eNOS

Produces nitric oxide (NO) which is implicated in vascular smooth muscle relaxation through a cGMP-mediated signal transduction pathway (PubMed:1378832). 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.

Variation Asp-298 in NOS3 may be associated with susceptibility to coronary spasm.

Phosphorylation by AMPK at Ser-1177 in the presence of Ca(2+)-calmodulin (CaM) activates activity. In absence of Ca(2+)-calmodulin, AMPK also phosphorylates Thr-495, resulting in inhibition of activity (By similarity). Phosphorylation of Ser-114 by CDK5 reduces activity.

Belongs to the NOS family.

Platelets, placenta, liver and kidney.

• Cell membrane
• Membrane
• Caveola
• Cytoplasm
• Cytoskeleton
• Golgi apparatus
• Specifically associates with actin cytoskeleton in the G2 phase of the cell cycle; which is favored by interaction with NOSIP and results in a reduced enzymatic activity.

Nitric oxide synthase 3, Constitutive NOS, EC-NOS, NOS type III, cNOS, NOSIII, Endothelial NOS, eNOS, NOS3

• entrezGene:4846
• omim:163729
• swissprot:P29474

Proteins

Oncology

• Cardiovascular
• Immuno-oncology

133275Da