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EGFR — NOX5

Text-mined interactions from Literome

Wang et al., Free Radic Biol Med 2005 : The increase in NADPH oxidase activity was mediated by EGFR activation
Cheng-Hsien et al., Pflugers Arch 2006 : Both NAD ( P ) H oxidase inhibitor, diphenyliodonium ( DPI ) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal regulated kinase ( ERK ) phosphorylation caused by ET-1
Murillo et al., Biochem J 2007 : Activation of NADPH oxidase by transforming growth factor-beta in hepatocytes mediates up-regulation of epidermal growth factor receptor ligands through a nuclear factor-kappaB dependent mechanism ... Results indicate that DPI ( diphenyleneiodonium ) and apocynin, two NOX ( NADPH oxidase ) inhibitors, and SB431542, an inhibitor of the TbetaR-I ( TGF-beta receptor I ), block up-regulation of EGFR ligands and Akt activation
Moody et al., J Pharmacol Exp Ther 2012 (Lung Neoplasms) : EGFR transactivation caused by the addition of PACAP to NCI-H838 cells was inhibited by N-acetyl-cysteine ( antioxidant ), tiron ( superoxide scavenger ), diphenylene iodonium ( NADPH oxidase inhibitor ), or 1- [ 6- [ [ ( 17ß ) -3-methoxyestra-1,3,5 ( 10 ) -trien-17-yl ] amino ] hexyl ] -1H-pyrrole-2,5-dione ( U73122 ; phospholipase C inhibitor ), but not N- [ 2- [ [ 3- ( 4-bromophenyl ) -2-propenyl ] amino ] ethyl ] -5-isoquinolinesulfonamide ( H89 ; protein kinase A inhibitor )
Tseng et al., Arch Toxicol 2012 : NADPH oxidase produced superoxide mediates EGFR transactivation by c-Src in arsenic trioxide stimulated human keratinocytes
Duru et al., Surgery 2012 : Urokinase requires NAD ( P ) H oxidase to transactivate the epidermal growth factor receptor
Norton et al., Antioxid Redox Signal 2013 (Anoxia) : As epidermal growth factor receptor (EGFR) mediates Rac1 dependent NOX activation in renal mesangial cells, we further sought to examine the role EGFR plays in this response ... Conclusion : CH augments membrane depolarization induced pulmonary VSM Ca ( 2+ ) sensitization and vasoconstriction through EGFR dependent stimulation of Rac1 and NOX 2