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
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1.6.3.1
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endothelial
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neutrophil
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artery
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p22phox
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dismutase
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angiotensin
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cardiovascular
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apocynin
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hypertension
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oxidases
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nicotinamide
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granulomatous
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cardiac
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fibrosis
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aortic
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atherosclerosis
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catalase
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sod
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leukocyte
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monocyte
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chemiluminescence
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tnf
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pkc
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phorbol
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diphenyleneiodonium
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ii-induced
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iodonium
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diphenylene
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myeloperoxidase
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endothelium-dependent
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hypothyroidism
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oxidase-derived
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renin-angiotensin
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fmlp
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dihydroethidium
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losartan
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tempol
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lucigenin
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nitrotyrosine
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peroxynitrite
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microbicidal
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oxidase-dependent
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vsmcs
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flavocytochrome
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rac2
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medicine
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ros-generating
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tiron
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oxidase-mediated
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synthesis
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agriculture
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fmlp-induced
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thyroperoxidase
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industry
- 1.6.3.1
- endothelial
- neutrophil
- artery
- p22phox
- dismutase
- angiotensin
- cardiovascular
- apocynin
- hypertension
- oxidases
- nicotinamide
- granulomatous
- cardiac
- fibrosis
- aortic
- atherosclerosis
- catalase
- sod
- leukocyte
- monocyte
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chemiluminescence
- tnf
- pkc
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phorbol
- diphenyleneiodonium
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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
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fmlp-induced
- thyroperoxidase
- industry
Reaction
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
1.6.3.1 NAD(P)H oxidase (H2O2-forming)Advanced search results
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results (Source Tissue
Source Tissue on EC 1.6.3.1 - NAD(P)H oxidase (H2O2-forming)
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SOURCE TISSUE 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
SOURCE
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isoform Nox4 is expressed at high levels in white and brown preadipocytes. Differentiation into adipocytes results in a decrease in their NOX4 mRNA content. In intact adipose tissue, the majority of NOX4 expressing cells are localized within the preadipocyte containing stromal/vascular fracftion. Alterations in NOX4 expression reflects changes in the ratio of adipocyte/interstitial fractions
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expression of isoform Nox4 mRNA in glioblastomas of WHO grade IV is significantly higher than other astrocytomas of WHO grades II and III
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expression of cytosolic subunits of NAD(P)H oxidase p47phox and p67phox is not altered by hypercholesterolemia, however, platelets and leukocytes from high cholesterol-fed mice exhibit elevated generation of reactive oxygen species compared to normal diet mice
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the cytosolic N-terminal segment, containing 4 calcium binding EF-hands is missing in Nox5S, a short calcium-insensitive variant, which is the dominant isoform in carcinoma cells, and expressed together with the long Nox5L in endothelial cells. Nox5S may be constitutively active or be a competitive inhibitor of calcium-dependent activation when present in the same tetrameric complex as Nox5L
