Polyclonal Anti-NOS3

Rabbit IgG polyclonal antibody for Nitric oxide synthase, endothelial (NOS3) detection. Tested with WB, IHC-P in Human;Mouse;Rat. \n

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SPECIFICATIONS

Price

200.00 USD

Catalog Number

PA1712

Size

100ug/vial

Applications

IHC, WB

Reactivities

Hum, Mouse, Rat

Form

Lyophilized

Format

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

Gene Id

NOS3

References

1.Ahsan, A., Norboo, T., Baig, M. A., Pasha, M. A. Q. Simultaneous selection of the wild-type genotypes of the G894T and 4B/4A polymorphisms of NOS3 associate with high-altitude adaptation. Ann. Hum. Genet. 69: 260-267, 2005.\n2.Chen, C.-A., Wang, T.-Y., Varadharaj, S., Reyes, L. A., Hemann, C., Talukder, M. A. H., Chen, Y.-R., Druhan, L. J., Zweier, J. L. S-glutathionylation uncouples eNOS and regulates its cellular and vascular function. Nature 468: 1115-1118, 2010. \n3.Fulton, D., Gratton, J.-P., McCabe, T. J., Fontana, J., Fujio, Y., Walsh, K., Franke, T. F., Papapetropoulos, A., Sessa, W. C. Regulation of endothelium-derived nitric oxide production by the protein kinase Akt. Nature 399: 597-601, 1999.\n

Swiss Prot

P29474

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 at the C-terminal of human NOS3, identical to the related rat and mouse sequences.

Scientific Background

NOS3(Nitric Oxide Synthase 3), also called ENOS, a nitric oxide synthase that generates NO in blood vessels and is involved with regulating vascular tone by inhibiting smooth muscle contraction andplatelet aggregation. The NOS3 gene is mapped on 7q36.1. Variations in this gene are associated with susceptibility to coronary spasm. Fulton et al. (1999) concluded the eNOS is an AKT substrate linking signal transduction by AKT to the release of the gaseous second messenger nitric oxide. AKT mediates the activation of eNOS, leading to increased nitric oxide production. Inhibition of the PI3K AKT pathway or mutation of the AKT site on eNOS protein at serine-1177 attenuated the serine phosphorylation and prevented the activation of eNOS. RT-PCR analysis showed that expression of NOS3 in human umbilical vein endothelial cells (HUVECs) and human aortic vascular smooth muscle cells (HAOVSMCs) was inversely proportional to that of NOS3AS.