◀ Back to EPHB2

EPHB2 — NOX4

Text-mined interactions from Literome

Viedt et al., Arterioscler Thromb Vasc Biol 2000 : JNK and p38 MAPK, but not ERK , activation was inhibited by an inhibitor of NAD ( P ) H oxidase
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
Xiao et al., Am J Physiol Cell Physiol 2002 (Cardiomegaly...) : We found that ARVM express gp91(phox), p22(phox), p67(phox), and p47(phox), four major components of NAD ( P ) H oxidase, and that alpha ( 1 ) -AR stimulated ERK1/2 activation was blocked by four structurally unrelated inhibitors of NAD ( P ) H oxidase [ diphenyleneiodonium, phenylarsine oxide, 4- ( 2-aminoethyl ) benzenesulfonyl fluoride, and cadmium ]
Schäfer et al., Circ Res 2003 (MAP Kinase Signaling System) : All three inhibitions suppressed the proliferative response : PD inhibited NAD ( P ) H oxidase activation ; p22phox antisense transfection did not inhibit ERK2 activation, but suppressed ROS production ; and MQ inhibited ERK2 activation and ROS production
Chen et al., Endocrinology 2004 (MAP Kinase Signaling System) : In addition, E2 and E2-BSA induced ERK2/1 activation and ICI 182,780 could inhibit NOx production by E2
Schneider et al., Proc Natl Acad Sci U S A 2003 : In neuroprogenitor, hypothalamic, and lymphoid cells, ERK1/2 activation is fully controlled by the NADPH oxidase dependent ROS production
Touyz et al., Arterioscler Thromb Vasc Biol 2005 : The p47phox : actin interaction, through cortactin, plays an important role in Ang II-mediated site directed assembly of functionally active NAD ( P ) H oxidase , ROS generation, and activation of redox-sensitive p38MAP kinase and Akt, but not ERK1/2
Kishida et al., J Neurochem 2005 : NADPH oxidase is required for NMDA receptor dependent activation of ERK in hippocampal area CA1
Chan et al., Circ Res 2005 : These results suggest that NADPH oxidase derived O2*- underlies the activation of p38 MAPK or ERK1/2 by Ang II in the ventrolateral medulla
Sturrock et al., Am J Physiol Lung Cell Mol Physiol 2006 : HPASMC activation of the MAP kinases ERK1/2 was reduced by the NAD ( P ) H oxidase inhibitors DPI and 4- ( 2-aminoethyl ) benzenesulfonyl fluoride, suggesting that TGF-beta1 may facilitate proliferation by upregulating Nox4 and ROS production, with transient oxidative inactivation of phosphatases and augmentation of growth signaling cascades
Zhang et al., Free Radic Biol Med 2006 : These results suggest that notoginsenoside R1 inhibits TNF-alpha induced ERK activation and subsequent fibronectin overexpression and migration in HASMCs by suppressing NADPH oxidase mediated ROS generation and directly scavenging ROS
Massaro et al., Proc Natl Acad Sci U S A 2006 : Western blots showed that DHA blocked nuclear p65 NF-kappaB subunit translocation by decreasing cytokine stimulated reactive oxygen species and ERK1/2 activation by effects on both NAD ( P ) H oxidase and PKCepsilon activities
Chen et al., Am J Physiol Heart Circ Physiol 2007 (Anoxia...) : Our findings underscore the important role of NADPH oxidase and its subunit p47(phox) in modulating Akt and ERK1/2 activation, angiogenic growth factor expression, and angiogenesis in myocardium undergoing I/R
Miller et al., Brain Res 2007 (Nerve Degeneration...) : Cytotoxicity of paraquat in microglial cells : Involvement of PKCdelta- and ERK1/2 dependent NADPH oxidase
Chan et al., J Hypertens 2007 : We tested the hypothesis that the NADPH oxidase dependent phosphorylation of ERK1/2 after the activation of conventional protein kinase C ( PKC ) mediates the AT1R dependent long-term pressor effects of angiotensin II via transcriptional induction of the proto-oncogene c-fos gene in RVLM
