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anti-Human NOX1 Antibodies:
anti-Rat (Rattus) NOX1 Antibodies:
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Human Polyclonal NOX1 Primary Antibody for ICC, IF - ABIN441545
Balasubramaniyan, Wright, Sharma, Davies, Sharifi, Habtesion, Mookerjee, Jalan: Ammonia reduction with ornithine phenylacetate restores brain eNOS activity via the DDAH-ADMA pathway in bile duct-ligated cirrhotic rats. in American journal of physiology. Gastrointestinal and liver physiology 2011
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Human Polyclonal NOX1 Primary Antibody for IHC (p), WB - ABIN3044132
Wang, Wang, Liu, Wang, Zhao, Wang, Yin: Cordyceps sinensis polysaccharide inhibits PDGF-BB-induced inflammation and ROS production in human mesangial cells. in Carbohydrate polymers 2015
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Mouse (Murine) Polyclonal NOX1 Primary Antibody for IHC (p), WB - ABIN3044251
Gu, Gong, Zhang, Dong, Zhao, Burczynski, Wang, Sun, Zhu, Han, Wang, Li: Regulation of transforming growth factor beta 1 gene expression by dihydropteridine reductase in kidney 293T cells. in Biochemistry and cell biology = Biochimie et biologie cellulaire 2013
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Human Polyclonal NOX1 Primary Antibody for WB - ABIN4893182
Quintela, Jiménez, Gómez-Guzmán, Zarzuelo, Galindo, Sánchez, Vargas, Cogolludo, Tamargo, Pérez-Vizcaíno, Duarte: Activation of peroxisome proliferator-activated receptor-β/-δ (PPARβ/δ) prevents endothelial dysfunction in type 1 diabetic rats. in Free radical biology & medicine 2012
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Cow (Bovine) Polyclonal NOX1 Primary Antibody for WB - ABIN2782754
Kuwano, Kawahara, Yamamoto, Teshima-Kondo, Tominaga, Masuda, Kishi, Morita, Rokutan: Interferon-gamma activates transcription of NADPH oxidase 1 gene and upregulates production of superoxide anion by human large intestinal epithelial cells. in American journal of physiology. Cell physiology 2006
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Human Polyclonal NOX1 Primary Antibody for IF (p), IHC (p) - ABIN702580
Kashiwabara, Ambe, Nakagawa, Watanabe: Immunohistochemical localization of Nox in mouse circumvallate papillae. in Tissue & cell 2015
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Human Polyclonal NOX1 Primary Antibody for ICC, IF - ABIN4335324
Fan, Hsiung, Cheng, Tzanakakis: Facile engineering of xeno-free microcarriers for the scalable cultivation of human pluripotent stem cells in stirred suspension. in Tissue engineering. Part A 2014
this study shows that NOX1 loss-of-function genetic variants in patients with inflammatory bowel disease
depletion of NOX1 and NOX4 partially rescued the growth inhibition of PARP1-deficient tumor xenografts. Our findings suggest that in addition to compromising the repair of DNA damage, PARP inhibition or depletion may exert extra antitumor effect by elevating oxidative stress in ovarian cancer cells
NOX activation might have a role in regulation of lymphocytic activity in patients with idiopathic nephrotic syndrome through the impairment of PDGF mitogenic function and might contribute toward pathogenesis of nephrotic syndrome.
The SUMO1/UBC9 axis may regulate Nox1mediated diabetic retinopathy by inhibiting reactive oxygen species generation and apoptosis.
Results show that the thrombospondin 1 (TSP1) and its receptor CD47 (CD47) axis selectively regulates NADPH oxidase 1 (Nox1) in the regulation of endothelial senescence and suggest potential targets for controlling the aging process at the molecular level.
in CAD, both mitochondria and NADPH oxidase contribute to flow-induced vasodilation through a redox mechanism in visceral arterioles.
NADPH oxidase-mediated redox signaling is important in the detrimental effect of C-reactive protein on pancreatic insulin secretion.
S340E mutation enhances Nox1 activation (Kaito et al., 2014), the present study suggests that betaPix can also play an inhibitory role in O2(-) production, depending on the sites of phosphorylation.
the anti-proliferative and pro-apoptotic effect of cambogin on breast adenocarcinoma is mediated via inducing NOX1-dependent ROS production and the dissociation of ASK1 and Trx1
Transcriptional regulation of NOX genes expression in human breast adenocarcinoma cells is modulated by adaptor protein CIN85.
the transition-state substrate analogue inhibitor of Prdx6 phospholipase A2 activity (MJ-33) was shown to suppress Nox1 activity, suggesting Nox1 activity is regulated by the phospholipase activity of Prdx6. Finally, wild type Prdx6, but not lipase or peroxidase mutant forms, supports Nox1-mediated cell migration in the HCT-116 colon epithelial cell model of wound closure
Cells redox environment mediated by NOX1 isozymes activation down-regulates BRCA1 expression and promotes DNA homologous recombination repair in cancer.
LRRC8A channels support TNFalpha-induced superoxide production by Nox1 which is required for receptor endocytosis.
These results are consistent with the hypothesis that antioxidants or NOX1/4 inhibition may be useful in blocking profibrotic effects of TGFbeta on dermal and gingival fibroblasts and warrant consideration for further development as potential antifibrotic agents
We demonstrated that rapid deletion of p22phox is possible and that the activity of Nox1 and Nox4 but not Nox5 exclusively depends on p22phox.
