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Validated All-in-One™ qPCR Primer for NOX1(NM_007052.4) Search again
Product ID:
HQP007453
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GP91-2, MOX1, NOH-1, NOH-1L, NOH1
Gene Description:
NADPH oxidase 1
Target Gene Accession:
NM_007052.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Voltage-gated proton (hydrogen) channels play an important role in cellular defense against acidic stress. They are unique among ion channels with respect to their extremely high selectivity, marked temperature dependence, and unitary conductance, which is 3 orders of magnitude lower than that of most other ion channels. NOX1 is a homolog of the catalytic subunit of the superoxide-generating NADPH oxidase of phagocytes, gp91phox.
Gene References into function
- Ionomycin-induced neutrophil NADPH oxidase activity is selectively inhibited by the serine protease inhibitor diisopropyl fluorophosphate
- The activity of leukocyte NADPH oxidase: regulation by p47PHOX cysteine and serine residues
- Nox1 partially restores the defective oxidases of gp91phox-deficient PLB-985 leukemia cells and peripheral blood stem cells of X-linked chronic granulomatous disease patients.
- our data strongly implicate Nox1 in redox-mediated signaling related to cellular activation of human keratinocytes at a more advanced stage of transformation.
- NOXO1 and NOXA1 activate Nox1 without the need for agonist activation, and this is mediated in part by binding of the NOXO1 PX domain to membrane lipids.
- Nox1 co-localizes with caveolin in punctate patches on the surface & along the cellular margins of vascular smooth muscle cells. Its role may be correlated with its compartamentalization in specific membrane signaling domains.
- aging-related cell surface NADH oxidase (arNOX) generates superoxide and is inhibited by coenzyme Q
- Cells expressed gp91phox homologs Nox1, Nox2, and Nox4. Keratinocytes expressed Nox distinct from phox isoform of phagocytes. Source of superoxide that may regulate cell proliferation and host defense in skin and oral mucosa.
- NADPH oxidase has a role in Cox-2 inhibition through ROS and GSH/GSSG reduction, and NF-kappaB suppression
- Nox1, in turn, was expressed at only low levels in a small number of patients, but when detected it was present in arteries and veins.
- p22phox directly interacts with Nox1 and Nox4, to form an superoxide-generating NADPH oxidase.
- no appropriate RNA splicing sites were found within Nox1 to account for NOH-1S formation, but repetitive sequence elements bordering the deleted region could promote intramolecular template switching during cDNA synthesis
- human prostate cancer frequently show both increased H(2)O(2) and Nox1
- NADPH oxidase has a role in fibrillar Abeta1-42 peptide-induced neuronal apoptosis
- Two identified isoforms of human Nox1 may be functionally distinct.
- Nuclear factor (NF)-kappaB was predominantly activated in adenoma and adenocarcinoma cells expressing abundant Nox1, suggesting that Nox1 may stimulate NF-kappaB-dependent antiapoptotic pathways in colon tumors.
- At the immunohistochemical level Nox1 expression was significantly increased in syncytiotrophoblast and endothelial cells in placentas from patients with preeclampsia as compared to gestational age-matched controls.
- activation of tie-2 receptors by Ang-1 triggers the production of ROS through activation of NADPH oxidase
- Results support a potential contribution of Nox1 to mucosal host defense and inflammation in the colon.
- Smooth muscle-specific Nox1 overexpression augments the oxidative, pressor, and hypertrophic responses to Angiotensin II supporting the concept that medial Nox1 participates in the development of cardiovascular pathologies.
- These results suggest that the formation of the complex consisting of Nox1, betaPix, and NoxO1 is likely to be a critical step in EGF-induced ROS generation.
- A study evaluating the relationship between phagocytic NADPH oxidase activity and oxidative stress and atherosclerosis in metabolic syndrome patients is presented.
- Chronic granulomatous disease (CGD) is a genetic disease caused by structural mutations in the enzyme NADPH oxidase that results in severe immunodeficiency.
- Inhibition of alphaIIbbeta3 activation by NAD(P)H oxidase inhibitors and superoxide scavengers was independent of NO/cGMP signaling demonstrating a direct role of platelet NAD(P)H oxidase-generated ROS for integrin alphaIIbbeta3 activation.
- Rac1 regulates both oxidases Nox1 and Nox3 through the Nox activators
- Rac1 activation provides a major trigger that acutely activates Nox1-dependent reactive oxygen species generation
- Rac1 directly participates in Nox1 activation via interacting with Noxa1.
- Data show that GM-CSF and TNF-alpha induce phosphorylation of Ser345 on p47phox, a cytosolic component of NADPH oxidase, in human neutrophils.
