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NADPH oxidase 1

NADPH oxidase
Voltage-gated proton (hydrogen) channels play an important role in cellular defense against acidic stress. They are unique among ion channels with respect to their extremely high selectivity, marked temperature dependence, and unitary conductance, which is 3 orders of magnitude lower than that of most other ion channels. NOX1 is a homolog of the catalytic subunit of the superoxide-generating NADPH oxidase of phagocytes, gp91phox. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
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Top mentioned proteins: Ros, V1a, CAN, Nox4, ACID
Papers using NADPH oxidase antibodies
Neutrophils from p40phox−/− mice exhibit severe defects in NADPH oxidase regulation and oxidant-dependent bacterial killing
Hawkins Phillip T. et al., In The Journal of Experimental Medicine, 2004
... Rac activation induces NADPH oxidase activity in transgenic COSphox cells, and the ...
Papers on NADPH oxidase
Cofactor Independent Human Antiphospholipid Antibodies Induce Venous Thrombosis in Mice.
Lackner et al., Mainz, Germany. In J Thromb Haemost, Feb 2016
We showed that cofactor independent human monoclonal aPL isolated from APS patients induce proinflammatory and procoagulant cellular responses by activating endosomal NADPH-oxidase-2 (NOX2).
Carrageenan-induced inflammation promotes ROS generation and neutrophil extracellular trap formation in a mouse model of peritonitis.
Donadio et al., Porto Alegre, Brazil. In Eur J Immunol, Feb 2016
Furthermore, although this polysaccharide was able to stimulate reactive oxygen species (ROS) generation by peritoneal neutrophils, NADPH oxidase-derived ROS were dispensable for NET formation by carrageenan.
NADPH oxidase 1 activity and ROS generation are regulated by Grb2/Cbl-mediated proteasomal degradation of NoxO1 in colon cancer cells.
Bae et al., South Korea. In Cancer Res, Feb 2016
In this study, we report a novel mechanism in which Nox1 activity is regulated through the proteasomal degradation of Nox organizer 1 (NoxO1).
Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease.
Kaplan et al., Seattle, United States. In Nat Med, Feb 2016
This was also observed in individuals with chronic granulomatous disease, who lack NADPH oxidase activity but still develop autoimmunity and type I IFN signatures.
Microglia antioxidant systems and redox signaling.
McBean et al., Copenhagen, Denmark. In Br J Pharmacol, Feb 2016
Microglia-derived oxidant production by NADPH oxidase (NOX2) is implicated in many CNS disorders.
Enzymatic oxidative biodegradation of nanoparticles: Mechanisms, significance and applications.
Kagan et al., Pittsburgh, United States. In Toxicol Appl Pharmacol, Feb 2016
We also accentuate the importance of peroxynitrite-driven pathways realized in macrophages via the engagement of NADPH oxidase- and NO synthase-triggered oxidative mechanisms.
Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.
Froehner et al., Sydney, Australia. In Physiol Rev, Jan 2016
In this review, we will consider the various proteins whose expression and function is changed in muscular dystrophies, focusing on Ca(2+)-permeable channels, nitric oxide synthase, NADPH oxidase, and caveolins.
A perspective on NETosis in diabetes and cardiometabolic disorders.
Avogaro et al., Padova, Italy. In Nutr Metab Cardiovasc Dis, Jan 2016
Protein kinase C (PKC) and NADPH oxidase (NOX) are two important targets to counter NETosis in the setting of diabetes.
Emerging Role of Nitric Oxide and Heat Shock Proteins in Insulin Resistance.
Manucha et al., Mendoza, Argentina. In Curr Hypertens Rep, Jan 2016
IR is connected to mitochondrial dysfunction, overproduction of oxidants, accumulation of fat, and an over-activation of the renin-angiotensin system linked to the NADPH oxidase activity.
Ncf1 polymorphism reveals oxidative regulation of autoimmune chronic inflammation.
