Endothelial NOS

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Nitric oxide synthase 3 (endothelial cell)
PDB 1m9j EBI.jpg
Rendering of 1M9J
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols NOS3 ; ECNOS; eNOS
External IDs OMIM163729 MGI97362 HomoloGene504 ChEMBL: 4803 GeneCards: NOS3 Gene
EC number 1.14.13.39
RNA expression pattern
PBB GE NOS3 205581 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 4846 18127
Ensembl ENSG00000164867 ENSMUSG00000028978
UniProt P29474 P70313
RefSeq (mRNA) NM_000603 NM_008713
RefSeq (protein) NP_000594 NP_032739
Location (UCSC) Chr 7:
150.69 – 150.71 Mb
Chr 5:
24.36 – 24.38 Mb
PubMed search [1] [2]

Endothelial NOS (eNOS), also known as nitric oxide synthase 3 (NOS3) or constitutive NOS (cNOS), is an enzyme that in humans is encoded by the NOS3 gene.[1]

Endothelial NOS is a nitric oxide synthase that generates NO in blood vessels and is involved with regulating vascular tone by inhibiting smooth muscle contraction and platelet aggregation. A constitutive Ca2+ dependent NOS provides a basal release of NO. eNOS is associated with plasma membranes surrounding cells and the membranes of Golgi bodies within cells.

Clinical significance[edit]

Variations in this gene are associated with susceptibility to coronary spasm.[2]

An association between a polymorphism in the gene and late-onset Alzheimer's disease in Chinese have been reported.[3]

Interactions[edit]

Endothelial NOS has been shown to interact with CAV1,[4] HSP90AA1[5][6][7] and GUCY1B3.[5]

References[edit]

  1. ^ Marsden PA, Schappert KT, Chen HS, Flowers M, Sundell CL, Wilcox JN, Lamas S, Michel T (August 1992). "Molecular cloning and characterization of human endothelial nitric oxide synthase". FEBS Lett. 307 (3): 287–93. doi:10.1016/0014-5793(92)80697-F. PMID 1379542. 
  2. ^ Yoshimura M, Yasue H, Nakayama M, Shimasaki Y, Sumida H, Sugiyama S, Kugiyama K, Ogawa H, Ogawa Y, Saito Y, Miyamoto Y, Nakao K (July 1998). "A missense Glu298Asp variant in the endothelial nitric oxide synthase gene is associated with coronary spasm in the Japanese". Hum. Genet. 103 (1): 65–9. doi:10.1007/s004390050785. PMID 9737779. 
  3. ^ Wang B, Tan S, Yang Z, Xie YC, Wang J, Zhou S, Li S, Zheng C, Ma X (February 2008). "Association between Alzheimer's disease and the NOS3 gene Glu298Asp polymorphism in Chinese". J. Mol. Neurosci. 34 (2): 173–6. doi:10.1007/s12031-007-9026-6. PMID 18183499. 
  4. ^ García-Cardeña G, Fan R, Stern DF, Liu J, Sessa WC (November 1996). "Endothelial nitric oxide synthase is regulated by tyrosine phosphorylation and interacts with caveolin-1". J. Biol. Chem. 271 (44): 27237–40. doi:10.1074/jbc.271.44.27237. PMID 8910295. 
  5. ^ a b Venema RC, Venema VJ, Ju H, Harris MB, Snead C, Jilling T, Dimitropoulou C, Maragoudakis ME, Catravas JD (August 2003). "Novel complexes of guanylate cyclase with heat shock protein 90 and nitric oxide synthase". Am. J. Physiol. Heart Circ. Physiol. 285 (2): H669–78. doi:10.1152/ajpheart.01025.2002. PMID 12676772. 
  6. ^ Harris MB, Ju H, Venema VJ, Blackstone M, Venema RC (September 2000). "Role of heat shock protein 90 in bradykinin-stimulated endothelial nitric oxide release". Gen. Pharmacol. 35 (3): 165–70. doi:10.1016/S0306-3623(01)00104-5. PMID 11744239. 
  7. ^ Stepp DW, Ou J, Ackerman AW, Welak S, Klick D, Pritchard KA (August 2002). "Native LDL and minimally oxidized LDL differentially regulate superoxide anion in vascular endothelium in situ". Am. J. Physiol. Heart Circ. Physiol. 283 (2): H750–9. doi:10.1152/ajpheart.00029.2002. PMID 12124224. 


Further reading[edit]