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Information on EC 1.6.3.1 - NAD(P)H oxidase (H2O2-forming) and Organism(s) Rattus norvegicus and UniProt Accession Q672K1
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1.6.3.1 NAD(P)H oxidase (H2O2-forming)IUBMB Comments
Requires FAD, heme and calcium. When calcium is present, this transmembrane glycoprotein generates H2O2 by transfering electrons from intracellular NAD(P)H to extracellular molecular oxygen. The electron bridge within the enzyme contains one molecule of FAD and probably two heme groups. This flavoprotein is expressed at the apical membrane of thyrocytes, and provides H2O2 for the thyroid peroxidase-catalysed biosynthesis of thyroid hormones.
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Word Map
- 1.6.3.1
- endothelial
- neutrophil
- artery
- p22phox
- dismutase
- angiotensin
- cardiovascular
- apocynin
- hypertension
- oxidases
- nicotinamide
- granulomatous
- cardiac
- fibrosis
- aortic
- atherosclerosis
- catalase
- sod
- leukocyte
- monocyte
-
chemiluminescence
- tnf
- pkc
-
phorbol
- diphenyleneiodonium
-
ii-induced
- iodonium
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diphenylene
- myeloperoxidase
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endothelium-dependent
- hypothyroidism
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oxidase-derived
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renin-angiotensin
- fmlp
- dihydroethidium
- losartan
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tempol
- lucigenin
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nitrotyrosine
- peroxynitrite
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microbicidal
-
oxidase-dependent
-
vsmcs
-
flavocytochrome
- rac2
- medicine
-
ros-generating
- tiron
-
oxidase-mediated
- synthesis
- agriculture
-
fmlp-induced
- thyroperoxidase
- industry
The taxonomic range for the selected organisms is: Rattus norvegicus
The expected taxonomic range for this enzyme is: Eukaryota, Bacteria, Archaea
The expected taxonomic range for this enzyme is: Eukaryota, Bacteria, Archaea
Synonyms
nad(p)h oxidase, p47phox, gp91phox, nadph-oxidase, p67phox, duox2, duox1, nadph oxidase 4, phagocyte nadph oxidase, nadph oxidase 2, 
more
topSYNONYM 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
dual oxidase
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Duox
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-
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large NOX
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-
-
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LNOX
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-
-
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NADPH oxidase
NOX1
Nox2
Nox4
p138 thyroid-oxidase
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-
-
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p138tox
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-
-
-
p47phox
ThOX
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-
-
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ThOX2
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-
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thyroid NADPH oxidase
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-
-
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thyroid oxidase
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-
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thyroid oxidase 2
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-
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NADPH oxidase
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NADPH oxidase
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REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
redox reaction
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oxidation
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-
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reduction
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-
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SYSTEMATIC NAME
IUBMB Comments
NAD(P)H:oxygen oxidoreductase (H2O2-forming)
Requires FAD, heme and calcium. When calcium is present, this transmembrane glycoprotein generates H2O2 by transfering electrons from intracellular NAD(P)H to extracellular molecular oxygen. The electron bridge within the enzyme contains one molecule of FAD and probably two heme groups. This flavoprotein is expressed at the apical membrane of thyrocytes, and provides H2O2 for the thyroid peroxidase-catalysed biosynthesis of thyroid hormones.
CAS REGISTRY NUMBER
COMMENTARY
9032-22-8
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SUBSTRATE
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
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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-
?
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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-
?
NADPH + H+ + O2
NADP+ + H2O2
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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 + 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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-
?
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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-
?
NATURAL SUBSTRATE
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
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
-
-
?
NADPH + O2
NADP+ + O2-
-
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
-
-
?
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
-
-
?
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
-
-
?
additional information
?
-
-
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
?
-
-
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
-
-
?
additional information
?
-
-
involvement of reactive oxygen species from NADPH oxidase in cytokine induction of secretory phospholipase A2-IIA in astrocytes
-
-
?
additional information
?
-
-
L-carnitine inhibits angiotensin II increased NADPH oxidase activity and intracellular ROS levels in cardiac fibroblasts
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-
?
COFACTOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
METALS and IONS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
4-(2-aminoethyl)benzenesulfonyl fluoride
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significantly reduces reactive oxygen species production, NADPH oxidase activity, and all the apoptotic events, and cell death induced by both 5 mM KCl and staurosporin
aminoethylbenzenesulfonylfluoride
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treatment blocks the induction of reactive oxygen species production by the dopaminergic toxin MPP+. Co-treatment with inhibitors aminoethylbenzenesulfonylfluoride, apocynin, or diphenylene iodinium significantly suppresses MPP*-induced cell death and attenuates MPP*-induced increases in caspase-3 enzymatic activity
angiotensin
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angiotensin-(1-7) decreases the elevated levels of renal NADPH oxidase activity and attenuates the activation of subunit NOX-4 gene expression in the diabetic hypertensive kidney. Angiotensin-(1-7) treatment increases sodium excretion but does not affect mean arterial pressure in diabetic hypertensive rats. The significant increase in urinary protein in the diabetic compared to control hypertensive rat is reduced by angiotensin-(1-7). Angiotensin-(1-7) treatment also attenuates the diabetes-induced increase in renal vascular responsiveness to endothelin-1, norepinephrine, and angiotensin II in hypertensive rats, but significantly increases the vasodilation of the renal artery of hypertensive and diabetic hypertensive rats to the vasodilator agonists
bilirubin
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bilirubin concentration-dependently reduces NADPH oxidase-dependent superoxide production stimulated by angiotensin II in vascular smooth muscle cells
N-[2-(4-hydroxy-phenyl)-ethyl]-2-(2, 5-dimethoxy-phenyl)-3-(3-methoxy-4-hydroxy-phenyl)-acrylamide
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i.e. FLZ, squamosamide derivative, mediates anti-inflammatory and neuroprotective effects in both lipopolysaccharide-and 1-methyl-4-phenylpyridinium-mediated models of Parkinson's disease. FLZ inhibits the translocation of the cytosolic subunit p47phox to the membrane and thus inhibits the activation of NAD(P)H oxidase
nitroglycerin
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in rats treated with nitroglycerin for three days, superoxide production is increased in all aortic layers, while expression of isoforms nox1, nox2 and nox4 is significantly decreased. In vascular smooth muscle cells exposed to nitroglycerin for 6-24 h, NAD(P)H oxidase activity is increased, in spite of nox1 downregulation
rosuvastatin
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rosuvastatin reduces systolic blood pressure in spontaneously hypertensive rats but does not change plasma lipid levels. Rosuvastatin treatment in spontaneously hypertensive rats significantly decreases reactive oxygen species levels, NAD(P)H activity in retinal ganglion cells, and increases retinal plasmalogen content in spontaneously hypertensive rats, but does not modify the electroretinogram response