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predominant expression in the dorsal part of zone VII of the endostyle
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
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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
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
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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
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expression of isoform Nox4 mRNA in glioblastomas of WHO grade IV is significantly higher than other astrocytomas of WHO grades II and III
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the plant hormone abscisic acid triggers production of reactive oxygen species in guard cells via the AtrbohD and AtrbohF NADPH oxidases, leading to stomatal closure. The ABA-activated SnRK2 protein kinase open stomata 1 (OST1) regulates AtrbohF activity
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
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infection by the pathogen Phytophthora infestans results in a radical burst mediated by mitogen-activated protein kinase cascades MEK2-SIPK/NTF4 and MEK1-NTF6. Silencing of the NAD(P)H oxidase Respiratory Burst Oxidase Homolog B, RBOHB eliminates generation of reactive oxygen speicies. INF1 elicitin, produced by the pathogen, regulates reactive oxygen species generation through mitogen-activiated protein kinase cascades
NOX2 and NOX4 are the main isoforms present in macula densa cells
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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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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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depleting Rac1 (a component of NADPH oxidase) in mouse rod photoreceptors protects them from photo-oxidative stress without affecting their structure or function
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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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neuroblastoma cell, cells differentiated by retinoic acid die after exposure to glycated albumin, a model of advanced glycation end product-modified protein. Undifferentiated cells are resistant to glycated albumin. Differentiated cells pre-treated with NAD(P)K oxidase inhibitor diphenyleneiodinium or with rottlerin, an inhibitor of protein kinase C delta, are able to prevent neuronal death induced by glycated albumin
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protein is localized to the rostral sperm head, with some labeling in the equatorial and post-acrosomal regions
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primary tracheobronchial epithelial cell. Study on enzyme isoforms Duox1 and Duox2 mRNA expression after treatment with multiple cytokines. Duox1 expression is increased severalfold by treatment with Th2 cytokines IL-4 and IL-13, and by polyinosine-polycytydilic acid and rhinovirus infection. Duox2 expression is highly induced following treatment with Th1-cytokine IFN-gamma
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NAD(P)H oxidase activity from 1-month-old tubers increases to a maximum 18-24 after wounding and then decreases to barely detecable levels by 72 h. Wound-induced responses are lost over a 25- to 30-month storage period. The initial burst of superoxide in response to wounding is mediated by isoform Strboh A
additional information
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Exposure of mouse aortic rings to hypoxia/reoxygenation significantly increases vessel outgrowth, whereas pharmacological inhibition of NADPH oxidase or genetic deletion of the NADPH oxidase subunit, p47phox significantly suppresses these changes. Increases in myocardial serine-threonine kinase Akt and ERK1/2 activation and vascular endothelial growth factor expression are markedly blunted in the subunit p47phox-deficient mouse subjected to myocardial ischemia-reperfusion compared with the wild-type mouse
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hemin treatment increases hemin oxidase-1 expression and activity in aorta and kidney of apolipoprotein E-deficient mice and significantly reduces both NADPH oxidase activity and superoxide generation in situ. Effects are reversed by tin protoporphyrin-IX and are not associated with changes in isoforms Nox2 or Nox4 protein levels. Inhibition of NADPH oxidase activity by hemin in the aorta is mimicked by bilirubin in vitro
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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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human pulmonary artery endothelial cell, induction of NAD(P)H oxidase by exposure to hyperoxia for 3 h. Pretreatment of cells with the actin-stabilizing agent phallacidin attenuates hyperoxia-induced cortical actin thickening and reactive oxygen species production, whereas cytochalasin D and latrunculin A enhance basal and hyperoxia-induced reactive oxygen species formation. A 3-h hyperoxic exposure enhances the tyrosine phosphorylation of cortactin and interaction between cortactin and subunit p47phox. Transfection of cells with cortactin small interfering RNA or myristoylated cortactin Src homology domain 3 blocking peptide attenuated reactive oxygen species production and the hyperoxia-induced translocation of p47phox to the cell periphery
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in the mesenteric arteries of streptozotocin-induced diabetic apoE-deficient mice the expression of nox4 and gp91phox, ie. nox2 subunits of NADPH oxidase are enhanced as are endothelial nitric oxide synthase mRNA and protein
