Biology:NOS1

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Short description: Protein-coding gene in the species Homo sapiens


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

Nitric oxide synthase 1 (neuronal), also known as NOS1, is an enzyme that in humans is encoded by the NOS1 gene.[1][2]

Function

Nitric oxide synthases (EC 1.14.13.39) (NOSs) are a family of synthases that catalyze the production of nitric oxide (NO) from L-arginine. NO is a chemical messenger with diverse functions throughout the body depending on its enzymatic source and tissue localization. In the brain and peripheral nervous system, where NOS1 is largely present, NO displays many properties of a neurotransmitter and may be involved in long term potentiation. It is implicated in neurotoxicity associated with stroke and neurodegenerative diseases, neural regulation of smooth muscle, including peristalsis and sphincter relaxation, and penile erection. NO is also responsible for endothelium-derived relaxing factor activity regulating blood pressure as produced from its related enzyme NOS3. In macrophages, NO mediates tumoricidal and bactericidal actions, as produced from its related enzyme NOS2. Various pharmacological inhibitors of NO synthases (NOS) block these effects, but further distinction of their function has been elucidated by animal models in which these specific genes have been inactivated. Neuronal NOS (NOS1), Endothelial NOS (NOS3), and Inducible NOS macrophage NOS are distinct isoforms.[3] Both the neuronal and the macrophage forms are unusual among oxidative enzymes in requiring several electron donors: flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), NADPH, and tetrahydrobiopterin.[4]

Clinical significance

It has been implicated in asthma,[5][6] schizophrenia,[7][8] restless leg syndrome,[9] and psychostimulant neurotoxicity. It has also been investigated with respect to bipolar disorder[10] and air pollution exposure.[11]

Interactions

NOS1 has been shown to interact with DLG4[12][13] and NOS1AP.[12]

See also

References

  1. ↑ "Localization of brain nitric oxide synthase (NOS) to human chromosome 12". Genomics 14 (3): 802–4. November 1992. doi:10.1016/S0888-7543(05)80192-2. PMID 1385308. 
  2. ↑ "Molecular cloning and expression of inducible nitric oxide synthase from human hepatocytes". Proc. Natl. Acad. Sci. U.S.A. 90 (8): 3491–5. April 1993. doi:10.1073/pnas.90.8.3491. PMID 7682706. Bibcode: 1993PNAS...90.3491G. 
  3. ↑ "Cloned and expressed macrophage nitric oxide synthase contrasts with the brain enzyme". Proc. Natl. Acad. Sci. U.S.A. 89 (15): 6711–5. August 1992. doi:10.1073/pnas.89.15.6711. PMID 1379716. Bibcode: 1992PNAS...89.6711L. 
  4. ↑ "Entrez Gene: NOS1 Nitric oxide synthase 1 (neuronal)". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=4843. 
  5. ↑ "Neuronal NO synthase (NOS1) is a major candidate gene for asthma". Clin. Exp. Allergy. 29 29 (Suppl 4): 39–41. December 1999. PMID 10641565. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0954-7894&date=1999&volume=29&issue=&spage=39. 
  6. ↑ "Nitric oxide synthase polymorphisms and asthma phenotypes in Chinese children". Clin. Exp. Allergy 35 (10): 1288–94. October 2005. doi:10.1111/j.1365-2222.2005.02342.x. PMID 16238787. 
  7. ↑ "Allelic association of the neuronal nitric oxide synthase (NOS1) gene with schizophrenia". Mol. Psychiatry 7 (6): 560–3. 2002. doi:10.1038/sj.mp.4001041. PMID 12140778. 
  8. ↑ "A neuronal nitric oxide synthase (NOS-I) haplotype associated with schizophrenia modifies prefrontal cortex function". Mol. Psychiatry 11 (3): 286–300. March 2006. doi:10.1038/sj.mp.4001779. PMID 16389274. 
  9. ↑ "Variants in the neuronal nitric oxide synthase (nNOS, NOS1) gene are associated with restless legs syndrome". Mov. Disord. 23 (3): 350–8. February 2008. doi:10.1002/mds.21647. PMID 18058820. 
  10. ↑ "No association between a neuronal nitric oxide synthase (NOS1) gene polymorphism on chromosome 12q24 and bipolar disorder". Am. J. Med. Genet. B Neuropsychiatr. Genet. 124B (1): 73–5. January 2004. doi:10.1002/ajmg.b.20040. PMID 14681919. 
  11. ↑ "Neuroinflammation induced by air pollution: gene expression analysis in laboratory animals". Master Thesis, GROUP T – Leuven Engineering College. 2013. https://www.researchgate.net/publication/236162904. 
  12. ↑ 12.0 12.1 "CAPON: a protein associated with neuronal nitric oxide synthase that regulates its interactions with PSD95". Neuron 20 (1): 115–24. January 1998. doi:10.1016/S0896-6273(00)80439-0. PMID 9459447. 
  13. ↑ "Interaction of nitric oxide synthase with the postsynaptic density protein PSD-95 and alpha1-syntrophin mediated by PDZ domains". Cell 84 (5): 757–67. March 1996. doi:10.1016/S0092-8674(00)81053-3. PMID 8625413. 

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.




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