NOX1 anticorps (AA 354-374)

N° du produit ABIN3031932

Détail du produit anti-NOX1 anticorps

Antigène: NOX1 (NADPH Oxidase 1 (NOX1))

Épitope: AA 354-374

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp NOX1 est non-conjugé

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

Purification: Antigen affinity

Immunogène: Amino acids 354-374 (HIRAAGDWTENLIRAFEQQYS-human) were used as the immunogen for this NOX1 antibody.

Isotype: IgG

Information d'application

Indications d'application: 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

Stockage

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

Stock: -20 °C

Stockage commentaire: 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.

Détails sur NOX1

Antigène: NOX1 (NADPH Oxidase 1 (NOX1))

Autre désignation: NOX1 (NOX1 Produits)

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

Sujet: 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. NOX1 is expressed in colon, prostate, uterus, and vascular smooth muscle, but not in peripheral blood leukocytes. The deduced 564-amino acid 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 NIH 3T3 cells increased superoxide generation and cell growth. Cells expressing the protein 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: Q9Y5S8

Pathways: Regulation of Systemic Arterial Blood Pressure by Hormones, Proton Transport