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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
NADH + H+ + O2
NAD+ + H2O2
NADPH + H+ + O2
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the protein shows NADH-ubiquinone-1 oxidoreductase activity (EC 1.6.5.3), NADPH oxidase (EC 1.6.3.1) and NADPH-ubiquinone-1 oxidoreductase (EC 1.6.5.2) activities
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NADPH + H+ + O2
NAD(P)+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
additional information
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
enzyme deficiency causes serious hypothyroidism
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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involved in Grave's disease
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
involved in Grave's disease
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H oxidase transfers electrons across membranes to oxygen and generate superoxide anions which rapidly dismutate to hydrogen peroxide
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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enzyme is an important factor for the generation of reactive oxygen species in astrocytes, and the reactive oxygen species generated by enzyme play an essential role in astrocyte survival
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
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production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NAD(P)H + H+ + O2
NAD(P)+ + H2O2
production of hydrogen peroxide in thyroid gland that is required for thyroid hormone synthesis
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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2 electrons are transferred from cytosolic NADPH to FAD and in succession across the membrane, via redox changes in heme irons. Finally, each electron reduces a molecule of oxygen to a superoxide radical, which is subsequently released outside the cell or in a topologically equivalent compartment, such as a vesicle lumen
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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oxidizes NADH and, less efficiently, NADPH
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NADH + H+ + O2
NAD+ + H2O2
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oxidizes NADH and, less efficiently, NADPH
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
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NADH + H+ + O2
NAD+ + H2O2
activity with NADPH is much lower than with NADH
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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687742, 710782, 711166, 711688, 711763, 712075, 712673, 712711, 712713, 713338, 724704, 724778, 741619, 742310, 742556, 742557, 743686 -
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
NOX3 is a relevant source of reactive oxygen species generation in the cochlear and vestibular systems. NOX3-dependent ROS generation might contribute to hearing loss and balance problems in response to toxic drugs
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
NOX3 is a relevant source of reactive oxygen species generation in the cochlear and vestibular systems. NOX3-dependent ROS generation might contribute to hearing loss and balance problems in response to ototoxic drugs
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NADPH + H+ + O2
NADP+ + H2O2
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the active enzyme complex produces O2 radicals, which are converted into superoxide-derived oxidants such as H2O2, hydroxyl radicals, and peroxynitrite
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NADPH + H+ + O2
NADP+ + H2O2
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oxidizes NADH and, less efficiently, NADPH (2fold lower activity)
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NADPH + H+ + O2
NADP+ + H2O2
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oxidizes NADH and, less efficiently, NADPH (2fold lower activity)
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
activity with NADPH is much lower than with NADH
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + H+ + O2
NADP+ + H2O2
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NADPH + O2
NADP+ + O2-
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NADPH + O2
NADP+ + O2-
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NADPH + O2
NADP+ + O2-
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NADPH + O2
NADP+ + O2-
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NADPH + O2
NADP+ + O2-
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enzyme is stimulated by phagocytizable particles
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NADPH + O2
NADP+ + O2-
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part of defense mechanism against a wide variety of bacteria
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NADPH + O2
NADP+ + O2-
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in pathological conditions where an increase in NADH concentration occurs, the NADH oxidation catalysed by xanthine dehydrogenase may constitute an important pathway for reactive oxygen species-mediated tissue injuries
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NADPH + O2
NADP+ + O2-
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reaction catalyzed by xanthine oxidase and xanthine dehydrogenase
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NADPH + O2
NADP+ + O2-
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additional information
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lignin deposition induced by cellulose biosynthesis inhibition is regulated by JAR1-1 and NADPH oxidase-dependent signalling processes
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additional information
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enzyme provides hydrogen peroxide for iodine metabolism in the thyroid
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additional information
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direct interaction of TLR4 with NAD(P)H oxidase 4 isozyme is essential for lipopolysaccharide-induced production of reactive oxygen species and activation of NF-kappaB
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additional information
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the production of reactive oxygen species is initiated by the phygocyte NADPH oxidase
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additional information
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enzyme isoform Nox3 plays an integral role in insulin-induced p42/44 MAPK signal transmission and VEGF-A production
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additional information
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essential role of enzyme-generated reactive oxigen species in insulin-stimulated activation of hypoxia-inducible factor 1
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additional information
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formation of a complex consisting of enzyme, guanine exchange factor for Rac, betaPix, and enzyme organizer NoxO1 is a critical step in EGF-induced generation of reactive oxygen species
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additional information
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active NAD(P)H oxidase is required for vascular endothelial growth factor activation of phosphoinositide 3-kinase-Akt-forkhead, and p38 mitogen-activated kinase, but not extracellular signal-related kinase 1/2 or c-Jnu N-terminal kinase. The permissive role of NADPH oxidase on phosphoinositide 3-kinase-Akt-forkhead signaling is mediated at post-vascular endothelial growth factor receptor levels and involves the nonreceptor tyrosine kinase Src
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additional information
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NAD(P)H oxidase plays an essential role in maintaining basal levels of reactive oxygen species in NB-4 cells
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additional information
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subunit p40phox functions primarily to regulate Fcgamma receptor-induced NADPH oxidase activity rather than assembly of the enzyme, and stimulates superoxide production via a phosphoinositol 3-phosphate signal that increases after phagosome internalization
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additional information