Wing et al., Stockholm, Sweden. In Immunol Rev, Jan 2016
We found that NCF1 and NADPH oxidase 2 (NOX2) complex-derived ROS is an important regulator of several chronic inflammatory disorders by using models for rheumatoid arthritis, multiple sclerosis, psoriasis and psoriasis arthritis, gout, and lupus.
Apocynin prevents mitochondrial burdens, microglial activation, and pro-apoptosis induced by a toxic dose of methamphetamine in the striatum of mice via inhibition of p47phox activation by ERK.
Kim et al., South Korea. In J Neuroinflammation, Dec 2015
BACKGROUND: Activation of NADPH oxidase (PHOX) plays a critical role in mediating dopaminergic neuroinflammation.
Ligation of Glycophorin A Generates Reactive Oxygen Species Leading to Decreased Red Blood Cell Function.
Ghiran et al., Kyoto, Japan. In Plos One, Dec 2015
In this study, using luminometric- and fluorescence-based methods, we show that ligation of glycophorin A (GPA) on human red blood cells (RBCs) results in a 2.1-fold, NADPH-oxidase-dependent increase in intracellular ROS that, in turn, trigger multiple downstream cascades leading to caspase-3 activation, ATP release, and increased band 3 phosphorylation.
Excess TGF-β mediates muscle weakness associated with bone metastases in mice.
Guise et al., Indianapolis, United States. In Nat Med, Nov 2015
We found that transforming growth factor (TGF)-β, released from the bone surface as a result of metastasis-induced bone destruction, upregulated NADPH oxidase 4 (Nox4), resulting in elevated oxidization of skeletal muscle proteins, including the ryanodine receptor and calcium (Ca(2+)) release channel (RyR1).
Cardiac-targeted NADPH oxidase 4 in the adaptive cardiac remodelling of the murine heart.
Shah et al., Tromsø, Norway. In Lancet, Mar 2015
NADPH oxidase (NOX) proteins produce reactive oxygen species (ROS) involved in redox signalling, and our recent studies have found that an increase in Nox4 during pressure overload protects the heart against failure.
Chemical approaches to discovery and study of sources and targets of hydrogen peroxide redox signaling through NADPH oxidase proteins.
Chang et al., In Annu Rev Biochem, 2014
In this context, a major source of H2O2 for redox signaling purposes is the NADPH oxidase (Nox) family of enzymes, which were classically studied for their roles in phagocytic immune response but have now been found to exist in virtually all mammalian cell types in various isoforms with distinct tissue and subcellular localizations.
Protein disulfide isomerase is required for platelet-derived growth factor-induced vascular smooth muscle cell migration, Nox1 NADPH oxidase expression, and RhoGTPase activation.
Laurindo et al., São Paulo, Brazil. In J Biol Chem, 2012
PDI is required to support Nox1/redox and GTPase-dependent VSMC migration.
NADPH oxidase 1 overexpression enhances invasion via matrix metalloproteinase-2 and epithelial-mesenchymal transition in melanoma cells.
Meyskens et al., Irvine, United States. In J Invest Dermatol, 2012
Nox1 was overexpressed in all melanoma cell lines examined, and enhanced cell invasion by MMP-2 upregulation and EMT induction
Hypoxia induces nitric oxide synthase in rheumatoid synoviocytes: consequences on NADPH oxidase regulation.
Borderie et al., Paris, France. In Free Radic Res, 2012
results provide evidence for upregulation of iNOS and NOX activities in rheumatoid arthritis synoviocytes under hypoxia conditions, associated to an increased peroxynitrite production
Novel role of NOX in supporting aerobic glycolysis in cancer cells with mitochondrial dysfunction and as a potential target for cancer therapy.
Huang et al., Houston, United States. In Plos Biol, 2011
Upregulation of NOX is important to maintain high glycolytic activity in cells with mitochondrial dysfunction. Cancer cells with compromised mitochondrial function due to p53 loss show elevated NOX activity and increased sensitivity to NOX inhibition.
Genetic interleukin-10 deficiency causes vascular remodeling via the upregulation of Nox1.
Sun et al., Oklahoma City, United States. In J Hypertens, 2011
IL-10KO-induced vascular structure damage may be mediated by the upregulation of Nox1
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