NADPH Oxidase 1
Subject Areas on Research
- A critical role for chloride channel-3 (CIC-3) in smooth muscle cell activation and neointima formation.
- Activation of NADPH oxidase 1 increases intracellular calcium and migration of smooth muscle cells.
- An oxidized extracellular oxidation-reduction state increases Nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation.
- Assessing activation states in microglia.
- Cigarette Smoke Initiates Oxidative Stress-Induced Cellular Phenotypic Modulation Leading to Cerebral Aneurysm Pathogenesis.
- Cytokine activation of nuclear factor kappa B in vascular smooth muscle cells requires signaling endosomes containing Nox1 and ClC-3.
- Drebrin attenuates atherosclerosis by limiting smooth muscle cell transdifferentiation.
- Increased expression of Nox1 in neointimal smooth muscle cells promotes activation of matrix metalloproteinase-9.
- Nox1 NADPH oxidase is necessary for late but not early myocardial ischaemic preconditioning.
- Nox1 transactivation of epidermal growth factor receptor promotes N-cadherin shedding and smooth muscle cell migration.
- Nox1 in cardiovascular diseases: regulation and pathophysiology.
- Nox4 NADPH oxidase contributes to smooth muscle cell phenotypes associated with unstable atherosclerotic plaques.
- Phosphorylation of Nox1 regulates association with NoxA1 activation domain.
- Platelet-derived growth factor (PDGF) regulates Slingshot phosphatase activity via Nox1-dependent auto-dephosphorylation of serine 834 in vascular smooth muscle cells.
- Redox Activation of Nox1 (NADPH Oxidase 1) Involves an Intermolecular Disulfide Bond Between Protein Disulfide Isomerase and p47phox in Vascular Smooth Muscle Cells.
- Role for Nox1 NADPH oxidase in atherosclerosis.