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Validated All-in-One™ qPCR Primer for NOX4(NM_016931.4) Search again
Product ID:
HQP012143
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
KOX, KOX-1, RENOX
Gene Description:
NADPH oxidase 4
Target Gene Accession:
NM_016931.4(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
This gene encodes a member of the NOX-family of enzymes that functions as the catalytic subunit the NADPH oxidase complex.
Gene References into function
- Nox4 is expressed in aortic media and either not at all or rarely in unaffected intima, while mRNA expression in cells is greatest in fibrofatty lesions.
- Nox4 co-localizes with vinculin in focal adhesions in vascular smooth muscle cells. Its role may be correlated with its
- Data suggest that Nox4 provides a novel link between the insulin receptor and the generation of cellular reactive oxygen species that enhances insulin signal transduction.
- 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.
- NOX4 has a role in inhibiting apoptosis with reactive oxygen species in pancreatic cancer cells
- A nox4-based oxidase appears proportionately more important in mammary arteries than in saphenous veins.
- p22phox directly interacts with Nox1 and Nox4, to form an superoxide-generating NADPH oxidase.
- Direct interaction of NADPH oxidase 4 with toll-like receptor 4 is involved in lipopolysaccharide-mediated generation of reactive oxygen species and NF-kappa B activation in HEK293T cells.
- NOX4 mediates 7-ketocholesterol-induced endoplasmic reticulum stress and apoptosis in aortic smooth muscle cells.
- Urotensin-II is a potent activator of reactive oxygen species generation by NADPH oxidase in pulmonary artery smooth muscle cells
- mRNA expression and localization of NOX4 in human umbilical vein endothelial cells.
- Nox4 exists as several isoforms that may have different functions in ROS-related cell signaling
- NOX2 and NOX4 have roles as redox messengers in the activation of intracellular signaling pathways leading (or contributing) to mitochondriogenesis, cell survival, and differentiation in hematopoietic stem cells
- The Nox4 associates with the protein p22phox on internal membranes, where ROS generation occurs.
- Downregulation of Nox4, which results in the reduction of ROS generation, is reported in the skin fibroblasts of patients wtih leprechaunism.
- Thus Nox4 appears to produce superoxide in the nucleus of HUVECs, thereby regulating gene expression via a mechanism for oxidative stress response.
- reactive oxygen species generated by Nox4, at least in part, transmit cell survival signals through the AKT-ASK1 pathway in pancreatic cancer cells and their depletion leads to apoptosis.
- We suggest that Nox4 may be involved in increased superoxide generation in vascular smooth muscle cells under proinflammatory conditions.
- The results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22(phox) expression, may be a novel and highly selective treatment for leukemia.
- In endothelial cells, NOX2 and NOX4, but not NOX1, equally contributed to ROS generation and proliferation under basal conditions, indicating that a complex relation between NOX homologues controls endothelial function.
- VHL protein exerts its tumor suppressor action, at least partially, via inhibition of p22phox-based Nox4/Nox1 NADPH oxidase-dependent reactive oxygen species generation
- Nox4 influences the pathobiochemistry of asthma by generating reactive oxygen species that promote TGF-beta1-induced proliferation and hypertrophy of human airway smooth muscle
- Reactive oxygen species production evolves in parallel with the catalytic activity of NOX and is suppressed by siNOX 4 (small interference oligonucleotide RNA directed against NOX 4) silencing.
- Upregulation of eNOS and a parallel downregulation of Nox4 lead to an increase in bioactive nitric oxide, which in turn could mediate some of the beneficial effects of danshen
- The close correlation between NOX4 mRNA and reactive oxygen species generation might hint towards a function as an inducible NOX isoform.
- Data suggest that decreased NOX4 mRNA content is a hallmark of adipocyte differentiation and that NOX4 expression measured in whole adipose tissue is not an unequivocal indicator of intact or impaired insulin action.
- In lungs from patients with idiopathic pulmonary arterial hypertension, NOX4 expression in the tunica media was 2.5-fold upregulated, supporting an important role for NOX4 in the vascular remodeling associated with pulmonary hypertension.
- Nox4 type NADPH oxidase promotes endothelial angiogenic responses in human microvascular endothelial cells in vitro.
- study shows HIV-1 Tat signaling, leading to concurrent but separate Nox4-dependent Ras/ERK activation, and Nox2-dependent JNK activation; Tat signaling, therefore, provides an example of Nox-specific differential control of MAP kinase pathways
- A novel signaling pathway, in which NADPH oxidase activation results in inhibition of protein tyrosine phosphatases, leading to enhanced and sustained phosphorylation of kinases (JAK2), and suppression of apoptosis is suggested in pancreatic neoplasms.
- Nox2 and Nox4-generated ROS modulate glucose uptake in a leukaemic cell line
- Enhanced expression of Nox4 appears to be involved in cell proliferation and survival in glioma cells.
- Nox4, a subtype of nonphagocytic NADPH oxidase, was found to play a key role in intracellular ROS generation and exogenous H(2)O(2)-induced MUC5AC gene expression in NHNE cells
- These data indicate that the specificity of intracellular reactive oxygen species-mediated signal transduction may be modulated by the localization of Nox isoforms within specific subcellular compartments.
- In hypoxia, NOX4 was significantly upregulated at mRNA & protein levels. A significant increase of NOX4 mRNA expression was seen under hypoxic conditions in pulmonary artery adventitial fibroblasts from idiopathic pulmonary arterial hypertension patients
- Upregulation of NOX4 by TGF-beta is required for its pro-apoptotic activity in hepatocytes
- analysis of distinct features of the Nox4-p22 phox complex
- Nox4 acts as a switch between differentiation and proliferation in preadipocytes.