EC Number   |
Natural Substrates |
|---|
   1.6.3.1 | NAD(P)H + H+ + O2 |
- |
| 1.6.3.1 | NADH + H+ + O2 |
- |
| 1.6.3.1 | NADPH + H+ + O2 |
- |
| 1.6.3.1 | NADPH + O2 |
- |
| 1.6.3.1 | NADH + H+ + O2 |
2 electrons are transferred from cytosolic NADPH to FAD and in succession across the membrane, via redox changes in heme irons. Finally, each electron reduces a molecule of oxygen to a superoxide radical, which is subsequently released outside the cell or in a topologically equivalent compartment, such as a vesicle lumen |
| 1.6.3.1 | more |
active NAD(P)H oxidase is required for vascular endothelial growth factor activation of phosphoinositide 3-kinase-Akt-forkhead, and p38 mitogen-activated kinase, but not extracellular signal-related kinase 1/2 or c-Jnu N-terminal kinase. The permissive role of NADPH oxidase on phosphoinositide 3-kinase-Akt-forkhead signaling is mediated at post-vascular endothelial growth factor receptor levels and involves the nonreceptor tyrosine kinase Src |
| 1.6.3.1 | more |
angiotensin II-evoked expression of endothelin-1 in adventitial fibroblasts is mediated, at least in part, by NADPH oxidase. This mechanism stimulates collagen expression thereby implicating the adventitia as a potential contributor to the vascular pathophysiology associated with oxidative stress and vascular remodeling |
| 1.6.3.1 | more |
calcium-dependent kinase CDPK5 induces phosphorylation of the catalytic subunit at resiude S82 and thereby regulates the oxidative burst |
| 1.6.3.1 | more |
chronic granulomatous disease is a rare inherited immunodeficiency syndrome caused by mutations in four genes encoding essential nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex components |
| 1.6.3.1 | more |
decreased hepatic fibrosis after chronic CCl4 administration in mice with NADPH oxidase deficiency occurs in the setting of greater necrosis and inflammation but decreased apoptosis |
