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The ROS (show ROS1 Proteins) levels of the study group decreased obviously before irradiation (P<0.01), however, the radiation-induced ROS (show ROS1 Proteins) of the study group was at a high level even when irradiation had been terminated for 2 h (P<0.01). Moreover, NOX2 (show CYBB Proteins) and NOX4 levels and total SOD (show SOD1 Proteins) activity decreased (P<0.01), while the levels of SOD1 (show SOD1 Proteins) were stably maintained (P>0.05).
NS5A contributes to reactive oxygen species production by activating expression of NADPH (show NQO1 Proteins) oxidases 1 and 4 as well as cytochrome P450 2E1 (show CYP2E1 Proteins).
Nox4 and Duox1/Duox2 (show DUOX1 Proteins) mediate redox activation of mesenchymal cell migration by PDGF (show PDGFA Proteins).
alkali burns markedly upregulated the transcription and expression of Nox2 (show CYBB Proteins) and Nox4 in human or mouse corneas.
The NOX4 and TLR2 pathways played important roles in the biological effects mediated by Bletilla striata polysaccharide b.
it was demonstrated that elevated uric acid promoted ROSinduced tubular cell apoptosis by upregulating Nox4 expression.
expression of MATER and NOX4 proteins are closely related to the follicular development and ovulation with particular regard for ovarian aging
Data indicate that endothelin receptor antagonist CPU0213 has an anti-apoptosis role through NADPH oxidase 4 (Nox4)-dependent O2-.production.
Oleic/[almitic acid treatment enhances reactive oxygen species production and cell apoptosis mainly by upregulating the protein levels of NOX4 and caspase3 activation in chondrocytes.
miR (show MLXIP Proteins)-99a directly regulates the invasion and migration in lung adenocarcinoma by targeting NOX4.
Peroxide derived from superoxide generated by Nox4 appears to maintain a basal relaxation in bovine pulmonary arteries under normoxic conditions, which is removed under hypoxia leading to hypoxic pulmonary vasoconstriction.
proteasome inhibition completely prevented endoplasmic reticulum stress-induced increase in NADPH oxidase (show NOX1 Proteins) activity, as well as increases in Nox4 isoform and protein disulfide isomerase (show P4HB Proteins) mRNA expression
Nox4 promotes tumour angiogenesis and may represent a novel target for anti-angiogenic tumour therapy.
of smooth muscle Nox4 inhibits atherosclerosis by suppressing sEH (show EPHX2 Proteins), which, at least in part, accounts for inhibition of SMC (show DYM Proteins) proliferation, migration and inflammation
the reduction of ROS generation and NOX4 expression by EA preconditioning might be involved in BBB recovery. Therefore, EA may serve as a potential preventive strategy for patients at high risk of ischemic stroke.
Deleterious effect of Nox4 expression in podocytes by promoting podocytopathy in association with albuminuria and extracellular matrix accumulation in experimental diabetes, emphasizes the role of NOX4 as a target for new renoprotective agents.
Data suggest that NOX4 and mitochondrial oxidative stress are mediators of cardiovascular disease in aging under hyperlipidemic conditions.
Downregulation of smooth muscle Nox4 inhibits neointimal hyperplasia by suppressing TSP1 (show GZMA Proteins).
TRAIL can promote angiogenesis following hindlimb ischemia in vivo via NOX4/eNOS (show NOS3 Proteins)/nitric oxide signaling.
NOX4 may thus associate with mitochondrial complex I proteins, but in cardiac and renal mitochondria under basal conditions, expression is beyond our detection limits.
IFNgamma induces oxidative stress, DNA damage and tumor cell senescence via TGFbeta/SMAD signaling-dependent induction of Nox4 and suppression of ANT2
MRTF down-regulation/inhibition suppresses TGFbeta (show TGFB1 Proteins)/contact disruption-provoked Nox4 protein and mRNA expression, Nox4 promoter activation, and reactive oxygen species production.
Nox4 NADPH oxidase (show NOX1 Proteins) mediates oxidative stress and apoptosis caused by TNF-alpha (show TNF Proteins) in cerebral vascular endothelial cells.
Nox4 NADPH oxidase (show NOX1 Proteins)-derived reactive oxygen species also initiate a cell survival mechanism by increasing production of carbon monoxide by constitutive heme oxygenase-2 (show HMOX2 Proteins).
This gene encodes a member of the NOX-family of enzymes that functions as the catalytic subunit the NADPH oxidase complex. The encoded protein is localized to non-phagocytic cells where it acts as an oxygen sensor and catalyzes the reduction of molecular oxygen to various reactive oxygen species (ROS). The ROS generated by this protein have been implicated in numerous biological functions including signal transduction, cell differentiation and tumor cell growth. A pseudogene has been identified on the other arm of chromosome 11. Alternative splicing results in multiple transcript variants.
NADPH oxidase 4
, predicted NADPH oxidase-4
, kidney oxidase-1
, kidney superoxide-producing NADPH oxidase
, renal NAD(P)H-oxidase
, superoxide-generating NADPH oxidase 4