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Rat (Rattus) NOX4 ELISA Kit for Sandwich ELISA - ABIN431602
El-Naga: Apocynin protects against ethanol-induced gastric ulcer in rats by attenuating the upregulation of NADPH oxidases 1 and 4. in Chemico-biological interactions 2015
Mouse (Murine) NOX4 ELISA Kit for Sandwich ELISA - ABIN424309
Vital, Castro, Ittmann: Oxidative stress promotes benign prostatic hyperplasia. in The Prostate 2016
Endoplasmic reticulum stress triggers a localized signaling module on the ER surface involving Nox4-dependent calcium mobilization, which directs local Ras activation through ER-associated, calcium-responsive RasGRF.
PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) signaling only occurs when FLT3 (show FLT3 ELISA Kits)-ITD is expressed at the plasma membrane and is required for the production of NOX-generated ROS (show ROS1 ELISA Kits). ER retention of FLT3 (show FLT3 ELISA Kits)-ITD resulted in NOX4 deglycosylation and p22(phox (show CYBA ELISA Kits)) protein degradation.
NOX4 upregulation confers anoikis resistance.
these data demonstrate that increased expression and activation of NOX4, which might result from increased TGFbeta1 (show TGFB1 ELISA Kits) levels seen during aging, induces a proinflammatory phenotype in VSMCs, enhancing atherosclerosis.
The ROS (show ROS1 ELISA Kits) levels of the study group decreased obviously before irradiation (P<0.01), however, the radiation-induced ROS (show ROS1 ELISA Kits) 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 ELISA Kits) and NOX4 levels and total SOD (show SOD1 ELISA Kits) activity decreased (P<0.01), while the levels of SOD1 (show SOD1 ELISA Kits) were stably maintained (P>0.05).
NS5A contributes to reactive oxygen species production by activating expression of NADPH (show NQO1 ELISA Kits) oxidases 1 and 4 as well as cytochrome P450 2E1 (show CYP2E1 ELISA Kits).
Nox4 and Duox1/Duox2 (show DUOX1 ELISA Kits) mediate redox activation of mesenchymal cell migration by PDGF (show PDGFA ELISA Kits).
alkali burns markedly upregulated the transcription and expression of Nox2 (show CYBB ELISA Kits) and Nox4 in human or mouse corneas.
The NOX4 and TLR2 (show TLR2 ELISA Kits) 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.
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 ELISA Kits) activity, as well as increases in Nox4 isoform and protein disulfide isomerase (show P4HB ELISA Kits) mRNA expression
These studies provide insight into the roles of Nox4/senescence in endothelial cells barrier responses.
NOX4-derived reactive oxygen species may play a role in the onset of insulin (show INS ELISA Kits) resistance and adipose tissue inflammation in obesity.
Brown adipose tissue, via Nox4-derived hydrogen peroxide, induces cyclic GMP-dependent protein kinase G type-1alpha activation, resulting in reduced vascular contractility.
this study shows that NOX4-derived oxidative stress plays a key role in psoriasis induced kidney dysfunction
Data (including data from studies using transgenic mice) suggest that Glut1 (glucose transporter type 1 (show SLC2A1 ELISA Kits)) is a critical downstream target of Hif1a (hypoxia-inducible factor 1 (show HIF1A ELISA Kits), alpha subunit (show POLG ELISA Kits)) mediating hyperglycemia-induced extracellular matrix accumulation in kidney via regulation of Nox4 (NADPH oxidase (show NOX1 ELISA Kits) type 4) expression in nephropathy due to diabetes type 1.
H2S recruits iNOS (show NOS2 ELISA Kits) to generate NO to inhibit high glucose-induced NOX4 expression, oxidative stress, and matrix protein accumulation in renal epithelial cells; the two gasotransmitters H2S and NO and their interaction may serve as therapeutic targets in diabetic kidney disease.
This study describes NOX4 as a major contributor to the initiation of neuropathic pain at early stages after nerve lesion.
Nox4 promotes tumour angiogenesis and may represent a novel target for anti-angiogenic tumour therapy.
MRTF down-regulation/inhibition suppresses TGFbeta (show TGFB1 ELISA Kits)/contact disruption-provoked Nox4 protein and mRNA expression, Nox4 promoter activation, and reactive oxygen species production.
Nox4 NADPH oxidase (show NOX1 ELISA Kits) mediates oxidative stress and apoptosis caused by TNF-alpha (show TNF ELISA Kits) in cerebral vascular endothelial cells.
Nox4 NADPH oxidase (show NOX1 ELISA Kits)-derived reactive oxygen species also initiate a cell survival mechanism by increasing production of carbon monoxide by constitutive heme oxygenase-2 (show HMOX2 ELISA Kits).
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