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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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porcine coronary artery endothelial cell, PCAEC. Exposure of cells to hypoxia for 2 h followed by 1 h of reoxygenation significantly increases reactive oxygen species formation. Pretreatment with the NADPH oxidase inhibitors, diphenyleneiodonium and apocynin , significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation. Exposure of PCAECs to hypoxia/reoxygenation causes a significant increase in serine-threonine kinase Akt and ERK1/2 activation. Exposure of PCAEC spheroids to hypoxia/reoxygenation significantly increases endothelial spheroid sprouting, whereas pharmacological inhibition of NADPH oxidase or genetic deletion of the NADPH oxidase subunit, p47phox (p47phox/), significantly suppresses these changes
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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
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
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in ischemic cardiomyocytes, Nox2 is upregulated in the cytosol and targeted to the nuclear pore complex
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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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Nox1 is most highly expressed in colon epithelium. In colon the cytosolic subunits p47phox and p67phox are not expressed and are replaced by Noxo1 and Noxa1
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L-carnitine inhibits angiotensin II increased NADPH oxidase activity and intracellular ROS levels in cardiac fibroblasts
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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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keratinocyte cell line. Long-term survival mechanisms in niacin deficient cells involve accumulation of reactive oxygen species and increased DNA damage with concomitant increase in expression and activity of NAD(P)H oxidase
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after myocardial infarction, NAD(P)H oxidase activity is markedly increased in remote left ventricular myocardium of wild-type mice but not in mice deficient in subunit p47phox. Increased myocardial xanthine oxidase activity is observed in wild-type, but not in p47phox-deficient mice after myocardial infarction. Left ventricular cavity dilatation and dysfunction 4 weeks after infarction are markedly attenuated in p47phox-deficient mice and cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis are substantially reduced as compared with wild-type. The survival rate is markedly higher in mice deficient in subunit p47phox
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induction of superoxide production by doxorubicin is much higher in hearts of wild-type mice than in subunit gp91phox knock-out mice. Superoxide production is similarly induced by addition of NADPH cytochrome P450 reductase
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the amount of NOX4 is elevated in hearts of db/db diabetic mice compared to wild-type mice
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the amount of NOX4 is elevated in hearts of db/db diabetic mice compared to wild-type mice
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rabbits with heart failure induced by myocardial infarction exhibit left ventricular dilatation and systolic dysfunction. Changes are associated with increases in NADPH oxidase activity, subunit p47phox protein expression, 8-hydroxydeoxyguanosine expression, 4-hydroxy-2-nonenal expression, myocyte apoptosis, and Bax protein and a decrease in Bcl-2 protein
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
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transfection of isoform Nox3-specific siRNA abrogates H2O2 production and inhibitis exclusively the second phase of p42/44 MAPK phosphorylation and Sp1 DNA binding thus preventing upregulation of VEGF-A mRNA expression
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taurolithocholylsulfate induces shrinkage in wild-type, but not in subunit p47phox-deficient hepatocytes. Hepatocytes from subunit p47phox knock-out mice are resistant towards taurolithocholylsulfate-induced apoptosis and fail to activate the CD95 system
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bilirubin concentration-dependently reduces NADPH oxidase-dependent superoxide production stimulated by phorbol 12-myristate 13-acetate
cochlear and vestibular system, NOX3 is highly expressed in specific portions of the inner ear
cochlear and vestibular system, NOX3 is highly expressed in specific portions of the inner ear
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
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hemin treatment increases hemin oxidase-1 expression and activity in aorta and kidney of apolipoprotein E-deficient mice and significantly reduces both NADPH oxidase activity and superoxide generation in situ. Effects are reversed by tin protoporphyrin-IX and are not associated with changes in isoforms Nox2 or Nox4 protein levels
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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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platelets and leukocytes from high cholesterol-fed mice exhibit elevated generation of reactive oxygen species compared to normal diet mice. Hypercholesterolemia-induced leukocyte recruitment is attenuated in Cu,Zn-superoxide dismutase transgenic, and NAD(P)H oxidase-knockout mice on high cholesterol diet. Platelets from NAD(P)H oxidase-knockout mice on high cholesterol diet exhibit low levels of adhesion comparable to those of wild-type on normal diet. Overexpression of Cu,Zn-superoxide dismutase or, to a lesser extent, NAD(P)H oxidase subunit gp91 deficiency restores arteriolar vasorelaxation responses toward normal diet wild-type levels
