Aliases for NOS3 Gene
External Ids for NOS3 Gene
Nitric oxide is a reactive free radical which acts as a biologic mediator in several processes, including neurotransmission and antimicrobial and antitumoral activities. Nitric oxide is synthesized from L-arginine by nitric oxide synthases. Variations in this gene are associated with susceptibility to coronary spasm. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, May 2009]
GeneCards Summary for NOS3 Gene
NOS3 (Nitric Oxide Synthase 3 (Endothelial Cell)) is a Protein Coding gene. Diseases associated with NOS3 include acute chest syndrome and stroke, ischemic. Among its related pathways are PI3K-Akt signaling pathway and Disease. GO annotations related to this gene include calmodulin binding and heme binding. An important paralog of this gene is NOS1.
UniProtKB/Swiss-Prot for NOS3 Gene
Produces nitric oxide (NO) which is implicated in vascular smooth muscle relaxation through a cGMP-mediated signal transduction pathway. NO mediates vascular endothelial growth factor (VEGF)-induced angiogenesis in coronary vessels and promotes blood clotting through the activation of platelets
Isoform eNOS13C: Lacks eNOS activity, dominant-negative form that may down-regulate eNOS activity by forming heterodimers with isoform 1
Endothelial nitric oxide synthase (eNOS), along with inducible nitric oxide synthase (iNOS) and neuronal nitric oxide synthase (nNOS), catalyze the generation of nitric oxide and L-citrulline from L-arginine and molecular oxygen. It is activated at concentrations of calcium greater than 100 nM and requires tetrahydrobiopterin, flavin adenine dinucleotide, flavin mononucleotide and NADPH for catalytic activity. eNOS is tightly regulated by co- and post-translational lipid modifications, phosphorylation by Akt/PKB, PKA and AMPK and protein-protein interactions. Negative protein-protein interactions are mediated by Hsp90 and Cav-1 in the Golgi and by NOSIP and NOSTRIN at the plasma membrane, whilst dynamin, porin and soluble guanylyl cyclase are positive regulators of eNOS activity. eNOS is a critical mediator of cardiovascular homeostasis through regulation of the diameter of blood vessels and maintenance of an antiproliferative and antiapoptotic environment in the vasculature. The human gene encoding eNOS is localized to chromosome 7q36.