sinomenine
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morphinan analog, inhibits NAD(P)H oxidase cytosolic subunit p47phox translocation to the cell membrane and thus reduces lipopolysaccharide-induced extracellular reactive oxygen species production. Protects neuron-glial cell cultures at both micro- and sub-picomolar concentrations against dopaminergic neuron death, but not protection is seen at nanomolar concentrations
tetramethylpyrazine
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inhibits the induction of NAD(P)H oxidase activity by angiotensin II and the concomitant increase of intracellular reactive oxygen species levels and ERK phosphorylation
VAS3947
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i.e. 3-benzyl-7-(2-oxazolyl)thio-1,2,3-triazolo[4,5-d]pyrimidine, specific low micromolar NADPH oxidase inhibitor
apocynin
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apocynin does not reduce arterial pressure acutely in spontaneously hpertensive rats when given orally over 1-week intervals or when given i.v. Apocynin potently inhibits granulocyte NADPH oxidase but not vascular NADPH-oxidase dependent oxygen radical formation unless exogenous peroxidase is added to vascular preparations. Apocynin dilates rat intrarenal and coronary arteries independently of pharmacological interventions that reduce vascular superoxide radical abundance and actions
apocynin
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apocynin reduces avascularity and apoptosis in the oxygen-induced retinopathy model
apocynin
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blocks up-regulation of epidermal growth factor receptor ligands and Akt activation by transforming growth factor-beta
apocynin
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inhibition of NAD(P)H oxidase in alveolar macrophage by apocynin results in down-regulation of arginase activity and decrease in arginase I mRNA
apocynin
-
prevents inflammation-mediated toxicity to motor neurons induced by lipopolysaccharide
apocynin
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smoking impaires acetylcholine-induced relaxations of carotid arteries, which can be improved by the NAD(P)H oxidase inhibitor apocynin. Vascular mRNA expression of the proinflammatory cytokines IL-1, IL-6, and TNF-alpha and that of inducible nitric oxide synthase is significantly increased by both smoking and cigarette smoke extract exposure, which can be prevented by apocynin, diphenyleneiodinium, or scavenging of H2O2
apocynin
-
treatment blocks the induction of reactive oxygen species production by the dopaminergic toxin MPP+. Co-treatment with inhibitors aminoethylbenzenesulfonylfluoride, apocynin, or diphenylene iodinium significantly suppresses MPP*-induced cell death and attenuates MPP*-induced increases in caspase-3 enzymatic activity
diphenylene iodinium
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significant suppression of release of reactive oxygen species in astrocytes caused by calcium ionophores or opsonized zymosan
diphenylene iodonium
-
significantly reduces reactive oxygen species production, NADPH oxidase activity, and all the apoptotic events, and cell death induced by both 5 mM KCl and staurosporin
diphenylene iodonium
-
treatment blocks the induction of reactive oxygen species production by the dopaminergic toxin MPP+. Co-treatment with inhibitors aminoethylbenzenesulfonylfluoride, apocynin, or diphenylene iodinium significantly suppresses MPP*-induced cell death and attenuates MPP*-induced increases in caspase-3 enzymatic activity
diphenyleneiodonium
-
blocks up-regulation of epidermal growth factor receptor ligands and Akt activation by transforming growth factor-beta
diphenyleneiodonium
-
vascular mRNA expression of the proinflammatory cytokines IL-1, IL-6, and TNF-alpha and that of inducible nitric oxide synthase is significantly increased by both smoking and cigarette smoke extract exposure, which can be prevented by apocynin, diphenyleneiodinium, or scavenging of H2O2
diphenyleneiodonium
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NAD(P)H oxidase inhibitor, complete inhibition at 0.001 mM
gp91ds-tat
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peptidyl inhibitor. Treatment of engineered tissue blocks of a chamber model significantly reduces the level of reactive oxygen species and retards the tissue formation process. Vessels in treated tissues have smaller lumens than control
additional information
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treatment of animals by oral administration of isoobtusilactone A for two weeks does not result in significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters
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additional information
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mGluR5 activation inhibits microglial NADPH oxidase activity
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additional information
-
trimer hydroxylated quinone is the major active compound in AOP-1, with strong inhibitory activity against vascular endothelial cell NADPH oxidase with an IC50 of 0.000031 mM at 22°C, pH not specified in the publication
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ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
(+)-(S)-2-(6-methoxynaphthalen-2-yl)propanoic acid
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i.e. naproxen, nonsteroidal anti-inflammatory drug. Marked increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin
2-(2-(2,6-dichlorophenylamino)-phenyl)acetic acid
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i.e. diclofenac, nonsteroidal anti-inflammatory drug. Marked increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin
4-(4-methylsulfonylphenyl)-3-phenyl-5H-furan-2-one
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i.e. rofecoxib, nonsteroidal anti-inflammatory drug. Moderate increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin
4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide
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i.e. celecoxib, nonsteroidal anti-inflammatory drug. Moderate increase in expression of isoforms Nox1, Nox2, Nox4, and p22phox. Up-regulation of NAD(P)H oxidases is associated with increased superoxide content in aorta and heart, which may be prevented by inhibitor apocynin
angiotensin II
-
potent stimulator of NAD(P)H oxidase O2- production in the vasculature
lipopolysaccharide
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exposure tolipopolysaccharide leads to the demise of motor neurons in a dose- and time-dependent manner, whereas interneurons are impaired relatively mildly. NADPH oxidase is activated upon lipopolysaccharide challenge, and inhibitor apocynin prevents inflammation-mediated toxicity to motor neurons
nitroglycerin
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in vascular smooth muscle cells exposed to nitroglycerin for 6-24 h, NAD(P)H oxidase activity is increased, in spite of isoform nox1 downregulation
thrombin
-
after addition to cell culture, expression of NADPH oxidase subunits p47phox and p67phox occurs, accompanied by up-regulation in the expression of cytosolic enzyme components Rac 1 and p67phox, and the translocation of cytosolic subunits p47phox and p67phox to the membrane. Thrombin-induced reactive oxygen species production, protein oxidation, and loss of cultured hippocampal neurons are partially attenuated by NADPH oxidase inhibition and/or by several antioxidants
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TNF-alpha
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activation of enzyme, resulting in an increase in intracellular H2O2 that stimulates Ca2+ sparks and transient Kca currents, leading to a reduction in global concentration of Ca2+ and vasodilation
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transforming growth factor-beta
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up-regulates isoform nox4 and increases the levels of Rac1 protein, a known regulator of both isoforms Nox1 and Nox2, in a transforming growth factor-beta receptor I-dependent manner and mediates activation of the nuclear factor-kappaB pathway. The inhibitors diphenyleneiodonium and apocynin, and SB431542, an inhibitor of the transforming growth factor-beta receptor I, block up-regulation of epidermal growth factor receptor ligands and Akt activation
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additional information
-
treatment of animals by oral administration of isoobtusilactone A for two weeks does not result in significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters
-
additional information
-
depolarization of membrane potential of endothelial cells leads to activation of NAD(P)H oxidase and, consequently, superoxide anion production
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ORGANISM
COMMENTARY
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SOURCE