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five splice variants of Nox4, named Nox4A through E, are found in lung epithelial cells
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presence of subunits NOX1, NOXA1, NOXO1, p22phox, p47phox, p40phox, p67phox, NOX2, and NOX4. Hypoxic conditions lead to upregulation exclusively of NOX4 mRNA, concomitant with increased levels in microdissected pulmonary arterial vessels. NOX4 mRNA and protein are localized predominantly in the media of small pulmonary arteries, with increased labeling intensities after chronic exposure to hypoxia. In isolated pulmonary arterial smooth muscle cells, NOX4 is localized primarily to the perinuclear space
Duox1 and Duox2 localize distinctly in lung epithelial cells as well as in ex-vivo differentiated lung epithelia. The localization of functional Duox-DuoxA heterodimers seems to be controlled by the associated DuoxA subunit
Duox1 and Duox2 localize distinctly in lung epithelial cells as well as in ex-vivo differentiated lung epithelia. The localization of functional Duox-DuoxA heterodimers seems to be controlled by the associated DuoxA subunit, including Duox2 expression in ciliated cells in an ex vivo differentiated lung epithelium
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Burkholderia cenocepacia resides in macrophage vacuoles displaying an altered recruitment of the NADPH oxidase complex at the phagosomal membrane
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alveolar macrophages. Inhibition of NAD(P)H oxidase by apocynin results in down-regulation of arginase
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subunit gp91phox gene expression is significantly higher in monocytes from sickle cell disease patients compared with normal controls. Monocytes from patients show higher levels of p47phox phosphorylation compared with normal controls
expressed highly in hemocytes, followed by comparable expression in hepatopancreas and moderate expression in brain, eyestalk and intestine, but with relatively low expressions in gill, heart and muscle
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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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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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hemorrhagic shock/resuscitation activates NAD(P)H oxidase by phosphorylation of subunit p47phox. Activation is significantly diminshed in C3H/HeJ mice, which are not responsive to lipopolysaccharide because of a point mutation of tlr4 affecting the TIR domain. In wild-type, in vitro stimulation of hemorrhagic shock/resuscitation-activated neutrophils with recombinant high-mobility group box HMGB1 causes TLR4-dependent activation of NAD(P)H oxidase as well as increased reactive oxygen species production through both MyD88-IRAK4-p38 MAPK and MyD88-IRAK4-Akt signaling pathways
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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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transcript levels of Nox1 increase in planta and during sclerotial development, transcript levels of Ssnox1 also increase during fungal interaction with plant tissue
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transcript levels of Nox1 increase in planta and during sclerotial development, transcript levels of Ssnox1 also increase during fungal interaction with plant tissue
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bilirubin concentration-dependently reduces NADPH oxidase-dependent superoxide production stimulated by angiotensin II in vascular smooth muscle cells
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protein is localized to the adluminal region of the seminiferous tubules
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NAD(P)H oxidase may have a role in the structural arrangement and mechanical properties of the airway tissue
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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
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in sarcoplasmic reticulum vesicles isolated after exercise and tachycardia, increase in NAD(P)H oxidase activity, ryanodine receptor-2 S-glutathionylation, and calcium release rates. Cardiac muscle displays significant colocalization of NADPH oxidase and ryanodine receptor-2
additional information
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different tissues screened for ThOX2, except for a weak signal in stomach ThOX2 in exclusively found in thyroid cells
additional information
different tissues screened for ThOX2, except for a weak signal in trachea ThOX2 in exclusively found in thyroid cells
additional information
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expression of isoform Duox2 in all tissues of the digestive tract examined. Enzyme is located at the apical membrane of the enterocytes in the brush border
additional information
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Nox5 expression is restricted to fewer tissues. Nox4 activity is constitutive, addition of cytosol to membrane fractions in transfected cells does not increase Nox4 activity, also transfection of organizer and activator subunits does not increase reactive oxygen species production
additional information
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chamber model using subcutaneous arteriovenous loop tissue
additional information
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expression of isoform Duox2 in all tissues of the digestive tract examined. Enzyme is located at the apical membrane of the enterocytes in the brush border
