NOX1 Antikörper (Middle Region)

Produktnummer ABIN3031931

Produktdetails anti-NOX1 Antikörper

Target: NOX1 (NADPH Oxidase 1 (NOX1))

Bindungsspezifität: Middle Region

Reaktivität: Ratte, Maus

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser NOX1 Antikörper ist unkonjugiert

Applikation: Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Aufreinigung: Antigen affinity

Immunogen: An amino acid sequence from the middle region of rat NOX1 (WYKFQRAHNKLKTQK) was used as the immunogen for this NOX1 antibody.

Isotyp: IgG

Anwendungsinformationen

Applikationshinweise: 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

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Buffer: 0.5 mg/mL if reconstituted with 0.2 mL sterile DI water

Lagerung: -20 °C

Informationen zur Lagerung: 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.

Details zu NOX1

Target: NOX1 (NADPH Oxidase 1 (NOX1))

Andere Bezeichnung: NOX1 (NOX1 Produkte)

Synonyme: GP91-2 antikoerper, MOX1 antikoerper, NOH-1 antikoerper, NOH1 antikoerper, NOX1a antikoerper, NOX1alpha antikoerper, Nox-1 antikoerper, Nox1 antikoerper, NADPH oxidase 1 antikoerper, NOX1 antikoerper, Nox1 antikoerper, nox1 antikoerper

Hintergrund: 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