eNOS (pT495) Pure 31/eNOS(pT495) 150ug

Nitric oxide synthase (NOS), a cell-type specific enzyme, catalyzes the synthesis of nitric oxide (NO). NO is a short-lived radical that

transmits signals involved in vasorelaxation, neurotransmission, and cytotoxicity. In neurons and endothelial cells, constitutive NOS (cNOS)

is activated by agonists that increase intracellular Ca2+ levels and enhance calmodulin binding. Neuronal NOS (nNOS) and endothelial NOS

(eNOS) have recognition sites for NADPH, FAD, FMN, and calmodulin. eNOS has a unique N-myristylation consensus sequence that may

explain its membrane localization. Various protein kinases have been implicated in regulation of eNOS activity, including AMPK, PKA,

PKB/Akt, PKC, and CaM Kinase II. During VEGF stimulation, eNOS is transiently phosphorylated at Ser-1177 by PKB/akt and

dephosphorylated at Thr-495. At later time points, VEGF stimulation leads to an increase in Thr-495 phosphorylation mediated by PKC and a

decrease in Ser-1177 phosphorylation. In addition, Ser-495, Ser-633, and Ser-1177 are phosphorylated by PKA and PKG in vitro. Thus,

eNOS activity may be regulated through complex phosphorylation events mediated by multiple kinases at various phosphorylation sites.

1.Since applications vary, each investigator should titrate the reagent to obtain optimal results.

2.Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.