cochlear and vestibular system, NOX3 is highly expressed in specific portions of the inner ear
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L-carnitine inhibits angiotensin II increased NADPH oxidase activity and intracellular ROS levels in cardiac fibroblasts
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dorsal root ganglion and sympathetic celiac ganglion. mRNA for the NAD(P)H oxidase subunits NOX1, NOX2, NOX4, p47phox, and p22phox is present in both celiac ganglion and dorsal root ganglion, mRNA for NOX4 is significantly higher in celiac ganglion than in dorsal root ganglion. Catalytic subunit p22phox mRNA and protein expression is greater in celiac ganglion of hypertensive rats but not in dorsal root ganglion. Subunit p47phox mRNA and protein, as well as Rac-1protein, are significantly decreased in hypertensive dorsal root ganglion but not in celiac ganglion. Subunit p47phox is translocated from cytoplasm to membrane in hypertensive celiac ganglion but not in hypertensive dorsal root ganglion
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primary culture of mixed glia. Incubation of cultures in the presence of fibrillar amyloid beta1-42 induces the assembly and the activation of NADPH oxidase, and triggers the production of superoxide anion-derived reactive oxygen species. Pretreatment of microglia with melatonin dose-dependently prevents the activation of NADPH oxidase and decreases the production of reactive oxygen species. Melatonin inhibits the phosphorylation of the p47phox subunit of NADPH oxidase via a PI3K/Akt-dependent signalling pathway, blocks the translocation of p47phox and p67phox subunit to the membrane, down-regulates the binding of p47phox to gp91phox, and impairs the assembly of NADPH oxidase
NOX2 and NOX4 are the main isoforms present in macula densa cells
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increased superoxide anion generation is present both in endothelial and smooth muscle cells after cigarette smoke extract exposure
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mesencephalic dopaminergic neuronal cells. Cells express key NAD(P)H oxidase subunits gp91phox and p67phox, and NAD(P)H oxidase are a key determinant of toxin MPP*-mediated dopaminergic degeneration
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NAD(P)H oxidase is most abundant in the pons compared to other regions of the brain. Cytoplasmic superoxide dismutase is equally distributed among different regions but catalase and glutathione peroxidase are more abundant in pons, hypothalamus and medulla and less so in the cortex and cerebellum
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(pro)renin receptor is constitutively expressed in renal glomeruli and tubules. Expression of the receptor is upregulated in diabetes via enhancement of angiotensin subtype 1 receptor-NADPH oxidase activity
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microinjection of lipopolysaccharide bilaterally into the rostral ventrolateral medulla induces progressive hypotension, bradycardia, and reduction in sympathetic vasomotor outflow. This is accompanied by an increase in superoxide anion production for 60-240 min, alongside phosphorylation of subunits p47phox or p67phox, upregulation of gp91phox or p47phox protein, and increase in Rac-1 or NADPH oxidase activity during 60-120 min, and a depression of mitochondrial respiratory enzyme activity during 120-240 min. Inhibition of NADPH oxidase or knockdown of the gp91phox or p47phox gene blunts the early phase of 60-150 min, coenzyme Q10 or mitochondrial KATP channel inhibitor antagonizes the delayed phase of 120-240 min of lipopolysaccharide-nduced increase in superoxide anion production in rostral ventrolateral medulla and cardiovascular depression
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primary cells. Glucose-mediated decreases in protein kinase G-I levels are inhibited by superoxide scavenger tempol or NAD(P)H oxidase inhibitors diphenylene iodonium or apocynin. High glucose exposure time-dependently increases superoxide production, which is abolished by tempol or apocynin treatment, but not by L-NAME, rotenone, or oxypurinol.Total protein levels and phosphorylated levels of subunit p47phox are increased after high glucose exposure. Transfection of cells with siRNA-p47phox abolishes glucose-induced superoxide production and restores protein kinase G-I protein levels
additional information
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chamber model using subcutaneous arteriovenous loop tissue
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aortas of transgenic rats harboring the mouse renin transgene exhibit greater NADPH oxidase activity, reactive oxygen species levels, C-reactive protein, tumor necrosis factor-alpha expression, apoptosis, and wall thickness, which are significantly attenuated by in vivo treatment with angiotensin type 1 receptor blockade by valsartan or the superoxide dismutase/catalase mimetic tempol
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study on enzyme activity, function, and expression in cerebral and systemic arteries. Superoxide production from enzyme is 10- to 100fold greater in intracranial arteries, basilar and middle cerebral arteries than in aorta, carotid, renal or mesenteric arteries. Isoform Nox4 shows 10fold higher expression in the basilar arteries versus aorta, carotid and mesenteric arteries
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smoking impaires acetylcholine-induced relaxations of carotid arteries, which can be improved by the NAD(P)H oxidase inhibitor apocynin. Both smoking and in vitro cigarette smoke extract exposure significantly increase vascular superoxide anion production
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primary culture. Proliferation induced by fibrillar beta-amyloid peptide Abeta1-40 is mediated both by microglial release of TNF-alpha and by production of hydrogen peroxide by enzyme
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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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primary culture. Proliferation induced by fibrillar beta-amyloid peptide Abeta1-40 is mediated both by microglial release of TNF-alpha and by production of hydrogen peroxide by enzyme
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(pro)renin receptor is constitutively expressed in renal glomeruli and tubules. Expression of the receptor is upregulated in diabetes via enhancement of angiotensin subtype 1 receptor-NADPH oxidase activity
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intrarenal infusions of angiotensin II both in vitro and in vivo increase renal vascular resistance, and alpha2-adrenoceptor agonist UK14,304 enhances this response. The interaction between angiotensin II and UK14,304 is blocked by inhibitors of NAD(P)H oxidase
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salt-sensitive rats consuming a low-salt diet exhibit significant increases in AT 1 receptor, cyclooxygenase-2, plasminogen activator inhibitor PAI and phospho-I kappaB in the kidney as compared to those found in salt-resistant rats. The high-salt diet results in severe hypertension and proteinuria in salt-sensitive but not salt-resistant rats, and marked elevations of renal tissue monocyte chemoattractant protein 1, p22phox, NADPH oxidase subunit 4, angiotensin-II-positive cell count, infiltrating T cells and macrophages and further increases in AT 1 receptor, cyclooxygenase-2, PAI-1 and phospho-IkappaB in the salt-sensitive group
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alveolar macrophages. Inhibition of NAD(P)H oxidase by apocynin results in down-regulation of arginase
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dorsomedial nucleus tractus solitarius neuron. In small dendritic processes, both angiotensin II and phenylephrine produce a decrease in intracellular subunit p47phox labeling selectively in dorsomedial nucleus tractus solitarius neurons. In intermediate-size dendritic profiles in the dorsomedial nucleus tractus solitarius region only, there is an increase in p47phox labeling in response to each hypertensive agent, although these changes occurre in different subcellular compartments. There is an increase in non-vesicular labeling in response to angiotensin II, but an increase in surface labeling with phenylephrine
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in primary cultures of cerebellar granule neuron, expression of the components of NADPH oxidase proteins, p40phox, p47phox and p67phox,and p22phox, as well as three homologues of the catalytic subunit, NOX1, 2, and 4
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retinal ganglion cell reactive oxygen species and retinal NAD(P)H oxidase activity are higher in spontaneously hypertensive rats than in wild-type rats
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bilirubin concentration-dependently reduces NADPH oxidase-dependent superoxide production stimulated by angiotensin II in vascular smooth muscle cells
LOCALIZATION
ORGANISM
UNIPROT
COMMENTARY
GeneOntology No.
