NOX1 antibody (Middle Region)
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- Target See all NOX1 Antibodies
- NOX1 (NADPH Oxidase 1 (NOX1))
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Binding Specificity
- Middle Region
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Reactivity
- Rat, Mouse
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Host
- Rabbit
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Clonality
- Polyclonal
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Conjugate
- This NOX1 antibody is un-conjugated
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Application
- Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))
- Purification
- Antigen affinity
- Immunogen
- An amino acid sequence from the middle region of rat NOX1 (WYKFQRAHNKLKTQK) was used as the immunogen for this NOX1 antibody.
- Isotype
- IgG
- Top Product
- Discover our top product NOX1 Primary Antibody
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- Application Notes
- The stated application concentrations are suggested starting amounts. Titration of the NOX1 antibody may be required due to differences in protocols and secondary/substrate sensitivity.\. Western blot: 0.5-1 μg/mL,IHC (Paraffin): 0.5-1 μg/mL
- Restrictions
- For Research Use only
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- Buffer
- 0.5 mg/mL if reconstituted with 0.2 mL sterile DI water
- Storage
- -20 °C
- Storage Comment
- After reconstitution, the NOX1 antibody can be stored for up to one month at 4°C. For long-term, aliquot and store at -20°C. Avoid repeated freezing and thawing.
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- Target
- NOX1 (NADPH Oxidase 1 (NOX1))
- Alternative Name
- NOX1 (NOX1 Products)
- Synonyms
- GP91-2 antibody, MOX1 antibody, NOH-1 antibody, NOH1 antibody, NOX1a antibody, NOX1alpha antibody, Nox-1 antibody, Nox1 antibody, NADPH oxidase 1 antibody, NOX1 antibody, Nox1 antibody, nox1 antibody
- Background
- NADPH OXIDASE 1, also known as NOH1, MOX1 or GP91-2, is an enzyme that in humans is encoded by the NOX1 gene. It is also a homolog of the catalytic subunit of the superoxide-generating NADPH oxidase of phagocytes, gp91phox. It is expressed in colon, prostate, uterus, and vascular smooth muscle, but not in peripheral blood leukocytes. The deduced 564-amino acid NOX1 protein, which is 58 % identical to CYBB, contains 6 membrane-spanning regions, conserved flavin and pyridine nucleotide-binding sites, and histidines possibly involved in heme ligation. Overexpression of NOX1 in NIH3T3 cells increased superoxide generation and cell growth. Cells expressing NOX1 had a transformed appearance, showed anchorage-independent growth, and produced tumors in athymic mice. Disruption of either Nox1 or Nox2 significantly delayed progression of motor neuron disease in these mice. However, 50 % survival rates were enhanced significantly more by Nox2 deletion than Nox1 deletion.
- UniProt
- Q9WV87
- Pathways
- Regulation of Systemic Arterial Blood Pressure by Hormones, Proton Transport
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