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1.6.3.1: NAD(P)H oxidase (H2O2-forming)

This is an abbreviated version!
For detailed information about NAD(P)H oxidase (H2O2-forming), go to the full flat file.

Word Map on EC 1.6.3.1

Reaction

NAD(P)H
+
H+
 +
O2
=
NAD(P)+
 +
H2O2

Synonyms

100787949, 100812342, 100820185, Atrbohc, AtrbohD NADPH oxidase, AtrbohF NADPH oxidase, BLI-3, cytochrome b-245 heavy chain, dual oxidase, Duox, Duox-DuoxA NADPH oxidase, Duox1, Duox2, Glyma.03G236300, Glyma.19G233900, Glyma.20G236200, GLYMA_10G152200, gp91phox, gp91phox/Nox2, KOD1, large NOX, LNOX, NAD(P)H oxidase, NAD(P)H oxidase 4, NADH oxidase, NADPH oxidase, NADPH oxidase 1, NADPH oxidase 2, NADPH oxidase 4, NADPH oxidase 5, NADPH oxidase type 4, NADPH-oxidase, NADPHox, NAPDH oxidase, NM_001184780, NOX, NOX1, Nox2, NOX3, Nox4, NOX4-art, NOX5, p138 thyroid-oxidase, p138tox, p47phox, p67phox, phagocyte NADPH oxidase, phox, RBOH, RBOHB, RbohF, RDH2, RdxA, renal oxidase, renox, Respiratory Burst Oxidase Homolog, respiratory burst oxidase homologue, rth5, SsNOX38, superoxide-generating NADPH oxidase, ThOX, ThOX2, thyroid NADPH oxidase, thyroid oxidase, thyroid oxidase 2, TK0304, TK0828, TK1186, TK1299, TK1481

ECTree

     1 Oxidoreductases
         1.6 Acting on NADH or NADPH
             1.6.3 With oxygen as acceptor
                1.6.3.1 NAD(P)H oxidase (H2O2-forming)

Expression

Expression on EC 1.6.3.1 - NAD(P)H oxidase (H2O2-forming)