LITERATURE
SOURCE
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subunit p47phox, in dorsomedial nucleus tractus solitarius neurons of saline-treated animals. Administration of angiotensin over 7 days, which produces elevated systemic blood pressure, is associated with a redistribution of p47phox immunolabeling away from intracellular organelles in the distal dendritic compartment, and toward non-vesicular targets in less distal, intermediate areas of dorsomedial nucleus tractus solitarius neurons. Chronic administration of phenylephrine, which produces increases in systolic blood pressure, is associated with a repartitioning of p47phox immunolabeling away from intracellular organelles in distal dendritic areas, andtoward the plasma membrane of intermediate dendritic areas of dorsomedial nucleus tractus solitarius neurons
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synaptic and extrasynaptic areas of the plasmalemma, localization of subunit p47phox, in dorsomedial nucleus tractus solitarius neurons of saline-treated animals. Chronic administration of phenylephrine, which produces increases in systolic blood pressure, is associated with a repartitioning of p47phox immunolabeling away from intracellular organelles in distal dendritic areas, and toward the plasma membrane of intermediate dendritic areas of dorsomedial nucleus tractus solitarius neurons
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GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
malfunction
metabolism
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mechanisms involved in the control of NO production involving the enzyme, NADPHox-mediated superoxide formation is involved in the inhibition of NO production, overview
physiological function
malfunction
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the inhibition of NAD(P)H oxidase-dependent nuclear factor-kappa B signaling reduces the increase in monocyte chemoattractant protein-1 production by glomerular endothelial cells induced by angiotensin II
malfunction
-
the inhibition of NADPH oxidase may contribute to lowered rate of renal gluconeogenesis, probably due to decreasing phosphoenolpyruvate carboxykinase activity
malfunction
-
blockade of NAD(P)H oxidase with apocynin or superoxide dismutationwith PEG-SOD prevents the increment in superoxide and changes in P-eNOSThr495 observed during apamin and triarylmethane-34 application
physiological function
-
in skeletal muscle and in heart the NADPH oxidase system is mainly involved in oxidative stress
physiological function
-
NAD(P)H derived superoxide generation is the underlying cause of vasoactive dysfunction in hyperglycemic Goto-Kakizaki arteries
physiological function
-
NAD(P)H oxidase is the major source of reactive oxygen species generation in the vasculature in response to high glucose and advanced glycation end-products. NAD(P)H oxidase in phagocytic cells releases reactive oxygen species as a defense against pathogens. Activation of NAD(P)H oxidase in diabetes leads to a cascade of reactive oxygen species production and impaired antioxidant defenses. In early stages of diabetes, NAD(P)H oxidase-derived reactive oxygen species may serve as intracellular mediators to regulate redox-sensitive transcription factors (e.g. Nrf2) involved in adaptive responses to oxidative stress
physiological function
-
NADPH oxidase is a major source of reactive oxygen species in aortas of spontaneously hypertensive rats
physiological function
while macula densa cells express the NOX2 and NOX4 isoforms, NOX 2 is primarily responsible for NaCl-induced O2- generation
physiological function
-
blockade of small-conductance and intermediate-conductance Ca2+-activated K+ channels activates NAD(P)H oxidase-dependent superoxide formation, which leads to inhibition of NO release through P-eNOSThr495
physiological function
-
the enzyme plays a significant role in promoting post-injury inflammation after spinal cord injury
UNIPROT
ENTRY NAME
ORGANISM
NO. OF AA
NO. OF TRANSM. HELICES
MOLECULAR WEIGHT[Da]
SOURCE
SEQUENCE
LOCALIZATION PREDICTION
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable).
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable). SUBUNIT
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
POSTTRANSLATIONAL MODIFICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
PROTEIN VARIANTS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
medicine
-
mRNA for the NAD(P)H oxidase subunits NOX1, NOX2, NOX4, p47phox, and p22phox is present in both celiac ganglion and dorsal root ganglion, mRNA for NOX4 is significantly higher in celiac ganglion than in dorsal root ganglion. Catalytic subunit p22phox mRNA and protein expression is greater in celiac ganglion of hypertensive rats but not in dorsal root ganglion. Subunit p47phox mRNA and protein, as well as Rac-1protein, are significantly decreased in hypertensive dorsal root ganglion but not in celiac ganglion. Subunit p47phox is translocated from cytoplasm to membrane in hypertensive celiac ganglion but not in hypertensive dorsal root ganglion
CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
a strong upregulation of NAD(P)H oxidase subunits p22phox and p47phox is observed in the hypertensive kidney of aortic coarcted rats
-
aequous extract of Tessaria absinthioides and Prosopis strombulifera inhibits at 5-40 mg/ml 10% fetal calf serum-induced cell proliferation in vascular smooth muscle cells, arrests cell in G2/M phase, reduces angiotensin II-induced reactive oxygen species generation, and decreases NADPH oxidase subunits NOX2 and NOX4 mRNA and protein expression
-
losartan administration significantly reduces oxidative stress generation by decreasing NAD(P)H oxidase expression
-
NADPH oxidase activity in the hippocampal CA1 region is significantly elevated in placebo versus sham control as early as 30 min after reperfusion, with peak NADPH oxidase activity levels observed at 3 h. 17Beta-estradiol attenuates NADPH oxidase activity in hippocampal CA1 after global cerebral ischemia
-
NADPH oxidase expression (p22phox and p47phox) and NADPH oxidase-dependent superoxide anion production are not modified in 12 week high-fat highsucrose diet-fed rats
-
the level of p47phox protein, an NAD(P)H oxidase subunit, is increased by angiotensin II treatment (0.01 mM) with a peak being reached at 8 h. This increase is reduced by 0.001 mM diphenyleneiodonium and 0.001 mM telmisartan treatment
-
tumor necrosis factor-alpha activates NADPH oxidase expression/activity. NAD(P)H oxidase is increased in the retina of diabetic rats
-
APPLICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
medicine
medicine
-
proliferation of microglial cells induced by fibrillar beta-amyloid peptide Abeta1-40 is mediated both by microglial release of TNF-alpha and by production of hydrogen peroxide by enzyme. TNF-alpha and enzyme, and its products, are potential targets to prevent Abeta-induced inflammatory neurodegeneration
medicine
-
TNF-alpha activates enzyme, resulting in an increase in intracellular H2O2 that stimulates Ca2+ sparks and transient Kca currents, leading to a reduction in global concentration of Ca2+ and vasodilation
medicine
-
(pro)renin receptor is constitutively expressed in renal glomeruli and tubules. Expression of the receptor is upregulated in diabetes via enhancement of angiotensin subtype 1 receptor-NADPH oxidase activity
medicine
-
after addition of thrombin to cell culture, expression of NADPH oxidase subunits p47phox and p67phox occurs, accompanied by up-regulation in the expression of cytosolic enzyme components Rac 1 and p67phox, and the translocation of cytosolic subunits p47phox and p67phox to the membrane. Thrombin-induced reactive oxygen species production, protein oxidation, and loss of cultured hippocampal neurons are partially attenuated by NADPH oxidase inhibition and/or by several antioxidants
