Anti-phospho-eNOS (Ser602) from rabbit

Nitric oxide synthase, endothelial (UniProt: P29473; also known as EC:1.14.13.39; constitutive NOS, EC-NOS, eNOS, NOS III, NOS type III) is encoded by the NOS3 gene (Gene ID: 287024) in bovine. The eNOS is mainly expressed in vascular endothelial cells and cardiomyocytes. It produces nitric oxide (NO) that 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. In endothelial cells, eNOS is localized in specialized plasmalemmal pockets known as caveolae, which contain a scaffolding protein termed caveolin. Acylation of eNOS by either myristate or palmitate targets it to caveolae, which facilitates enzyme activation following receptor stimulation. In a resting cell, eNOS is inhibited by its interaction with caveolin. Following agonist activation, eNOS dissociates from caveolin and translocates to the cytosol. The eNOS is generally activated in response to an increase in intracellular Ca2+ following stimulation with receptor-dependent agonists such as acetylcholine. However, shear stress can also activate this enzyme independently of Ca2+ level changes, via a tyrosine kinase-dependent mechanism involving its phosphorylation and redistribution. Perturbations of eNOS phosphorylation have been reported in a number of diseases. The primary sites where eNOS gets phosphorylated are multiple serine residues and, to a lesser extent, on tyrosine and threonine residues. Ser 602 is reported to lie at the N-terminal edge of the 42-residue eNOS autoinhibitory element and is phosphorylated by ERK. Low concentrations of nitric oxide in the endothelial cells prevent their apoptotic death and maintain their integrity during inflammation and atherosclerosis. Distorted production of nitric oxide in endothelial cells has been linked to hypertension, hypercholesterolemia, diabetes, and even cardiac failure. (Ref.: Rafikov, R., et al. (2011). J. Endocrinol. 210(3): 271-284).