NOS3

NOS3
Structures disponibles
PDB	Recherche d'orthologue : PDBe RCSB
Identifiants PDB
	1M9J, 1M9K, 1M9M, 1M9Q, 1M9R, 1NIW, 2LL7, 3EAH, 3NOS, 2MG5, 4D1O, 4D1P
Identifiants
Alias	NOS3, Nitric Oxyde Synthase 3
IDs externes	OMIM: 163729 MGI: 97362 HomoloGene: 504 GeneCards: NOS3
Nomenclature EC	1.14.13.39
Position du gène (humain)
Chr.	Chromosome 7 humain
Fin	151,014,588 bp
Position du gène (souris)
Chr.	Chromosome 5 (souris)
Fin	24,589,472 bp
Expression génique
	Fortement exprimé dans
	rate; ; apex of heart; ; auricule de l'oreillette droite; ; upper lobe of left lung; ; left uterine tube; ; ventricule gauche; ; body of uterus; ; right lobe of thyroid gland; ; artère coronaire gauche; ; artère coronaire droite;
	Fortement exprimé dans
	ventricule droit; ; subcutaneous adipose tissue; ; tunica adventitia of aorta; ; tunica media of zone of aorta; ; tissu adipeux blanc; ; endocardial cushion; ; tissu adipeux brun; ; muscle digastrique; ; septum interventriculaire; ; gastrula;
	Plus de données d'expression de référence
	Plus de données d'expression de référence
Gene Ontology
Fonction moléculaire	FMN binding; actin monomer binding; flavin adenine dinucleotide binding; scaffold protein binding; arginine binding; tetrahydrobiopterin binding; liaison ion métal; fixation de la calmoduline; liaison protéique; heme binding; NADP binding; activité d'oxydoréductase; cadmium ion binding; nitric-oxide synthase activity; NADPH-hemoprotein reductase activity;
Composant cellulaire	cytoplasme; endocytic vesicle membrane; cytosol; appareil de Golgi; membrane; Golgi membrane; membrane plasmique; cavéole; cytosquelette; noyau; membrane d'une vésicule;
Processus biologique	negative regulation of muscle hyperplasia; ovulation from ovarian follicle; positive regulation of guanylate cyclase activity; nitric oxide biosynthetic process; regulation of systemic arterial blood pressure by endothelin; regulation of sodium ion transport; développement des poumons; negative regulation of blood pressure; removal of superoxide radicals; regulation of nitric-oxide synthase activity; mitochondrion organization; response to heat; in utero embryonic development; negative regulation of hydrolase activity; cell redox homeostasis; arginine catabolic process; response to fluid shear stress; regulation of blood pressure; negative regulation of platelet activation; blood vessel remodeling; negative regulation of extrinsic apoptotic signaling pathway via death domain receptors; angiogenèse; negative regulation of potassium ion transport; nitric oxide mediated signal transduction; negative regulation of calcium ion transport; smooth muscle hyperplasia; regulation of the force of heart contraction by chemical signal; endothelial cell migration; lipopolysaccharide-mediated signaling pathway; negative regulation of cell population proliferation; vasodilatation; positive regulation of blood vessel endothelial cell migration; positive regulation of angiogenesis; aortic valve morphogenesis; pulmonary valve morphogenesis; endocardial cushion morphogenesis; positive regulation of gene expression; homeostasis of number of cells within a tissue; ventricular septum morphogenesis; negative regulation of biomineral tissue development; response to hormone; response to lipopolysaccharide; regulation of nervous system process; positive regulation of Notch signaling pathway;
	Sources:Amigo / QuickGO
Orthologues
	4846
	18127
	ENSG00000164867
	ENSMUSG00000028978
	P29474
	P70313
	NM_000603; NM_001160109; NM_001160110; NM_001160111
	NM_008713
	NP_000594; NP_001153581; NP_001153582; NP_001153583
	NP_032739
	Wikidata
Voir/Editer Humain	Voir/Editer Souris

Le NOS3 (pour « Nitric Oxyde Synthase 3 ») est une enzyme de type oxyde nitrique synthase exprimée au niveau de l'endothélium vasculaire. Son gène est NOS3 situé sur le chromosome 7 humain.

Action

Il permet la synthèse du monoxyde d'azote (NO). Son activité est régulé par le calcium et la calmoduline. L'augmentation du taux de NO dans les cellules endothéliales a une activité vasodilatatrice, avec baisse de la pression artérielle.

En médecine

Certains variants du gène augmentent le risque d'hypertension artérielle. D'autres, entraînant une forme plus active de l'enzyme, font baisser la tension artérielle et diminuent le risque de survenue d'une maladie cardiovasculaire.

Notes et références

1 2 3 GRCh38: Ensembl release 89: ENSG00000164867 - Ensembl, May 2017
1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000028978 - Ensembl, May 2017
↑ « Publications PubMed pour l'Homme », sur National Center for Biotechnology Information, U.S. National Library of Medicine
↑ « Publications PubMed pour la Souris », sur National Center for Biotechnology Information, U.S. National Library of Medicine
↑ Förstermann U, Closs EI, Pollock JS, Nakane M, Schwarz P, Gath I, Kleinert H, Nitric oxide synthase isozymes: characterization, purification, molecular cloning, and functions, Hypertension, 1994;23:1121–1131
↑ Salvi E, Kutalik Z, Glorioso N et al. Genomewide association study using a high-density single nucleotide polymorphism array and case-control design identifies a novel essential hypertension susceptibility locus in the promoter region of endothelial NO synthase, Hypertension, 2012;59:248–255
↑ Emdin CA, Khera AV, Klarin D et al. Phenotypic consequences of a genetic predisposition to enhanced nitric oxide signaling, Circulation, 2018;137:222–232

Portail de la biologie cellulaire et moléculaire

Portail de la médecine

[refGRCh38Ensembl-1] 1 2 3 GRCh38: Ensembl release 89: ENSG00000164867 - Ensembl, May 2017

[refGRCm38Ensembl-2] 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000028978 - Ensembl, May 2017

[3] « Publications PubMed pour l'Homme », sur National Center for Biotechnology Information, U.S. National Library of Medicine

[4] « Publications PubMed pour la Souris », sur National Center for Biotechnology Information, U.S. National Library of Medicine

[Förstermann_1994-5] Förstermann U, Closs EI, Pollock JS, Nakane M, Schwarz P, Gath I, Kleinert H, Nitric oxide synthase isozymes: characterization, purification, molecular cloning, and functions, Hypertension, 1994;23:1121–1131

[Salvi_2012-6] Salvi E, Kutalik Z, Glorioso N et al. Genomewide association study using a high-density single nucleotide polymorphism array and case-control design identifies a novel essential hypertension susceptibility locus in the promoter region of endothelial NO synthase, Hypertension, 2012;59:248–255

[Emdin_2018-7] Emdin CA, Khera AV, Klarin D et al. Phenotypic consequences of a genetic predisposition to enhanced nitric oxide signaling, Circulation, 2018;137:222–232