medicine
-
angiotensin-(1-7) decreases the elevated levels of renal NADPH oxidase activity and attenuates the activation of subunit NOX-4 gene expression in the diabetic hypertensive kidney. Angiotensin-(1-7) treatment increases sodium excretion but does not affect mean arterial pressure in diabetic hypertensive rats. The significant increase in urinary protein in the diabetic compared to control hypertensive rat is reduced by angiotensin-(1-). Angiotensin-(1-7) treatment also attenuates the diabetes-induced increase in renal vascular responsiveness to endothelin-1, norepinephrine, and angiotensin II in hypertensive rats, but significantly increases the vasodilation of the renal artery of hypertensive and diabetic hypertensive rats to the vasodilator agonists
medicine
-
aortas of transgenic rats harboring the mouse renin transgene exhibit greater NADPH oxidase activity, reactive oxygen species levels, C-reactive protein, tumor necrosis factor-alpha expression, apoptosis, and wall thickness, which are significantly attenuated by in vivo treatment with angiotensin type 1 receptor blockade by valsartan or the superoxide dismutase/catalase mimetic tempol
medicine
-
apocynin reduces avascularity and apoptosis in the oxygen-indunced retinopathy model. The antioxidant properties of N-acetylcysteine are not effective in reducing intravitreous neovasicularization or avascular retina
medicine
-
chronic administration of agents that induce hypertension can also produce changes in the subcellular localization in subunit p47phox in dorsomedial nucleus tractus solitarius neurons. Systemic hypertension may produce alterations in the trafficking of proteins associated with superoxide production in central autonomic neurons. Administration of angiotensin over 7 days, which produces elevated systemic blood pressure, is associated with a redistribution of p47phox immunolabeling away from intracellular organelles in the distal dendritic compartment, and toward non-vesicular targets in less distal, intermediate areas of dorsomedial nucleus tractus solitarius neurons. Chronic administration of phenylephrine, which produces increases in systolic blood pressure, is associated with a repartitioning of p47phox immunolabeling away from intracellular organelles in distal dendritic areas, andtoward the plasma membrane of intermediate dendritic areas of dorsomedial nucleus tractus solitarius neurons
medicine
-
diabetes-induced translocation of protein kinase C, specifically PKC-alpha to renal membranes is associated with increased NADPH-dependent superoxide production. In both diabetic animals and in advanced glycation end products-treated mesangial cells, blockade of NADPH oxidase or PKC-alpha attenuates cytosolic superoxide and protein kinase C activation and increases vascular endothelial growth factor
medicine
-
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
medicine
-
incubation of microglial cultures in the presence of fibrillar amyloid beta1-42 induces the assembly and the activation of NADPH oxidase, and triggers the production of superoxide anion-derived reactive oxygen species. Pretreatment of microglia with melatonin dosedependently prevents the activation of NADPH oxidase and decreases the production of reactive oxygen species. Melatonin inhibits the phosphorylation of the p47phox subunit of NADPH oxidase via a PI3K/Akt-dependent signalling pathway, blocks the translocation of p47phox and p67phox subunit to the membrane, down-regulates the binding of p47phox to gp91phox, and impairs the assembly of NADPH oxidase
medicine
-
intrarenal infusions of angiotensin II both in vitro and in vivo increase renal vascular resistance, and alpha2-adrenoceptor agonist UK14,304 enhances this response. The interaction between angiotensin II and UK14,304 is blocked by inhibitors of NAD(P)H oxidase
medicine
-
intravitreal injections of angiotensin II can result in retinal leukostasis, which appears to be mediated via increasing superoxide generation by NAD(P)H oxidase, and by vasular endothelial growth factor. The activity of NAD(P)H oxidase is required for leukostasis to occur in the diabetic retina
medicine
-
microinjection of lipopolysaccharide bilaterally into the rostral ventrolateral medulla induces progressive hypotension, bradycardia, and reduction in sympathetic vasomotor outflow. This is accompanied by an increase in superoxide anion production for 60-240 min, alongside phosphorylation of subunits p47phox or p67phox, upregulation of gp91phox or p47phox protein, and increase in Rac-1 or NADPH oxidase activity during 60-120 min, and a depression of mitochondrial respiratory enzyme activity during 120-240 min. Inhibition of NADPH oxidase or knockdown of the gp91phox or p47phox gene blunts the early phase of 60-150 min, coenzyme Q10 or mitochondrial KATP channel inhibitor antagonizes the delayed phase of 120-240 min of lipopolysaccharide-nduced increase in superoxide anion production in rostral ventrolateral medulla and cardiovascular depression
medicine
-
on a high-salt diet of 4% NaC1, male and obese rats have significantly higher mean arterial blood pressure relative to female and lean rats and reduced renal cortical nitric oxide synthase activity. Lean female rats have the highest outer medullary protein levels of several NADPH oxidase subunits, including gp91phox, p47phox, and p67phox, however, renal NADPH activity is not increased in lean females, but is significantly increased in obese rats of both sexes
medicine
-
rosuvastatin reduces systolic blood pressure in spontaneously hypertensive rats but does not change plasma lipid levels. Rosuvastatin treatment in spontaneously hypertensive rats significantly decreases reactive oxygen species levels , NAD(P)H activity in retinal ganglion cells, and increases retinal plasmalogen content in spontaneously hypertensive rats, but does not modify the electroretinogram response
medicine
-
salt sensitivity in the salt-sensitive rat is associated with upregulations of the intrarenal angiotensin system, reactive oxygen species-generating and proinflammatory/profibrotic proteins and an inability to raise antioxidant enzymes and maximally suppress plasma renin activity in response to high salt intake
medicine
-
the morphinan analog, sinomenine inhibits NAD(P)H oxidase cytosolic subunit p47phox translocation to the cell membrane and thus reduces lipopolysaccharide-induced extracellular reactive oxygen species production. Sinomenine protects neuron-glial cell cultures at both micro- and sub-picomolar concentrations against dopaminergic neuron death, but not protection is seen at nanomolar concentrations
medicine
-
treatment of animals by oral administration of isoobtusilactone A for two weeks does not result in significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters
medicine
-
treatment with peptidyl inhibitor gp91ds-tat reduces proliferation and migration of cultured microvascular endothelial cells
medicine
-
water-soluble components of cigarette smoke activate the vascular NAD(P)H oxidase. NAD(P)H oxidase-derived H2O2 activates NF-kappaB, leading to proinflammatory alterations in vascular phenotype, which likely promotes development of atherosclerosis
medicine
-
as NAD(P)H oxidase activation may have dual actions in diabetes, selective targeting of the deleterious effects of sustained NAD(P)H oxidase activation, such as eNOS uncoupling, mitochondrial dysfunction, and impaired antioxidant gene expression, may prove beneficial in the treatment of diabetes
REF.
