eNOS

Function

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.

Involvement in disease

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

Post-translational modifications

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.

Sequence similarities

Belongs to the NOS family.

Tissue specificity

Platelets, placenta, liver and kidney.

Cellular localization

• 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.

Alternative names

• Constitutive NOS
• EC-NOS
• Endothelial NOS
• NOS type III
• cNOS
• eNOS
• NOSIII
• NOS3

Database links

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

Target type

Proteins

Primary research area

Oncology

Other research areas

• Cardiovascular
• Immuno-oncology

Molecular weight

133275Da