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chronic granulomatous disease is a rare inherited immunodeficiency syndrome caused by mutations in four genes encoding essential nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex components
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additional information
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Duox NADPH oxidases generate hydrogen peroxide at the air-liquid interface of the respiratory tract and at apical membranes of thyroid follicular cells
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additional information
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Duox NADPH oxidases generate hydrogen peroxide at the air-liquid interface of the respiratory tract and at apical membranes of thyroid follicular cells
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additional information
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NADPH oxidase mediates angiotensin II-stimulated protein synthesis downstream of the type 1 receptor AT1 in myometrium smooth muscle cells
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additional information
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the membrane-bound NADPH oxidase in phagocytes, gp91phox/Nox2, produces superoxide, a precursor of microbicidal oxidants, thereby playing a crucial role in host defense. Activation of gp91phox/Nox2 requires assembly with the cytosolic proteins p67phox and p47phox, each containing two SH3 domains. p67phox-SH3(N) specifically functions in gp91phox/Nox2 activation probably via facilitating oxidase assembly
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additional information
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the potent anti-inflammatory, cytokine interleukin-10, acts as a down-regulator of the Nox1-based oxidase in the colon, and suggests an important role of ROS derived from Nox1-based oxidase in the initiation of inflammatory responses of the colon
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additional information
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Nox4 can produce a higher hydrogen peroxide to superoxide ratio than Nox1 and Nox2. NOX2-produced superoxide can be released outside the cell when Nox2 is located at the plasma membrane, thus allowing it to intercept, e.g., with endothelial-derived nitric oxide before it reaches the adjacent smooth muscle cell layer in vessels
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additional information
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NOX1 generates superoxide when coexpressed with the p47(phox) and p67(phox) subunits of the phygocyte NADPH oxidase but not when expressed by itself
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additional information
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reactive oxygen species generated by the transverse tubule NADPH oxidase enzyme activate via redox modification the neighboring RyR1 Ca2+ release channels
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additional information
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angiotensin II-evoked expression of endothelin-1 in adventitial fibroblasts is mediated, at least in part, by NADPH oxidase. This mechanism stimulates collagen expression thereby implicating the adventitia as a potential contributor to the vascular pathophysiology associated with oxidative stress and vascular remodeling
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additional information
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superoxide anions play a key role in suppressing K +secretion during K+ restriction and isoform NoxII is involved in mediating the effect of low K +intake on renal K+ secretion and ROMK channel activity
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additional information
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decreased hepatic fibrosis after chronic CCl4 administration in mice with NADPH oxidase deficiency occurs in the setting of greater necrosis and inflammation but decreased apoptosis
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additional information
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NADPH oxidase is an important molecular sources responsible for superoxide overproduction after high-glucose exposure
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additional information
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NADPH oxidase may play a potential role in oxidative stress-induced arterial tetrahydrobiopterin and GTP cyclohydrolase I deficiency, resulting in endothelial dysfunction in Ins2Akita type 1 diabetic mice fed a high-cholesterol diet
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additional information
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isoform NOX-1 is required for sexual and asexual development, and normal hyphal growth, while isoform NOX-2 is specifically involved in sexual spore function. Regulatory subunit NOR-1 is required for NOX-1 and NOX-2 functions at different developmental stages
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additional information
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hypoosmotic swelling of cardiac myocytes activates volume-sensitive Cl- current via the angiotensin II-reactive oxygen species signalling cascade
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additional information
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enzyme-derived reactive oxigen species modulate cerebral vascular tone under physiological conditions
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additional information
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glucose-mediated down-regulation of protein kinase G-I expression in vascular smooth muscle cells occurs through protein kinase C-dependent activation of NAD(P)H oxidase derived superoxide production, contributing to diabetes-associated vessel dysfunctions
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additional information
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NAD(P)H oxidase/superoxide and RhoA/Rho kinase are involved in the interaction between alpha2-adrenoceptors and angiotensin II on renal vascular resistance by mediating signaling events downstream of the phospholipase C/protein kinase C/c-src pathway
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additional information
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involvement of reactive oxygen species from NADPH oxidase in cytokine induction of secretory phospholipase A2-IIA in astrocytes
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additional information
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L-carnitine inhibits angiotensin II increased NADPH oxidase activity and intracellular ROS levels in cardiac fibroblasts
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additional information
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the activated Nox enzyme complex generates superoxide from oxygen by utilizing NADPH as an electron donor, thereby leading to the formation of other species of reactive oxygen
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additional information
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the activated Nox enzyme complex generates superoxide from oxygen by utilizing NADPH as an electron donor, thereby leading to the formation of other species of reactive oxygen
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additional information
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calcium-dependent kinase CDPK5 induces phosphorylation of the catalytic subunit at resiude S82 and thereby regulates the oxidative burst
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additional information
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the initial burst of superoxide in response to wounding is mediated by isoform Strboh A
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additional information
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KOD1 (TkNOX) catalyzes oxidation of NADH and NADPH with oxygen from atmospheric air as an electron acceptor
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additional information
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plasma membrane NADPH oxidase participates in the Ni-induced production of reactive oxygen species, and Ca2+ may be involved in the oxidative stress induced by nickel in wheat roots
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