PAK4 downregulation decreased PPARgamma-mediated Nox1 expression and suppressed EMT in IR-treated glioma cells.
Nox1-SHH-Grem1 signaling axis in pulmonary vascular endothelium that is likely to contribute to Pulmonary hypertension.
5-HT1B receptor-dependent cellular Src-related kinase-Nox1-pathways contribute to vascular remodeling in pulmonary arterial hypertension.
NOX1 has a role in maintaining the proliferative phenotype of some colon cancers and has potential as a therapeutic target in this disease
NOX1 mRNA was undetectable in the gastric mucosa.
these data show a role for NOX1-produced reactive oxygen species in maintaining homeostasis of the gut microbiota
Its pathway may promote reactive oxygen species generation in the early stage of Alzheimer's disease and eventually contribute to the exacerbation of pathological phenotype.
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.
these data demonstrate that altered zinc distribution leading to accumulation of zinc in the mitochondria increases mitochondrial ROS production causing NF-kappaB activation which in turn upregulates Nox1 expression inducing senescence of vascular smooth muscle cells
our data identify EBP50 as a previously unidentified regulator of Nox1 and support that it promotes Nox1 activity by binding p47(phox) This interaction is pivotal for agonist-induced smooth muscle ROS, hypertrophy, and vasoconstriction and has implications for ROS-mediated physiological and pathophysiological processes.
We examined the pattern of NOX expression in spinal cords of patients and mouse models of ALS and analyzed the impact of genetic deletion of the NOX1 and 2 isoforms as well as pharmacological NOX inhibition in the SOD1(G93A) ALS mouse model.In contrast to previous publications, survival of SOD1(G93A) mice was not modified upon breeding with constitutive NOX1 and NOX2 deficient mice.
NOX-derived superoxide intesifies diabetogenic antiviral macrophage responses and protect from virus-induced diabetes
Both Nox1 and Duox2 induce exfoliation of crypt epithelium, but only Nox1 induces apoptosis. NOX1 and DUOX2 may be potential therapeutic targets for treating ileocolitis in human patients suffering inflammatory bowel disease (IBD).
we used the Ang II infused hph-1 mice to examine the roles of NOX isoforms in the development of AAA. We generated double mutants of hph-1-NOX1, hph-1-NOX2, hph-1-p47phox, and hph-1-NOX4
C-kit-positive hematopoietic stem/progenitor cells expressed significantly higher of Nox1 and catalase, but less of lactoperoxidase than in matured mononuclear cells.
Nox1 deletion reduces oxidant load and restores microvascular health in obese mice.
Data suggests that ROS produced during primitive endoderm differentiation is dependent in part on increased NOX1 and NOX4 levels, which is under the control of GATA6. Furthermore, these results suggest that the combined activity of multiple NOX proteins is necessary for the differentiation of F9 cells to primitive endoderm.
Gp91phox NADPH oxidase modulates litter size by up-regulating mucin1 expression in the uterus of mice.
NOX4- and NOX1-derived ROS contribute to atherosclerosis in the aortic sinus of diabetic ApoE knockout mice.
Data show that pan-NOX-inhibitor APX-115 treatment decreased NADPH oxidase (Nox) Nox1, Nox2, and Nox4 protein expression in the kidney.
NOX1 is selectively important in GPCR-dependent intracellular ROS generation but dispensable for GPVI-ITAM-dependent ROS generation in blood platelets..
Plasmid driven elevation of NOX-1 resulted in elevated ROSreactive oxygen species, loss of glucose-stimulated-insulin-secretion and increased apoptosis. These outcomes on beta cell function are analogous to cytokine treatment.
Nox1-knockout (Nox1-KO) mice were not more sensitive to S. Tm colonization and infection than WT B6 mice.
NADPH oxidase plays an important role in proMMP-2 expression and activation and MMP-2 mediated SMC proliferation occurs through the involvement of Spm-Cer-S1P signaling axis under ANG II stimulation of PASMCs
Differential Roles of Protein Complexes NOX1-NOXO1 and NOX2-p47phox in Mediating Endothelial Redox Responses to Oscillatory and Unidirectional Laminar Shear Stress.
The current study was designed to determine mechanisms underlying 20-hydroxyeicosatetraenoic acid -stimulated nitric oxide (NO) release, and particularly the role of NADPH oxidase, reactive oxygen species, and PI3-kinase in stimulated NO release.
NEP expression is down-regulated in vascular endothelial cells by physiological laminar shear, possibly via a mechanotransduction mechanism involving NADPH oxidase-induced reactive oxygen species production.
The nox1 expression in zebrafish during early nervous system development from 12 to 48 hours post fertilization.
Over inhibition of the NADPH oxidase by the NADPH Inhibitor DPI may reduce the cell even the tissue in the progress of healing after the injury, in zebrafish liver cells.
This gene encodes a member of the NADPH oxidase family of enzymes responsible for the catalytic one-electron transfer of oxygen to generate superoxide or hydrogen peroxide. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
NADH/NADPH mitogenic oxidase subunit P65-MOX
, NADPH oxidase homolog-1
, mitogenic oxidase (pyridine nucleotide-dependent superoxide-generating)
, mitogenic oxidase 1
, NADH/NADPH mitogenic oxidase subunit p65-mox
, GP91 phox homolog
, NADPH oxidase 1 alpha
, NADPH oxidase-1
, predicted NADPH oxidase-1
, NADPH oxidase 1