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ANGPT2 — NOX5

Text-mined interactions from Literome

Frank et al., Endocrinology 2000 : In the presence of a NADH/NADPH oxidase inhibitor, diphenyleneiodonium ( DPI ) or an antioxidant, alpha-tocopherol, Ang II-induced protein tyrosine phosphorylation of two major proteins ( p120, p70 ) and ERK activation were markedly reduced , whereas ERK activation by epidermal growth factor was unaffected
de Gasparo et al., Heart Fail Rev 2002 : Through its AT(1) receptor, Ang II stimulates the long-term increase of several membrane component of NADPH oxidase such as P ( 22 ) phox or nox-1 and causes an increased activity of NADPH oxidase with inactivation of NO leading to impaired endothelium dependent vasorelaxation, vascular smooth muscle cell hypertrophy, proliferation and migration, extracellular matrix formation, thrombosis, cellular infiltration and inflammatory reaction
Gorin et al., American journal of physiology. Renal physiology 2003 : These data provide the first evidence that activation by AA of a Rac1 regulated, Nox4 based NAD ( P ) H oxidase and subsequent generation of ROS mediate the effect of ANG II on Akt/PKB activation and protein synthesis in MCs
Xie et al., J Cell Physiol 2004 : Diphenylene iodonium ( DPI ), inhibitor of NAD ( P ) H oxidase , and tiron, superoxide scavenger, inhibited Ang II- and Ang II+ IL-1beta stimulated increases in OPN mRNA
Andresen et al., American journal of physiology. Renal physiology 2005 (Hypertension, Renal) : ANG II activation of phospholipase D ( PLD ) is required for ERK and NAD ( P ) H oxidase activation, both of which are involved in hypertension
Luchtefeld et al., Biochem Biophys Res Commun 2005 (Cardiomyopathies...) : Since reactive oxygen species ( ROS ) induce MMP-2 and angiotensin II (ANG II) enhances NADPH-oxidase dependent ROS formation, we assessed whether ANG II induces MMP-2 in a NADPH-oxidase dependent manner
Fujii et al., J Biol Chem 2005 : Ang II-induced NFAT activation was suppressed by diphenyleneiodonium ( an NADPH oxidase inhibitor ), dominant negative ( DN ) -Rac, DN-p47(phox), and an inhibitor of Galpha(12/13) ( Galpha(12/13)-specific regulator of G protein signaling domain of p115RhoGEF, p115-regulator of G protein signaling (RGS) )
Yamagishi et al., Cell Tissue Res 2005 : Furthermore, PEDF inhibited Ang-II induced up-regulation of mRNA levels of p22phox, Nox4, and gp91phox/Nox2 , which are membrane components of NADPH oxidase, and its enzymatic activity in HUVEC
Chan et al., Circ Res 2005 : We tested the hypothesis that NADPH oxidase derived superoxide anion ( O2*- ) in the RVLM mediates Ang II-induced pressor response via activation of mitogen activated protein kinase ( MAPK ) signaling pathways
Pech et al., Am J Hypertens 2006 (Disease Models, Animal...) : In response to ANG II , Nox subunits protein expression increased in HS but not in the NS or LS rats
Yusof et al., Am J Physiol Heart Circ Physiol 2007 (Disease Models, Animal...) : Our work suggests that ANG II , formed by the enzymatic activity of ACE and chymase, plays an important role in inducing postischemic LR and LA, effects that involve the engagement of both AT(1) and AT(2) receptors and may be mediated by CGRP and NADPH oxidase
Choi et al., J Biol Chem 2008 : The effects of constitutively active alpha subunits of G proteins and of various pharmacological agents implicated signaling by a pathway comprising AT(1)R, Galpha ( q/11 ), phospholipase C-beta, and protein kinase C as largely, but not exclusively, responsible for Ang II-induced activation of Nox1 and Nox2 in the reconstituted cells
Sampaio et al., Hypertension 2007 : Ang II significantly increased activation of c-Src, ERK1/2, and NAD ( P ) H oxidase and reduced phosphorylation of SHP-2 ( P < 0.05 ) in human endothelial cells
Montezano et al., Arterioscler Thromb Vasc Biol 2008 : Aldo and Ang II costimulation induced c-Src dependent activation of NAD ( P ) H oxidase and c-Src independent activation of ERK1/2 ( P < 0.05 ), without effect on ERK5, p38MAPK, or JNK
Hirata et al., Regul Pept 2009 : Ang II activates NAD ( P ) H oxidase in several tissues with important function in the control of insulin secretion ... Considering the concomitant occurrence of hypertension, insulin resistance and pancreatic B cell secretion impairment in the development of type II diabetes the aim of the present study was to evaluate the effect of ANG II on NAD ( P ) H oxidase activation in isolated pancreatic islets
White et al., Am J Physiol Cell Physiol 2009 : Since ANG II activates NADPH oxidase , we tested the hypothesis that NADPH oxidase mediates the pump inhibition
Montezano et al., Circ Res 2010 (Inflammation) : Human ECs possess functionally active Nox5 , regulated by Ang II and ET-1 through Ca ( 2+ ) /calmodulin dependent, Rac-1 independent mechanisms ... Nox5 activation by Ang II and ET-1 induces ROS generation and ERK1/2 phosphorylation
Herrera et al., J Biol Chem 2010 : In some cells, Ang II stimulates protein kinase C ( PKC ), whose a isoform ( PKCa ) can activate NADPH oxidase
Shanmugam et al., J Mol Cell Cardiol 2011 (Cardiomyopathy, Hypertrophic) : AT1 was physically associated with NOX2 both in vitro and in vivo, and Ang-II increased this interaction in vivo ... These results demonstrate that Ang-II induced cardiomyocyte hypertrophy is mediated through AT1, NOX2 and the induction of WISP1, and may involve the direct interaction of AT1 with NOX2
Fang et al., American journal of physiology. Renal physiology 2013 (Renal Insufficiency, Chronic) : Activation of AMPK with 5-aminoimidazole-4-carboxamide-1-ß-d-ribofuranoside ( AICAR ) mimicked, while inhibition of AMPK with compound C abrogated, the effect of adiponectin on ANG II-induced activation of NADPH oxidase