EC Number   |
General Information |
Reference |
|---|
   1.6.3.1 | malfunction |
a lesion in BLI-3's NADPH oxidase domain increases sensitivity to pathogen and diminishes lifespan |
743573 |
| 1.6.3.1 | 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 |
-, 725062 |
| 1.6.3.1 | malfunction |
DelTASsnox1 strains have reduced reactive oxygen species levels, are unable to develop sclerotia, and unexpectedly correlate with significantly reduced oxalate production. Inactivation of the Nox2 gene results in limited sclerotial development, but the organism remains fully pathogenic |
-, 724012 |
| 1.6.3.1 | malfunction |
excessive NADPH oxidase activation and reactive oxygen species overproduction are believed to participate in disorders such as joint, lung, vascular and intestinal inflammation |
724704 |
| 1.6.3.1 | malfunction |
in pathological circumstances, excess Nox2 can lead to oxidative stress and disease development. NOX2 V204A mutant is a competitive inhibitor of wild-type p67phox. Binding of the PB1 domain of NOX2 to p40phox is abolished by a K355A mutation in NOX2. Depletion or mutation of p40phox impairs reactive oxygen species production in neutrophils and endothelial cells. Upregulation of Nox1 can lead to oxidative stress in the cardiovascular system |
724778 |
| 1.6.3.1 | malfunction |
inhibition of NAD(P)H oxidase abolishes endothelial dysfunction in AMP-activated protein kinase alpha2-deficient mice |
711763 |
| 1.6.3.1 | malfunction |
isozyme Nox4 is involved in a variety of diseases such as idiopathic pulmonary fibrosis, pulmonary arterial hypertension, diabetic nephropathy, and complications such as diabetic cardiomyopathy and neuropathy and retinopathy or cancers like metastatic renal cell carcinoma |
712713 |
| 1.6.3.1 | malfunction |
lentiviral silencing of Nox4 in an Ang2-sufficient bEnd cell line decreases Ang2 mRNA levels and greatly impairs hemangioma growth in vivo |
712573 |
| 1.6.3.1 | malfunction |
mice deficient in NOX4 of either sex, but not those deficient for NOX1 or NOX2, are largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia |
713338 |
| 1.6.3.1 | malfunction |
NAD(P)H oxidase inhibition by apocynin might suppress reactive oxygen species production and confer neuroprotection in premature infants with intraventricular hemorrhage |
713521 |
