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Oxygenases nitric oxide synthases

In the rat retina, ischemia upregulates expression of the neuronal nitric oxide synthase and cyclo-oxygenase-2 these effects can be effectively inhibited by lutein (Choi et al., 2006). [Pg.335]

Enzymes Nitric Oxide Synthase and Heme Oxygenase... [Pg.652]

Enzymes Nitric Oxide Synthase and Heme Oxygenase Thomas L. Poulos, Huiying Li,... [Pg.476]

E. D., Stuehr, D. J.,Tainer, J. A., The structure of nitric oxide synthase oxygenase domain and inhibitor complexes, Science 278 (1997),... [Pg.275]

STRUCTURES OF GAS-GENERATING HEME ENZYMES NITRIC OXIDE SYNTHASE AND HEME OXYGENASE... [Pg.243]

Fig. 3. Mechanisms of vasocontraction and vasorelaxation in endothelial and smooth muscle cells. COX cyclooxygenase, eNOS endothelial nitric oxide synthase, HO-1 heme oxygenase-1, EET epoxyeicosatrienoic acid, EDHF endothelium-derived hyperpolariz-ing factor, PGI2 prostaglandin I2, NO nitric oxide, CO carbon monoxide, PLC phospholipase C, IP3 inositol 1,4,5-trisphosphate, DAG diacylglycerol, ER/SR endo-plasmic/sarcoplasmic reticulum, AC adenylyl cyclase, cAMP cyclic adenosine monophosphate, sGC soluble guanylyl cyclase, cGMP cyclic guanosine monophosphate. Fig. 3. Mechanisms of vasocontraction and vasorelaxation in endothelial and smooth muscle cells. COX cyclooxygenase, eNOS endothelial nitric oxide synthase, HO-1 heme oxygenase-1, EET epoxyeicosatrienoic acid, EDHF endothelium-derived hyperpolariz-ing factor, PGI2 prostaglandin I2, NO nitric oxide, CO carbon monoxide, PLC phospholipase C, IP3 inositol 1,4,5-trisphosphate, DAG diacylglycerol, ER/SR endo-plasmic/sarcoplasmic reticulum, AC adenylyl cyclase, cAMP cyclic adenosine monophosphate, sGC soluble guanylyl cyclase, cGMP cyclic guanosine monophosphate.
Hara E., Takahashi K., Tominaga T., Kumabe T., Kayama T., Suzuki H., Fujita H., Yoshi-moto T., Shirato K., and Shibahara S. (1996). Expression of heme oxygenase and inducible nitric oxide synthase mRNA in human brain tumors. Biochem. Biophys. Res. Commun. 224 153-158. [Pg.232]

In 1989, BH4 was found to be a cofactor for nitric oxide synthase (NOS) [ 126, 127]. BH4 is also involved in dimerization of NOS, as NOS is catalytically active in a homodimer structure. Three isoforms of NOS exist neuronal NOS (NOS 1), inducible NOS (NOS 2) and endothelial NOS (NOS 3). BH4 is essential for all NOS isoforms. The NOS isoforms share approximately 50-60% sequence homology. Each NOS polypeptide is comprised of oxygenase and reductase domains. An N-terminal oxygenase domain contains iron protoporphyrin IX (heme), BH4 and an arginine binding site, and a C-terminal reductase domain contains flavin mononucleotide (FMN), and a reduced nicotin-amide adenine dinucleotide phosphate (NADPH) binding site. [Pg.160]

Crane, B.R, Arvai, A.S., Ghosh, D.K., Wu, C., Getzoff, E.D., Stuehr, D.J., and Tainer, J.A. (1998) Structure of nitric oxide synthase oxygenase dimer with pterin and substrate, Science 279, 2121-2126. [Pg.195]

Baranano, David E. Snyder, Solomon H. Neural roles for heme oxygenase Contrasts to nitric oxide synthase. PNAS, No. 20 10996-11002 2001. [Pg.81]

At the same time there are differences between CO and NO. For example, NO is an unstable gas and radical while CO is a stable gas and not a radical. CO binds only ferrous heme but NO binds to both ferrous and ferric hemoprotein (Hartsfield, 2002). The combination rate of NO with hemoglobin is faster and dissociation slower than that of CO (Sharma and Ranney, 1978) so that the affinity of NO for hemoglobin is 1,500 times that of CO (Foresti and Motterlini, 1999). Formation of endogenous CO in a variety of tissues has been demonstrated (Marks et al, 2002). Given the complexity of colocalization and activities of heme oxygenase and nitric oxide synthase, it has been speculated that CO and NO could function in a synergistic, compensatory, and/or counterregulatory way (Hartsfield, 2002). [Pg.282]

Increased synthesis of Metallothionein, inducible nitric oxide synthase, heme oxygenase, manganese superoxide dismutase, and tissue inhibitor of metalloproteinase-1... [Pg.103]

Rensing H, Jaeschke H, Bauer 1, Patau C, Datene V, Pannen BH and Bauer M, Differential activation pattern of redox-sensitive transcription factors and stress-inducible dilator systems heme oxygenase-1 and inducible nitric oxide synthase in hemorrhagic and endotoxic shock. Cril Care Med 29(10) 1962-71,2001. [Pg.128]

Motterlini, R., Foresti, R., Bassi, R., Calabrese, V., Clark, J. E. and Green, C. J. Endothelial heme oxygenase-1 induction by hypoxia modulation by inducible nitric oxide synthase and S-nitrosothiols. Journal of Biological Chemistry 27S 13613-13620 2000. [Pg.352]


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See also in sourсe #XX -- [ Pg.1069 , Pg.1070 , Pg.1071 ]




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