Polyclonal Anti-NOX1

Rabbit IgG polyclonal antibody for NADPH oxidase 1 (NOX1) detection. Tested with WB, IHC-P in Human. \n\n

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SPECIFICATIONS

Price

200.00 USD

Catalog Number

PA1739

Size

100ug/vial

Applications

IHC, WB

Reactivities

Hum

Form

Lyophilized

Format

Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.

Gene Id

NOX1

References

1. Banfi, B., Maturana, A., Jaconi, S., Arnaudeau, S., Laforge, T., Sinha, S., Ligeti, E., Demaurex, N., Krause, K.-H. A mammalian H+ channel generated through alternative splicing of the NADPH oxidase homolog NOH-1. Science 287: 138-141, 2000.\n2. Behrens, M. M., Ali, S. S., Dao, D. N., Lucero, J., Shekhtman, G., Quick, K. L., Dugan, L. L. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science 318: 1645-1647, 2007.\n3. Lachgar A, Sojic N, Arbault S, et al. (1999). \"Amplification of the inflammatory cellular redox state by human immunodeficiency virus type 1-immunosuppressive tat and gp160 proteins.\"\n

Swiss Prot

Q9Y5S8

Storage Temp

At -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquotted and stored frozen at -20 degree C for a longer time.Avoid repeated freezing and thawing.

Additional Info

A synthetic peptide corresponding to a sequence in the middle region of human NOX1.

Scientific 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.