No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Mouse (Murine) Antibodies:
anti-Rat (Rattus) Antibodies:
Go to our pre-filtered search.
Cow (Bovine) Polyclonal NOX4 Primary Antibody for ICC, IHC (fro) - ABIN189715
Maranchie, Zhan: Nox4 is critical for hypoxia-inducible factor 2-alpha transcriptional activity in von Hippel-Lindau-deficient renal cell carcinoma. in Cancer research 2005
Show all 64 Pubmed References
Human Polyclonal NOX4 Primary Antibody for FACS, ICC - ABIN4340462
Weyemi, Caillou, Talbot, Ameziane-El-Hassani, Lacroix, Lagent-Chevallier, Al Ghuzlan, Roos, Bidart, Virion, Schlumberger, Dupuy: Intracellular expression of reactive oxygen species-generating NADPH oxidase NOX4 in normal and cancer thyroid tissues. in Endocrine-related cancer 2010
Show all 40 Pubmed References
Polyclonal NOX4 Primary Antibody for IHC (fro), WB - ABIN540366
Kim, Park, Park: Increased superoxide formation induced by irradiation preconditioning triggers kidney resistance to ischemia-reperfusion injury in mice. in American journal of physiology. Renal physiology 2009
Show all 2 Pubmed References
Human Polyclonal NOX4 Primary Antibody for IHC (p), WB - ABIN3044011
Meyer, Fredette, Daniel, Sharma, Amann, Arterburn, Barton, Prossnitz: Obligatory role for GPER in cardiovascular aging and disease. in Science signaling 2017
Show all 2 Pubmed References
Human Polyclonal NOX4 Primary Antibody for IHC, WB - ABIN5692899
Liu, Hong, Li, Ren, Wang, Xu, Shi, Xu: A Cross Talk Between BRG1 and Males Absent on the First Contributes to Reactive Oxygen Species Production in a Mouse Model of Nonalcoholic Steatohepatitis. in Antioxidants & redox signaling 2018
Show all 2 Pubmed References
Human Polyclonal NOX4 Primary Antibody for IHC, IHC (p) - ABIN409683
Zhang, Liu, Hu: Inhibiting cancer metastasis via targeting NAPDH oxidase 4. in Biochemical pharmacology 2013
Dog (Canine) Polyclonal NOX4 Primary Antibody for IF (p), IHC (p) - ABIN737526
Khan, Byer, Khan: Exposure of Madin-Darby canine kidney (MDCK) cells to oxalate and calcium oxalate crystals activates nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase. in Urology 2014
Human Polyclonal NOX4 Primary Antibody for ELISA, IHC - ABIN6263695
Shen, Tian, Shen, Sun, Liu: Alpha-Lipoic Acid Protects Human Aortic Endothelial Cells Against H2O2-Induced Injury and Inhibits Atherosclerosis in Ovariectomized Low Density Lipoprotein Receptor Knock-Out Mice. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2018
Human Polyclonal NOX4 Primary Antibody for ELISA, ICC - ABIN4340464
Murley, Arbiser, Weichselbaum, Grdina: ROS modifiers and NOX4 affect the expression of the survivin-associated radio-adaptive response. in Free radical biology & medicine 2018
High NOX4 expression is associated with Tuberin Deficiency Syndrome.
this study shows that silencing of NADPH Oxidase 4 attenuates hypoxia-induced chemoresistance in neuroblastoma cells by Inhibiting PI3K/Akt-dependent glycolysis
NOX4 expression correlated with tumor size and prognosis of gastric cancer. NOX4 regulated gastric cancer cell growth and cell apoptosis via the generation of reactive oxygen species (ROS), subsequently activating the GLI1 protein pathway.
HIC-5 regulates mitochondrial ROS production in tumor cells while requiring activated KRAS to mediate its effect on NOX4 in oncogene-induced senescence and tumor invasiveness.
Integrin engagement during cell attachment activates Poldip2/Nox4 to oxidize actin, which modulates filamentous actin assembly and its interaction with vinculin.
Nox4-induced ROS production appears to be an essential actor in the osteoarthritis process [review]
Our results suggest that increased expression of NOX4 in the hippocampal DG in the 6-OHDA-treated mouse induces Abeta expression and oligomer A11 production, thereby reducing cognitive function.
miR-423-5p overexpression protected high-glucose-induced podocyte damage by inhibiting ROS generation via targeting Nox4
this study shows that NADPH oxidase 4 contributes to endothelial dysfunction mediated by histone methylations in metabolic memory
NOX4-derived ROS production may play a key role in the development of pulmonary hypertension in chronic obstructive pulmonary disease by promoting distal pulmonary vascular remodeling.
MiR-99a-5p affected the vitality and proliferation, migration together with the invasion of oral tumor cells through targeting NOX4.
Levels of NADPH oxidase subunits NOX2 and NOX4 proteins in peripheral blood mononuclear cells of the sevoflurane group were lower than the propofol group (p=0.033, p<0.001, p<0.001and p<0.001, respectively).
NOX4 plays a considerable role in the cycle-dependent changes in the normal endometrium and in the biology of endometrial cancer.
Integrated analyses of heterodimerization, trafficking, and catalytic activity identified determinants for the NOX4-p22(phox) interaction, such as heme incorporation into NOX4 and hot spot residues in transmembrane domains 1 and 4 in p22(phox) .
Metabolic syndrome in Brazilian NAFLD patients most likely results from common allelic variants in a large number of genes, including CYBA and NOX4, that interact with each other, each of which alone determines a modest risk.
