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N2783

Sigma-Aldrich

Nitric Oxide Synthase, Inducible from mouse

recombinant, expressed in E. coli, buffered aqueous solution

Synonym(s):

Inducible Nitric Oxide Synthase, NOS II, iNOS, macNOS

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About This Item

Enzyme Commission number:
MDL number:
UNSPSC Code:
12352303
NACRES:
NA.32

recombinant

expressed in E. coli

Quality Level

form

buffered aqueous solution

specific activity

≥4.0 units/mg protein

mol wt

130 kDa (homodimer)
130 kDa (subunit, homodimer)

UniProt accession no.

shipped in

dry ice

storage temp.

−70°C

Gene Information

mouse ... Nos2(18126)

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General description

Inducible nitric oxide synthase (iNOS), also known as inflammatory nitric oxide synthase, is a calcium independent isoenzyme, involved in synthesis of nitric oxide (NO). It is a soluble enzyme encoded by the gene mapped to mouse chromosome 11. iNOS is active in dimeric form and its activity is induced by cytokines and various other stimuli. iNOS is expressed in various inflammatory conditions.

Application

Nitric Oxide Synthase, Inducible from mouse has been used in immunohistochemical studies. It is also used to evaluate the therapeutic efficacy of inducible nitric oxide synthase (NOS) on reperfusion-induced microcirculatory alterations and hemodynamic adverse effects in the microvasculature of skeletal muscle.

Biochem/physiol Actions

Tumor-derived inducible nitric oxide synthase (iNOS) plays a vital role in stimulating tumor growth and vessel maturation. Therefore, it is considered to be a potential therapeutic target for anti-vascular cancer therapies. Unchecked activity of iNOS leads to overproduction of nitric oxide (NO), which is toxic for living cells. iNOS activity can be controlled at both transcription and translational level by regulating protein stability, dimerization, phosphorylation, cofactor binding and availability of oxygen and L-arginine as substrates. iNOS plays a vital role in excisional wound repair and exhibits gene therapy strategy to advance wound healing process in iNOS-deficient conditions such as diabetes and steroid treatment.
NOS is responsible for the biosynthesis of nitric oxide from L-arginine. iNOS is not calcium/calmodulin dependent and has a Km = 16 μM for L-arginine.

Unit Definition

One unit will produce 1.0 μmol of nitric oxide per minute at 37 °C in 50 mM HEPES, pH 7.4, containing 1 mM arginine, 1 mM magnesium acetate, 0.15 mM NADPH, 4.5 μM oxyhemoglobin, 18 μM tetrahydrobiopterin and 180 μM DTT.

Physical form

Solution in 50 mM HEPES, pH 7.4, with 10% glycerol, 8 μM tetrahydrobiopterin

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

常规特殊物品

Certificates of Analysis (COA)

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Mapping of the gene for inducible nitric oxide (NO) synthase of mouse macrophages to chromosome 11, close to Evi-2, nu, and Idd-4.
Jenkins NA
Genomics, 19(2), 402-404 (1994)
Investigating the role of tumour cell derived iNOS on tumour growth and vasculature in vivo using a tetracycline regulated expression system.
Papaevangelou E
International Journal of Cancer. Journal International Du Cancer, 138(11), 2678-2687 (2016)
P A Marsden et al.
FEBS letters, 307(3), 287-293 (1992-08-03)
The constitutive calcium/calmodulin-dependent nitric oxide (NO) synthase expressed in vascular endothelium shares common biochemical and pharmacologic properties with neuronal NO synthase. However, recent cloning and molecular characterization of NO synthase from bovine endothelial cells indicated the existence of a family
H Luss et al.
Journal of molecular and cellular cardiology, 29(4), 1153-1165 (1997-04-01)
There is evidence that nitric oxide (NO) may mediate some of the functional myocardial changes caused by bacterial LPS and inflammatory cytokines. The expression of the inflammatory or inducible NO synthase (iNOS) in human cardiac myocytes, however, has not been
Enhancing Nitric Oxide Bioavailability via Exogen Nitric Oxide Synthase and L-Arginine Attenuates Ischemia-Reperfusion-Induced Microcirculatory Alterations.
Engel H
Annals of Plastic Surgery (2014)

Articles

Cellular oxidative stress is countered by enzymatic scavengers and antioxidant modulators against reactive oxygen species damage.

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