Any feedback?
Please rate this page
(all_enzymes.php)
(0/150)

BRENDA support

1.14.13.39: nitric-oxide synthase (NADPH)

This is an abbreviated version!
For detailed information about nitric-oxide synthase (NADPH), go to the full flat file.

Word Map on EC 1.14.13.39

Reaction

2 L-arginine + 2 NADPH + 2 H+ + 2 O2 = 2 Nomega-hydroxy-L-arginine + 2 NADP+ + 2 H2O

Synonyms

bacterial nitric oxide synthase, bacterial nitric-oxide synthase, bNOS, bsNOS, cb-NOS, cytokine inducible NOS, DNOS, e-NOS, EC-NOS, endothelial nitric oxide synthase, endothelial nitric-oxide synthase, endothelial NO synthase, endothelial NOS, endothelium-derived relaxation factor-forming enzyme, endothelium-derived relaxing factor synthase, eNOS, i-NOS, inducible nitric oxide synthase, inducible nitric-oxide synthase, inducible NO synthase, inducible NOS, iNOS, mitochondrial NO synthase, mitochondrial-specific nitric oxide synthase, mtNOS, n-NOS, NADPH diaphorase, NADPH-d, NADPH-diaphorase, NADPHd, neuronal nitric oxide synthase, neuronal nitric-oxide synthase, neuronal NO synthase, neuronal NOS, nicotinamide adenine dinucleotide phosphate-diaphorase, nitric oxid synthase, nitric oxide synthase, nitric oxide synthase-like protein, nitric oxide synthetase, nitric-oxide synthase, nNOS, nNOSalpha, NO synthase, NO synthase type I, NO synthase type II, NO synthase type III, NO-synthase, NOS, NOS I, NOS-2, NOS1, NOS2, NOS3, synthetase, nitric oxide

ECTree

     1 Oxidoreductases
         1.14 Acting on paired donors, with incorporation or reduction of molecular oxygen
             1.14.13 With NADH or NADPH as one donor, and incorporation of one atom of oxygen into the other donor
                1.14.13.39 nitric-oxide synthase (NADPH)

Expression

Expression on EC 1.14.13.39 - nitric-oxide synthase (NADPH)

Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
0.001 mg thyroxin significantly increases nNOS protein level to 178% compared to control
0.01 mM 2-phenyl-ethenesulfonic acid phenyl ester, 2-phenyl-ethenesulfonic acid 4-chlorophenyl ester, and 2-methyl-4-nitro-quinoline 1-oxide inhibit the expression of inducible nitric oxide synthase protein, 4-nitro-quinoline 1-oxide reveals no significant expression-downregulating activity at 0.01 mM
-
0.1 mg 6-n-propyl-2-thyouracil decreases nNOS protein level to 19% compared to control
exposure of primary cortical astrocytes to a low concentration of Mn2+ (0.01 mM) potentiates expression of NOS2 mRNA and protein
expression of both the eNOS protein and gene is significantly reduced in tight-skin 1-mouse skin tissue
expression of eNOS mRNA and protein does not change in mild to moderate chronic obstructive pulmonary disease, but is reduced in the more severe stages of chronic obstructive pulmonary disease
expression of isozyme NOS1 protein is decreased in the cytoplasmic and plasma membrane fractions, although maintained in the intracellular membrane fraction, in response to high salt
expression of isozyme NOS3 protein is unaffected by high salt
expression of neuronal NOS and endothelial NOS is upregulated during the odontoblastic differentiation of dental papilla cells (DPCs)
in Portunus trituberculatus challenged with the Hematodinium parasite, transcripts in hemocytes are significantly induced at 12 and 24 h, followed by significant suppression at 96 and 192 h
in the peripheral lung of chronic obstructive pulmonary disease patients iNOS mRNA expression is increased at earlier stages of the disease but decreases in the most severe patients, pro-inflammatory cytokine-induced iNOS expression is decreased by oxidative stress, such as H2O2, cigarette smoke conditioned media, and the peroxyntrite generator SIN1
investigated the effect of imiquimod (IMQ)-induced psoriatic inflammation on kidney function and inflammation in a murine model. Psoriatic inflammation in mice is associated with kidney dysfunction as reflected by increased serum creatinine and blood urea nitrogen. Kidney dysfunction is paralleled by upregulation of reactive oxygen species (ROS) generating enzymes such as NOX2, NOX4 and iNOS
lung tissue from patients with severe and very severe chronic obstructive pulmonary disease have graded increases in nNOS (mRNA and protein) compared with non-smokers and normal smokers
mitogen-activated protein kinase phosphatase-1 may negatively regulate iNOS expression by controlling the expression of microRNA-155 and consequently the signal transducer and activator of transcription pathway via suppressor of cytokine signaling-1
neither interleukin-1 nor tissue necrosis factor-alpha is capable of inducing nNOS synthesis for up to 48 h treatment, treatment with insulin-like growth factor-1 or transforming growth factor-beta for up to 48 h has no effect on the levels of nNOS
nitric oxide synthase activity and expression are decreased in the paraventricular nucleus of pregnant rats
nitric oxide synthase activity is significantly affected in ipsilateral and contralateral testes cells after vasal and epididymal ligation
nitric oxide synthase activity is significantly affected in ipsilateral and contralateral testes cells after vasal and epididymal ligation, eNOS immunoreactivity increases markedly after ipsilateral vasal ligation
treatment with a selective G protein-coupled ER agonist decreases NADPH-diaphorase expression in the supraoptic and paraventricular nuclei of the hypothalamus. Treatment with the selective G protein-coupled estrogen receptor agonist in combination with an antagonist effectively rescues the decrease in NADPH-diaphorase expression in both brain regions
-
treatment with insulin-like growth factor-1 or transforming growth factor-beta for up to 48 h has no effect on the levels of iNOS
treatment with interleukin-1 or tissue necrosis factor-alpha for 16 h significantly increases iNOS levels to 429.4% of the control
up-regulation of the inflammatory gene encoding for iNOS is observed in a population of amoeboid microglial cells from Parkinson's disease patients, iNOS up-regulation in microglia seems to play an important role in the onset of inflammatory processes in Parkinsons's disease and acts synergistically with other inflammatory mediators, Parkinsons's disease-inducing drugs such as rotenone and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine or dopamine overexposure provoke activation of iNOS expression
urothelial and endothelial i-NOS expression are significantly increased in neuromodulated rats
urothelial n-NOS expression is significantly increased in neuromodulated rats