| Title | New Insights into eNOS Signaling in Microvascular Permeability. | | Author(s) | Yuan SY | | Institution | Surgery, University of California a Davis School of Medicine, Sacramento, California, United States. | | Source | Am J Physiol Heart Circ Physiol 2006 May 26. | | Abstract | Since the original discovery that nitric oxide (NO) is the endothelium-derived relaxing factor, extensive investigation has been carried out to study the role of this signaling molecule in control of vascular homeostasis. We now know that endothelial nitric oxide synthase (eNOS) is the primary physiological source of NO in the vascular system, where exposure of the endothelium to physical stress or circulating factors causes eNOS activation and NO production. Such responses often occur via a calcium/calmodulin-dependent transduction pathway, and the downstream effects involve the formation of cyclic guanosine monophosphate (cGMP) (21). The post-translational regulation of eNOS is mediated by fatty acid modification and phosphorylation of the enzyme, as well as protein-protein interactions with other effector molecules (28). Furthermore, the intracellular localization of eNOS may be an important determinant of its activity (29). Mechanisms of eNOS trafficking between different subcellular compartments represent an active area of investigation. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 16731639 |
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