This genome-wide association study of severe diabetic retinopathy suggests new evidence for the involvement of the NOX4 gene.
These results suggest the specific involvement of Nox4 and Nox2 subunits as physiologically relevant endothelial sources of H2O2 generation that contribute to the endothelium-dependent vasodilatation of renal arteries and therefore have a protective role in kidney vasculature.
NOX4 is induced in early alcoholic liver injury and regulates CCR2/CCL2 mRNA stability thereby promoting recruitment of inflammatory cells and production of proinflammatory cytokines.
Study reveals the novel function of NOX4 in reprogramming aerobic glycolysis initiated by activated Kras and inactivated p16 in pancreatic ductal adenocarcinoma (PDAC), indicating its potential as a therapeutic target for PDAC and other cancers.
In beta-actin null cells, we show evidence that the enhanced TGF-b signaling relies on the active utilization of latent TGF-b1 in the cell culture medium. TGF-b signaling activation contributes to the elevated reactive oxygen species production, which is likely mediated by the upregulation of Nox4.
In conclusion, using unique in vivo models and ex vivo techniques we provide evidence that Nox4-derived ROS contribute to podocyte injury via, at least in part, podocyte TRPC6 channels. Furthermore, Nox4 produces the majority of AngII-elicited H2O2 in the glomerulus and its absence attenuates the podocytic calcium signaling dysfunction that occurs in diabetes.
NOX4 deletion is partially protective against EtOH effects on osteoblast differentiation, but may predispose bone to osteogenic impairments
The downregulation of miRNA30e induced the protein expression of Snai1, transforming growth factor (TGF)beta and mothers against decapentaplegic homolog 2 (Smad2) and suppressed that of NADPH oxidase 4 (Nox4) in vitro.
Cardiomyocyte as well as endothelial cell Nox4 contributes to protection against chronic hemodynamic overloadinduced cardiac remodelling, at least in part through common effects on myocardial capillary density.
The up-regulated levels of Hsp47 were observed in both the cochlea and heart of NOX4-TG mice.
We evidenced the pathological relevance of NOX4 overexpression in the progression of the aortic aneurysm in a murine Marfan model.
TGF-beta1 induced collagen production via NOX4 activation and reactive oxygen species generation in LmcMF cells.
The results of this study implicate a functional role for NOX4 in traumatic brain injury induced oxidative damage and neurodegeneration
Data indicate the reactive oxygen species (ROS)-generating NADPH oxidase-4 (Nox4) as an essential regulator of exercise performance in mice.
Nox4 is expressed in primary cultured neural stem/precursor cells (NS/PCs) and in those of the adult mouse brain. Nox inhibitors VAS 2870 and GKT137831 or Nox4 deletion attenuated bFGF-induced proliferation of cultured NS/PCs, while lentivirus-mediated Nox4 overexpression increased the production of H2O2, the phosphorylation of Akt, and the proliferation of cultured NS/PCs.
The Nox4-dependent ROS production was involved in CVB3-induced myocardial apoptosis.
Results provide evidence that Nox4-mediated reactive oxygen species generation plays a central role in MIF production and resistance to Toxoplasma gondii infection.
TRPC1 deficiency potentiates Reactive Oxygen Species generation via Nox4-containing NADPH oxidase, which exacerbates cerebral Ischemia/Reperfusion injury.
Data suggest that Nox4 aggravates cisplatin-induced nephrotoxicity (acute kidney injury) by promoting ROS-mediated programmed cell death (oxidative stress and apoptosis) and by promoting inflammation in mouse kidney, mouse/human renal tubular cells, and transformed human kidney cell line. (ROS = reactive oxygen species)
Gene analysis indicated that soluble epoxide hydrolase 2 (sEH) was significantly upregulated in Nox4DN endothelial cells (EC). Inhibition of sEH activity in Nox4DN EC suppressed inflammation and macrophage adhesion to EC.
Our study provides strong evidence that Egr1 is a transcriptional activator of NOX4 in oxidative stress of DKD. Egr1 contributes to diabetic kidney disease by enhancing EMT, in part by targeting NOX4.
High glucose induced histone H3K27 acetylation enrichment at the promoters of Nox1/4/5 genes in SMCs. The novel data of this study indicate that HDACs mediate vascular Nox up-regulation in diabetes. HDAC inhibition reduces vascular ROS production in experimental diabetes, possibly by a mechanism involving negative regulation of Nox expression.
Identify Nox4 as a key source of radical oxygen species involved in development of hypertension and the metabolic syndrome.
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.
MRTF down-regulation/inhibition suppresses TGFbeta/contact disruption-provoked Nox4 protein and mRNA expression, Nox4 promoter activation, and reactive oxygen species production.
Nox4 NADPH oxidase mediates oxidative stress and apoptosis caused by TNF-alpha in cerebral vascular endothelial cells.
Nox4 NADPH oxidase-derived reactive oxygen species also initiate a cell survival mechanism by increasing production of carbon monoxide by constitutive heme oxygenase-2.
proteasome inhibition completely prevented endoplasmic reticulum stress-induced increase in NADPH oxidase activity, as well as increases in Nox4 isoform and protein disulfide isomerase mRNA expression
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.
, kidney superoxide-producing NADPH oxidase
, renal NAD(P)H-oxidase
, superoxide-generating NADPH oxidase 4
, NADPH oxidase 4
, predicted NADPH oxidase-4