Clone REA451 recognizes the human endothelial nitric oxide synthase (eNOS) antigen regardless of phosphorylation status. eNOS catalyzes the production of nitric oxide (NO) from l-arginine within the endothelium to regulate vascular tone via cGMP signaling in vascular smooth muscle, mitochondrial respiration, platelet function, inflammation, and angiogenesis. Physiologically, the most important stimulus for the continuous formation of NO is the shear stress generated by the streaming blood on the endothelial layer. Serine/threonine protein kinase Akt/PKB mediates the activation of eNOS, leading to increased NO production. Inhibition of the phosphatidylinositol-3-OH kinase/Akt pathway or mutation of the Akt site on eNOS protein attenuates the serine phosphorylation and prevents the activation of eNOS.
Additional information: Clone REA451 displays negligible binding to Fc receptors.
NOS3, ECNOS, NOS type III, EC-NOS, NOS III
Technical specifications