AUTHORS
TITLE
JOURNAL
VOL.
PAGES
YEAR
ORGANISM (UNIPROT)
PUBMED ID
SOURCE
De Deken, X.; Wang, D.; Dumont, J.E.; Miot, F.
Characterization of ThOX proteins as components of the thyroid H2O2-generating system
Exp. Cell Res.
273
187-196
2002
Canis lupus familiaris, Homo sapiens, Rattus norvegicus
Banfi, B.; Malgrange, B.; Knisz, J.; Steger, K.; Dubois-Dauphin, M.; Krause, K.H.
NOX3, a superoxide-generating NADPH oxidase of the inner ear
J. Biol. Chem.
279
46065-46072
2004
Mus musculus (Q672J9), Rattus norvegicus (Q672K1)
Cheranov, S.Y.; Jaggar, J.H.
TNF-alpha dilates cerebral arteries via NAD(P)H oxidase-dependent Ca2+ spark activation
Am. J. Physiol.
290
C964-C971
2006
Rattus norvegicus
Liu, Q.; Kang, J.; Zheng, R.
NADPH oxidase produces reactive oxygen species and maintains survival of rat astrocytes
Cell Biochem. Funct.
23
93-100
2005
Rattus norvegicus
Miller, A.A.; Drummond, G.R.; Schmidt, H.H.; Sobey, C.G.
NADPH oxidase activity and function are profoundly greater in cerebral versus systemic arteries
Circ. Res.
97
1055-1062
2005
Rattus norvegicus
Maia, L.; Vala, A.; Mira, L.
NADH oxidase activity of rat liver xanthine dehydrogenase and xanthine oxidase-contribution for damage mechanisms
Free Radic. Res.
39
979-986
2005
Rattus norvegicus
Jekabsone, A.; Mander, P.K.; Tickler, A.; Sharpe, M.; Brown, G.C.
Fibrillar beta-amyloid peptide Abeta1-40 activates microglial proliferation via stimulating TNF-alpha release and H2O2 derived from NADPH oxidase: a cell culture study
J. Neuroinflammation
3
24
2006
Rattus norvegicus
Wong, K.L.; Wu, K.C.; Wu, R.S.; Chou, Y.H.; Cheng, T.H.; Hong, H.J.
Tetramethylpyrazine inhibits angiotensin II-increased NAD(P)H oxidase activity and subsequent proliferation in rat aortic smooth muscle cells
Am. J. Chin. Med.
35
1021-1035
2007
Rattus norvegicus
Chandramohan, G.; Bai, Y.; Norris, K.; Rodriguez-Iturbe, B.; Vaziri, N.D.
Effects of dietary salt on intrarenal angiotensin system, NAD(P)H oxidase, COX-2, MCP-1 and PAI-1 expressions and NF-kappaB activity in salt-sensitive and -resistant rat kidneys
Am. J. Nephrol.
28
158-167
2008
Rattus norvegicus
Benter, I.F.; Yousif, M.H.; Dhaunsi, G.S.; Kaur, J.; Chappell, M.C.; Diz, D.I.
Angiotensin-(1-7) prevents activation of NADPH oxidase and renal vascular dysfunction in diabetic hypertensive rats
Am. J. Nephrol.
28
25-33
2008
Rattus norvegicus
Orosz, Z.; Csiszar, A.; Labinskyy, N.; Smith, K.; Kaminski, P.M.; Ferdinandy, P.; Wolin, M.S.; Rivera, A.; Ungvari, Z.
Cigarette smoke-induced proinflammatory alterations in the endothelial phenotype: role of NAD(P)H oxidase activation
Am. J. Physiol. Heart Circ. Physiol.
292
H130-H139
2007
Rattus norvegicus
Chen, P.; Guo, A.M.; Edwards, P.A.; Trick, G.; Scicli, A.G.
Role of NADPH oxidase and ANG II in diabetes-induced retinal leukostasis
Am. J. Physiol. Regul. Integr. Comp. Physiol.
293
R1619-R1629
2007
Rattus norvegicus
Murillo, M.M.; Carmona-Cuenca, I.; Del Castillo, G.; Ortiz, C.; Roncero, C.; Sanchez, A.; Fernandez, M.; Fabregat, I.
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
Biochem. J.
405
251-259
2007
Rattus norvegicus
Sicard, P.; Acar, N.; Gregoire, S.; Lauzier, B.; Bron, A.M.; Creuzot-Garcher, C.; Bretillon, L.; Vergely, C.; Rochette, L.
Influence of rosuvastatin on the NAD(P)H oxidase activity in the retina and electroretinographic response of spontaneously hypertensive rats
Br. J. Pharmacol.
151
979-986
2007
Rattus norvegicus
Campese, V.M.; Sindhu, R.K.; Ye, S.; Bai, Y.; Vaziri, N.D.; Jabbari, B.
Regional expression of NO synthase, NAD(P)H oxidase and superoxide dismutase in the rat brain
Brain Res.
1134
27-32
2007
Rattus norvegicus
Li, B.; Guo, Y.S.; Sun, M.M.; Dong, H.; Wu, S.Y.; Wu, D.X.; Li, C.Y.
The NADPH oxidase is involved in lipopolysaccharide-mediated motor neuron injury
Brain Res.
1226
199-208
2008
Rattus norvegicus
Schlueter, T.; Steinbach, A.C.; Steffen, A.; Rettig, R.; Grisk, O.
Apocynin-induced vasodilation involves Rho kinase inhibition but not NADPH oxidase inhibition
Cardiovasc. Res.