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
2 mM metformin induces suppression of NAD(P)H oxidase activity by 45% in high glucose (30 mM) and by 60% in normal glucose concentrations (5.6 mM)
-
5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside-induced suppression of NAD(P)H oxidase subunit expression is AMP-activated protein kinase alpha2-dependent
a strong upregulation of NAD(P)H oxidase subunits p22phox and p47phox is observed in the hypertensive kidney of aortic coarcted rats
-
adiponectin suppresses NADPH oxidase expression/activity
-
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
-
during sunlight exposure, UV attenuation significantly loweres plasma membrane NADPH oxidase activity
-
enzyme expression is upregulated in diabetes
-
expression increases 100fold upon challenge with Sclerotina sclerotiorum
expression increases 20fold upon challenge with Sclerotina sclerotiorum
expression increases 50fold upon challenge with Sclerotina sclerotiorum
expression of NOX4 mRNA is significantly higher 12 h and 24 h after transient middle cerebral artery occlusion in the basal ganglia and neocortex of wild type mice than in sham-operated controls
-
fatty acids activate NADPH oxidase expression/activity
-
high glucose concentration (30 mM) increases NAD(P)H oxidase activity by about 27%
-
hyperglycemia induces increases in NAD(P)H oxidase activity
-
in Portunus trituberculatus challenged with the Hematodinium parasite, transcripts in hemocytes are ignificantly enhanced from 3 h to 24 h (P < 0.05), then recovered to the normal level and reduced significantly from 96 h to 192 h
in Portunus trituberculatus challenged with the Hematodinium parasite, transcripts in hemocytes are significantly enhanced from 3 h to 24 h (P < 0.05), then recovered to the normal level and reduced significantly from 96 h to 192 h
interleukin-3 incubation stimulates the synthesis of Nox2 cytosolic sub-unit p47phox
-
investigated the effect of imiquimod (IMQ)-induced psoriatic inflammation on kidney function and inflammation in a murine model. Psoriatic inflammation in mice is associated with kidney dysfunction as reflected by increased serum creatinine and blood urea nitrogen. Kidney dysfunction is paralleled by upregulation of reactive oxygen species (ROS) generating enzymes such as NOX2, NOX4 and iNOS
ischemia/reperfusion injury stimulates the expression of a 28000 Da NOX4 spliced isoform
-
leptin suppresses NADPH oxidase expression/activity
-
losartan administration significantly reduces oxidative stress generation by decreasing NAD(P)H oxidase expression
-
loss of AMP-activated protein kinase activity increases NAD(P)H oxidase subunit expression (gp91phox, p47phox, p67phox, NOX1 and -4) and NAD(P)H oxidase-mediated superoxide production
NAD(P)H oxidase activity is increased in hypertension
NAD(P)H oxidase activity is increased in noninfarcted left ventricular tissues from mice in the high fat diet plus myocardial infarction group
-
NAD(P)H oxidase activity is not increased in mice from the normal diet plus myocardial infarction group
-
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 activity is significantly increased in both the periventricular region and cortex of pups with intraventricular hemorrhage than glycerol- and saline-treated controls at 6h age, and remains substantially elevated at 24h postnatal age
-
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
-
NOX1 is upregulated by angiotensin II, PDGF, PGF, LDL, TNF-alpha, oscillatory shear stress BMP4, aldosterone plus salt, IFN-gamma, ET-1, T3, urokinase8, oxidized LDL, and vascular injury. NOX2 is upregulated by angiotensin II, ET-1, TGF-beta, IFN-gamma, oxidized LDL oscillatory shear stress, aldosterone plus salt, Ischemia, and vascular injury.NOX4 is upregulated by TGF-beta, thromboxane, TNF-alpha. IFN-gamma, urotensin, urokinase, oscillatory shear stress, hypoxia, hyperoxia vascular injury. NOX5 iss upregulated by angiotensin II, ET-1, thromboxane A2, TNF-alpha, atherosclerosis. Nox5 can be upregulated and activated by minute concentrations of hydrogen peroxide. In ischemic cardiomyocytes, Nox2 is upregulated in the cytosol and targeted to the nuclear pore complex
-
NOX2 and NOX4 activity is induced by 70 and 140 mM NaCl
NOX4 gene expression is stronger in brain samples from stroke patients compared to healthy controls
-
Nox4 is downregulated in angiopoietin 2 heterozygous cells
-
Nox4 mRNA expression increases to 88% in fibroblasts cultured on 3-deoxyglucosone-collagen for 24 h compared to fibroblasts cultured on native collagen
-
oxidized low-density lipoprotein increases the amounts of NADPH oxidase in fibroblasts. Treatment with physiologically relevant levels of glycated low-density lipoprotein increases superoxide and H2O2 release and the levels of NOX4 and p22phox, an essential component of multiple NOX complexes, in wild-type or HSF1-deficient mouse embryonic fibroblasts. Small interfering RNA for p22phox prevents the increase in expression of Nox4 in fibroblasts. The results suggest that glyLDL increases the abundance of NOX4 or p22phox via an HSF1-independent pathway, but that of PAI-1 via an HSF1-dependent manner
the BRAFV600E oncogene upregulates the enzyme NOX4 via TGF-beta1 signaling pathway in papillary thyroid cancer cell line
-
the enzyme is elevated in human radio-induced thyroid tumors and in sporadic thyroid tumors
-
the enzyme is up-regulated after spinal cord injury
-
the expression of isoforms NOX2 and NOX4 is increased after spinal cord injury
-
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
-
transcript levels of Ssnox1 increase during fungal interaction with plant tissue
tumor necrosis factor-alpha activates NADPH oxidase expression/activity. NAD(P)H oxidase is increased in the retina of diabetic rats
-