 2008 (Encephalitis...) : Neurotoxic activation of microglia is promoted by a nox1 dependent NADPH oxidase
Jaulmes et al., Thromb Res 2009 (MAP Kinase Signaling System) : The aim of the present study was to characterize the role of NADPH oxidase and in particular Nox4 in the regulation of PAI-1 expression in cultured Human Umbilical Venous Endothelial Cells ( HUVECs )
Wang et al., Free Radic Biol Med 2010 (Radiation Injuries, Experimental) : The induction of chronic oxidative stress in HSCs by TBI is probably attributable to the up-regulation of NADPH oxidase 4 (NOX4), because irradiated HSCs expressed an increased level of NOX4 , and inhibition of NOX activity with diphenylene iodonium but not apocynin significantly reduced TBI induced increases in ROS production, oxidative DNA damage, and DNA DSBs in HSCs and dramatically improved HSC clonogenic function
McCarty et al., Med Hypotheses 2010 (Atrial Fibrillation...) : Nox2- and Nox4 dependent NADPH oxidase activity appears to be a major source of this oxidative stress, and oxidants can induce conformational changes in xanthine dehydrogenase, nitric oxide synthase, and the mitochondrial respiratory chain which increase their capacity to generate superoxide as well
Souvannakitti et al., J Neurosci 2010 (Anoxia) : IH treatment increased NADPH oxidase ( NOX ) activity, upregulated NOX2 and NOX4 transcription in adrenal medullae, and a NOX inhibitor prevented the effects of IH on hypoxia evoked chromaffin cell secretion
Edderkaoui et al., J Biol Chem 2011 (Pancreatic Neoplasms) : Up-regulation of p22(phox) by the growth factors results in increased Nox4-p22(phox) complex formation and activation of NADPH oxidase
Moe et al., J Cell Mol Med 2011 (Ventricular Remodeling) : Nox2 and Nox4 siRNA were used to determine whether or not Nox2 and Nox4 mediated TNF-a induced ROS and upregulation of IL-1ß and IL-6 in adult human cardiomyocytes
Shimada et al., BMC urology 2011 (Carcinoma, Transitional Cell...) : NOX4 was overexpressed in several UC cell lines and the NOX inhibitor, diphenylene iodonium reduced intracellular ROS and induced p16 dependent cell cycle arrest at the G1 phase
Youn et al., Diabetologia 2012 (Diabetes Mellitus, Experimental) : Our data demonstrate for the first time that the p47(phox) and NOXO1 dependent activation of NOX1 , but not that of NOX2, NOX4 or mitochondrion, mediates diabetic uncoupling of eNOS
Aoyama et al., Hepatology 2012 (Liver Cirrhosis) : The NOX1/4 inhibitor, GKT137831, attenuated liver fibrosis and ROS production in both SOD1mu and WT mice as well as messenger RNA expression of fibrotic and NOX genes ... Both Ang II and tumor growth factor beta up-regulated NOX4 , but Ang II required NOX1
Weaver et al., Mol Cell Endocrinol 2013 : Inhibition of NADPH oxidase activity blocked stimulated NOX-1 expression ( p < 0.05 )
Peshavariya et al., PloS one 2013 (Inflammation) : Surprisingly, Nox4 gene expression was reduced by TNFa whilst expression of Nox2 , p22phox and p67phox remained unchanged