Data sheet
| Size | 100ug/vial |
| Storage | At -20C for one year. After reconstitution, at 4C for one month. |
| Form | lyophilized |
| Ig type | rabbit IgG |
| Immunogen/Antigen | A synthetic peptide corresponding to a sequence in the middle of |
| Reconstitution | 0.2ml of distilled water will yield a concentration of 500μg/ml. |
More info
Background
NOX1(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.The NOX1 gene is mapped to Xq22.1. NOX1 was 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 MOX1 in NIH 3T3 cells increased superoxide generation and cell growth. Cells expressing MOX1 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.
NOX1(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.The NOX1 gene is mapped to Xq22.1. NOX1 was 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 MOX1 in NIH 3T3 cells increased superoxide generation and cell growth. Cells expressing MOX1 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.