Nitric Oxide Synthase, Inducible from mouse

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.

NOS is responsible for the biosynthesis of nitric oxide from L-arginine. iNOS is not calcium/calmodulin dependent and has a K_m = 16 μM for L-arginine.

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.

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.

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.

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