- This study identifies a role for p40(phox) and PI(3)P in coupling FcgammaR-mediated phagocytosis to activation of the NADPH oxidase.
- there is a signaling link between the mitochondria and Nox1, which is crucial for the sustained accumulation of ROS and cell death in serum withdrawal-induced signaling
- Nox1 expression and activation inhibited TNF-alpha-induced inhibitor of kappaB kinase (IKK), and NF-kappaB while promoting JNK activation and cell death.
- Deletion of GSTT1 gene might be considered as protective factor for hypertension.
- VHL protein exerts its tumor suppressor action, at least partially, via inhibition of p22phox-based Nox4/Nox1 NADPH oxidase-dependent reactive oxygen species generation
- Potential candidate genes in these regions that have been implicated in diabetic nephropathy and/or renal damage in models of hypertension include CYBA (or P22PHOX) (16q24), NOX1 (10q22), and NOX3 (6q25.1-q26).
- Nox1 has a role in inducing resistance against differentiation-induced cell death
- cortactin and actin have roles in hyperoxia-induced activation of NADPH oxidase and ROS generation in human lung endothelial cells
- UVA activates Nox1-based NADPH oxidase to produce ROS that stimulate PGE2 synthesis, and that Nox1 may be an appropriate target for agents designed to block UVA-induced skin injury.
- NADPH oxidase-derived ROS selectively modulate some but not all the effects of VEGF on endothelial cell phenotypes
- PKA-phosphorylated NoxA1 is a new binding partner of 14-3-3 protein; this forms the basis of a novel mechanism regulating the formation of ROS by Nox1 and, potentially, other NoxA1-regulated Nox family members
- Overexpression of the hNOX1 complex increased the steady-state levels of DNA 8-oxo-7,8-dihydroguanine and caused a threefold increase in the HPRT mutation rate in HeLa cells.
- These data indicate that developmental, tissue-restricted transcription factors play a key role in NOX1 regulation in vivo.
- Nox1 activation by arachidonic acid metabolism occurs through 12-lipoxygenase and protein kinase C delta, and controls cell migration by affecting integrin alpha 2 subunit turn-over
- Nox1-based oxidase system may be a potential marker of neoplastic transformation and play an important role in oxygen radical- and inflammation-dependent carcinogenesis in the stomach.
- Nox1 overexpression may function as a reversible signal for cellular proliferation with relevance for a common human tumor.
- Subsequently, ROS generation by PA-LPS releases transforming growth factor-alpha (TGF-alpha), which in turn, leads to up-regulate MUC5AC expression.
- 12-lipoxygenase pathway is upstream of Nox1 activation and controls cell spreading and proliferation, while Nox1 specifically affects cell proliferation.
- nox1, nox2, and p47 have distinct roles in NADPH oxidase activity in human veins.
- The physical interaction of AP-1 with p22(phox) gene promoter facilitates NADPHox regulation.
- the local distribution and organization of The plasma membrane NADPH-oxidase (NOX) in human haematopoietic stem cell (HSC) was characterized via fluorescence scanning near-field optical microscopy approach.
- Rac1-dependent Noxs play a critical role in activating c-Src following hypoxia/reoxygenation injury
- Nox1 mRNA and protein are overexpressed in colon cancer and are strongly correlated with activating mutations in K-Ras.
- Genotypes prevalence in AH patients was as follows: GG 58,8%, GA 32,3%, AA 8,9%, and CC 48,2%, CT 44,9%, TT 6.9%. In the control group: GG 53%, GA 36%, AA 11% and CC 42%, CT 54%, TT 4%.
- data show that calcium influx in HL-60 cells relies on TRPC channels 1,3, and 6, and Orai1 for allowing NADPH oxidase activation
- upregulation of transcription is caused by oncogenic Ras signaling through MEK-ERK-dependent phosphorylation of GATA-6
- c-Src is an important regulator of Nox1 activity
- Exogenous hydrogen sulfide inhibits superoxide formation, NOX-1 expression and Rac1 activity in human vascular smooth muscle cells.
- The activated forms of Rac1 and NOXA1 are essentially involved in Nox1 activation and their interactions might be responsible for regulating the O(2)(-)-producing activity in Caco-2 cells.
- ET1, via ETB1, inhibited NADPH oxidase activity in vascular endothelial cells by suppressing the Pyk2-Rac1-Nox1 pathway
- Data demonstrate that Vibrio vulnificus induces death of Jurkat T-cells via reactive oxygen species-dependent activation of p38 MAPK, and that NADPH oxidase plays a major role in ROS generation in V. vulnificus-exposed cells.
- Nox1 associates with ERp72, which involves its N-terminus encompassing a Ca(2+)-binding site and the first TRX-like motif.