80
271-279
2008
Mus musculus, Rattus norvegicus
Thallas-Bonke, V.; Thorpe, S.R.; Coughlan, M.T.; Fukami, K.; Yap, F.Y.; Sourris, K.C.; Penfold, S.A.; Bach, L.A.; Cooper, M.E.; Forbes, J.M.
Inhibition of NADPH oxidase prevents advanced glycation end product-mediated damage in diabetic nephropathy through a protein kinase C-alpha-dependent pathway
Diabetes
57
460-469
2008
Rattus norvegicus
Matthiesen, S.; Lindemann, D.; Warnken, M.; Juergens, U.R.; Racke, K.
Inhibition of NADPH oxidase by apocynin inhibits lipopolysaccharide (LPS) induced up-regulation of arginase in rat alveolar macrophages
Eur. J. Pharmacol.
579
403-410
2008
Rattus norvegicus
Glass, M.J.; Chan, J.; Frys, K.A.; Oselkin, M.; Tarsitano, M.J.; Iadecola, C.; Pickel, V.M.
Changes in the subcellular distribution of NADPH oxidase subunit p47phox in dendrites of rat dorsomedial nucleus tractus solitarius neurons in response to chronic administration of hypertensive agents
Exp. Neurol.
205
383-395
2007
Rattus norvegicus
Siragy, H.M.; Huang, J.
Renal (pro)renin receptor upregulation in diabetic rats through enhanced angiotensin AT1 receptor and NADPH oxidase activity
Exp. Physiol.
93
709-714
2008
Rattus norvegicus
Chen, C.Y.; Liu, T.Z.; Chen, C.H.; Wu, C.C.; Cheng, J.T.; Yiin, S.J.; Shih, M.K.; Wu, M.J.; Chern, C.L.
Isoobtusilactone A-induced apoptosis in human hepatoma Hep G2 cells is mediated via increased NADPH oxidase-derived reactive oxygen species (ROS) production and the mitochondria-associated apoptotic mechanisms
Food Chem. Toxicol.
45
1268-1276
2007
Homo sapiens, Rattus norvegicus
Sheh, Y.L.; Hsu, C.; Chan, S.H.; Chan, J.Y.
NADPH oxidase- and mitochondrion-derived superoxide at rostral ventrolateral medulla in endotoxin-induced cardiovascular depression
Free Radic. Biol. Med.
42
1610-1623
2007
Rattus norvegicus
Liu, S.; Ma, X.; Gong, M.; Shi, L.; Lincoln, T.; Wang, S.
Glucose down-regulation of cGMP-dependent protein kinase I expression in vascular smooth muscle cells involves NAD(P)H oxidase-derived reactive oxygen species
Free Radic. Biol. Med.
42
852-863
2007
Rattus norvegicus
Coyoy, A.; Valencia, A.; Guemez-Gamboa, A.; Moran, J.
Role of NADPH oxidase in the apoptotic death of cultured cerebellar granule neurons
Free Radic. Biol. Med.
45
1056-1064
2008
Rattus norvegicus
Riazi, S.; Madala-Halagappa, V.K.; Dantas, A.P.; Hu, X.; Ecelbarger, C.A.
Sex differences in renal nitric oxide synthase, NAD(P)H oxidase, and blood pressure in obese Zucker rats
Gend. Med.
4
214-229
2007
Rattus norvegicus
Wei, Y.; Whaley-Connell, A.T.; Chen, K.; Habibi, J.; Uptergrove, G.M.; Clark, S.E.; Stump, C.S.; Ferrario, C.M.; Sowers, J.R.
NADPH oxidase contributes to vascular inflammation, insulin resistance, and remodeling in the transgenic (mRen2) rat
Hypertension
50
384-391
2007
Rattus norvegicus
Datla, S.R.; Dusting, G.J.; Mori, T.A.; Taylor, C.J.; Croft, K.D.; Jiang, F.
Induction of heme oxygenase-1 in vivo suppresses NADPH oxidase derived oxidative stress
Hypertension
50
636-642
2007
Homo sapiens, Mus musculus, Rattus norvegicus
Cao, X.; Dai, X.; Parker, L.M.; Kreulen, D.L.
Differential regulation of NADPH oxidase in sympathetic and sensory ganglia in deoxycorticosterone acetate salt hypertension
Hypertension
50
663-671
2007
Rattus norvegicus
Jackson, E.K.; Gillespie, D.G.; Zhu, C.; Ren, J.; Zacharia, L.C.; Mi, Z.
Alpha2-adrenoceptors enhance angiotensin II-induced renal vasoconstriction: role for NADPH oxidase and RhoA
Hypertension
51
719-726
2008
Rattus norvegicus
Szoecs, K.; Lassegue, B.; Wenzel, P.; Wendt, M.; Daiber, A.; Oelze, M.; Meinertz, T.; Muenzel, T.; Baldus, S.
Increased superoxide production in nitrate tolerance is associated with NAD(P)H oxidase and aldehyde dehydrogenase 2 downregulation
J. Mol. Cell. Cardiol.
42
1111-1118
2007
Rattus norvegicus
Qian, L.; Xu, Z.; Zhang, W.; Wilson, B.; Hong, J.S.; Flood, P.M.
Sinomenine, a natural dextrorotatory morphinan analog, is anti-inflammatory and neuroprotective through inhibition of microglial NADPH oxidase
J. Neuroinflammation
4
23
2007
Rattus norvegicus
Zhang, D.; Hu, X.; Wei, S.; Liu, J.; Gao, H.; Qian, L.; Wilson, B.; Liu, G.; Hong, J.
Squamosamide derivative FLZ protects dopaminergic neurons against inflammation-mediated neurodegeneration through the inhibition of NADPH oxidase activity
J. Neuroinflammation
5
21
2008
Mus musculus, Rattus norvegicus
Park, K.W.; Jin, B.K.
Thrombin-induced oxidative stress contributes to the death of hippocampal neurons: role of neuronal NADPH oxidase
J. Neurosci. Res.
86
1053-1063
2008
Rattus norvegicus
Li, H.; Hortmann, M.; Daiber, A.; Oelze, M.; Ostad, M.A.; Schwarz, P.M.; Xu, H.; Xia, N.; Kleschyov, A.L.; Mang, C.; Warnholtz, A.; Muenzel, T.; Foerstermann, U.
Cyclooxygenase 2-selective and nonselective nonsteroidal anti-inflammatory drugs induce oxidative stress by up-regulating vascular NADPH oxidases
J. Pharmacol. Exp. Ther.
326
745-753
2008
Homo sapiens, Rattus norvegicus
Zhou, J.; Zhang, S.; Zhao, X.; Wei, T.
Melatonin impairs NADPH oxidase assembly and decreases superoxide anion production in microglia exposed to amyloid-beta(1-42)
J. Pineal Res.
45
157-165
2008
Rattus norvegicus
Hachisuka, H.; Dusting, G.J.; Abberton, K.M.; Morrison, W.A.; Jiang, F.