Abid et al., J Biol Chem 2007 : We show that NADPH oxidase activity is required for VEGF activation of phosphoinositide 3-kinase-Akt-forkhead, and p38 MAPK, but not ERK1/2 or JNK
Wu et al., J Biol Chem 2007 (MAP Kinase Signaling System) : Rac1, therefore, bifurcates Tat signaling, leading to concurrent but separate Nox4 dependent Ras/ERK activation, and Nox2 dependent JNK activation
Sampaio et al., Hypertension 2007 : Ang II-induced phosphorylation of c-Src, extracellular signal regulated kinase ( ERK ) 1/2, and SHP-2 and activation of NAD ( P ) H oxidase were assessed in the absence and presence of Ang- ( 1-7 ) ( 10 ( -6 ) mol/L, 15 minutes ) by immunoblotting and lucigenin enhanced chemiluminescence, respectively
Wójcicka et al., Life Sci 2008 (Disease Models, Animal...) : NADPH oxidase inhibitor, apocynin, prevented leptin 's effect on BP, ERK , Na ( + ), K ( + ) -ATPase/Na ( + ) excretion and NO formation at all time points
Anilkumar et al., Arterioscler Thromb Vasc Biol 2008 : Nox4 overexpression induced basal activation of ERK1/2 and JNK whereas Nox2 transfected cells showed a modest increase in p38MAPK activation
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
Schröder et al., Arterioscler Thromb Vasc Biol 2009 : Consequently, downregulation of Nox4 promoted ERK1/2 signaling : Proliferation was increased and through phosphorylation of the inhibitory site serine612, ERK1/2 inhibited the activation of the insulin-receptor substrate-1 (IRS-1) and thereby prevented differentiation in response to insulin
Zhu et al., Biochem J 2009 : NAD ( P ) H oxidase mediated menadione induced ROS production, which then stimulated phosphorylation of p38 MAPK ( mitogen activated protein kinase ) and ERK1/2 ( extracellular-signal regulated kinase 1/2 ), and increased actin polymerization and cytoskeletal protrusions
Wu et al., Br J Pharmacol 2009 : Effects of tripterine were investigated on endothelial barrier function, inducible nitric oxide synthase (iNOS) expression, nicotinamide adenine dinucleotide phasphate ( NADPH ) oxidase activity, 3-nitrotyrosine formation, protein phosphatase type 2A (PP2A) activity, activation of extracellular regulated kinase (ERK) , c-Jun terminal kinase (JNK) and Janus kinase ( Jak2 ), and degradation of IkappaB in microvascular endothelial cells exposed to pro-inflammatory stimulus [ lipopolysaccharide (LPS) + interferon gamma (IFNgamma) ] and on vascular permeability in air pouches of mice injected with LPS + IFNgamma
Banerjee et al., Toxicol Appl Pharmacol 2011 (Calcium Signaling) : The NADPH oxidase inhibitor apocynin and diphenyleneiodonium chloride also inhibited ERK activation indicating activation of ERK in arsenic exposed HKM also depends on signals from NADPH oxidase pathway
Sancho et al., Free Radic Biol Med 2011 : Finally, we determined that NOX4 induction by PGE ( 2 ) was dependent on ERK1/2 signaling
Robin et al., J Mol Cell Cardiol 2011 (Arrhythmias, Cardiac) : Moreover, NADPH oxidase inhibition or antioxidant MPG prevented both A ( 1 ) AR-mediated arrhythmias and ERK phosphorylation
Askarova et al., Neuroscience 2011 : Ab ( RAGE ) as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aß42 induced ERK1/2 and cPLA2 phosphorylation in CECs
Abdala-Valencia et al., PloS one 2011 : VCAM-1 activation of endothelial cell NADPH oxidase/PKCa/PTP1B induces transient ERK1/2 activation that is necessary for VCAM-1 dependent leukocyte TEM
Nakanishi et al., Int J Mol Med 2013 : Blocking of the activity of Nox with diphenylene iodonium inhibited ROS production, activation of extracellular signal regulated kinase ( ERK ), and the expression of RANK, PU.1 and MITF
Ramkhelawon et al., FASEB J 2013 : NADPH oxidase inhibition with apocynin prevented both the colocalization of AT1R with Cav1 and the induction of ERK1/2 by shear stress