NOS3

1M9J, 1M9K, 1M9M, 1M9Q, 1M9R, 1NIW, 2LL7, 3EAH, 3NOS, 2MG5, 4D1O, 4D1P

NOS3
NOS3
Structures disponibles
PDBRecherche d'orthologue : PDBe RCSB
Identifiants
AliasNOS3, Nitric Oxyde Synthase 3
IDs externesOMIM: 163729 MGI: 97362 HomoloGene: 504 GeneCards: NOS3
Nomenclature EC1.14.13.39
Wikidata
Voir/Editer HumainVoir/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[5]. 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[6]. 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[7].

Notes et références

  1. ↑ a b et c GRCh38: Ensembl release 89: ENSG00000164867 - Ensembl, May 2017
  2. ↑ a b et c 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
  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
  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
  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

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