Role of NADPH oxidase in tissue growth in a tissue engineering chamber in rats
J. Tissue Eng. Regen. Med.
2
430-435
2008
Rattus norvegicus
Saito, Y.; Geisen, P.; Uppal, A.; Hartnett, M.E.
Inhibition of NAD(P)H oxidase reduces apoptosis and avascular retina in an animal model of retinopathy of prematurity
Mol. Vis.
13
840-853
2007
Rattus norvegicus
Anantharam, V.; Kaul, S.; Song, C.; Kanthasamy, A.; Kanthasamy, A.G.
Pharmacological inhibition of neuronal NADPH oxidase protects against 1-methyl-4-phenylpyridinium (MPP+)-induced oxidative stress and apoptosis in mesencephalic dopaminergic neuronal cells
Neurotoxicology
28
988-997
2007
Rattus norvegicus
Chao, H.H.; Chen, C.H.; Liu, J.C.; Lin, J.W.; Wong, K.L.; Cheng, T.H.
L-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation
J. Nutr. Biochem.
21
580-588
2010
Rattus norvegicus
Jensen, M.D.; Sheng, W.; Simonyi, A.; Johnson, G.S.; Sun, A.Y.; Sun, G.Y.
Involvement of oxidative pathways in cytokine-induced secretory phospholipase A2-IIA in astrocytes
Neurochem. Int.
55
362-368
2009
Rattus norvegicus
El-Benna, J.; Dang, P.M.; Perianin, A.
Peptide-based inhibitors of the phagocyte NADPH oxidase
Biochem. Pharmacol.
80
778-785
2010
Homo sapiens, Rattus norvegicus
Pan, Q.; Yang, X.H.; Cheng, Y.X.
Angiotensin II stimulates MCP-1 production in rat glomerular endothelial cells via NAD(P)H oxidase-dependent nuclear factor-kappa B signaling
Braz. J. Med. Biol. Res.
42
531-536
2009
Rattus norvegicus
Gao, L.; Mann, G.E.
Vascular NAD(P)H oxidase activation in diabetes: a double-edged sword in redox signalling
Cardiovasc. Res.
82
9-20
2009
Bos taurus, Homo sapiens, Mus musculus, Rattus norvegicus
Winiarska, K.; Grabowski, M.; Rogacki, M.K.
Inhibition of renal gluconeogenesis contributes to hypoglycaemic action of NADPH oxidase inhibitor, apocynin
Chem. Biol. Interact.
189
119-126
2011
Oryctolagus cuniculus, Rattus norvegicus
Morgan, D.; Rebelato, E.; Abdulkader, F.; Graciano, M.F.; Oliveira-Emilio, H.R.; Hirata, A.E.; Rocha, M.S.; Bordin, S.; Curi, R.; Carpinelli, A.R.
Association of NAD(P)H oxidase with glucose-induced insulin secretion by pancreatic beta-cells
Endocrinology
150
2197-2201
2009
Rattus norvegicus
Feillet-Coudray, C.; Sutra, T.; Fouret, G.; Ramos, J.; Wrutniak-Cabello, C.; Cabello, G.; Cristol, J.P.; Coudray, C.
Oxidative stress in rats fed a high-fat high-sucrose diet and preventive effect of polyphenols: Involvement of mitochondrial and NAD(P)H oxidase systems
Free Radic. Biol. Med.
46
624-632
2009
Rattus norvegicus
Zhang, R.; Harding, P.; Garvin, J.L.; Juncos, R.; Peterson, E.; Juncos, L.A.; Liu, R.
Isoforms and functions of NAD(P)H oxidase at the macula densa
Hypertension
53
556-563
2009
Rattus norvegicus (Q924V1)
Zhang, Q.G.; Raz, L.; Wang, R.; Han, D.; De Sevilla, L.; Yang, F.; Vadlamudi, R.K.; Brann, D.W.
Estrogen attenuates ischemic oxidative damage via an estrogen receptor alpha-mediated inhibition of NADPH oxidase activation
J. Neurosci.
29
13823-13836
2009
Rattus norvegicus
Gupte, S.; Labinskyy, N.; Gupte, R.; Csiszar, A.; Ungvari, Z.; Edwards, J.G.
Role of NAD(P)H oxidase in superoxide generation and endothelial dysfunction in Goto-Kakizaki (GK) rats as a model of nonobese NIDDM
PLoS ONE
5
e11800
2010
Rattus norvegicus
Polizio, A.H.; Balestrasse, K.B.; Gornalusse, G.G.; Gorzalczany, S.B.; Santa-Cruz, D.M.; Yannarelli, G.G.; Pena, C.; Tomaro, M.L.
Losartan exerts renoprotection through NAD(P)H oxidase downregulation in a renovascular model of hypertension
Regul. Pept.
156
28-33
2009
Rattus norvegicus
Gaete, P.S.; Lillo, M.A.; Ardiles, N.M.; Perez, F.R.; Figueroa, X.F.
Ca2+-activated K+ channels of small and intermediate conductance control eNOS activation through NAD(P)H oxidase
Free Radic. Biol. Med.
52
860-870
2012
Rattus norvegicus, Rattus norvegicus Sprague-Dawley
De Blasio, M.J.; Ramalingam, A.; Cao, A.H.; Prakoso, D.; Ye, J.M.; Pickering, R.; Watson, A.M.D.; de Haan, J.B.; Kaye, D.M.; Ritchie, R.H.
The superoxide dismutase mimetic tempol blunts diabetes-induced upregulation of NADPH oxidase and endoplasmic reticulum stress in a rat model of diabetic nephropathy
Eur. J. Pharmacol.
807
12-20
2017
Rattus norvegicus
Matsumoto, M.; Katsuyama, M.; Iwata, K.; Ibi, M.; Zhang, J.; Zhu, K.; Nauseef, W.M.; Yabe-Nishimura, C.
Characterization of N-glycosylation sites on the extracellular domain of NOX1/NADPH oxidase
Free Radic. Biol. Med.
68
196-204
2014
Homo sapiens, Mus musculus, Rattus norvegicus
Cooney, S.J.; Zhao, Y.; Byrnes, K.R.
Characterization of the expression and inflammatory activity of NADPH oxidase after spinal cord injury
Free Radic. Res.
48
929-939
2014
Rattus norvegicus
Quesada, I.; de Paola, M.; Alvarez, M.S.; Hapon, M.B.; Gamarra-Luques, C.; Castro, C.
Antioxidant and anti-atherogenic properties of Prosopis strombulifera and Tessaria absinthioides aqueous extracts modulation of NADPH oxidase-derived reactive oxygen species
Front. Physiol.
12
662833
2021
Mus musculus, Rattus norvegicus
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Release 2023.1 (January 2023)
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