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Gene Review

NANOS3  -  nanos homolog 3 (Drosophila)

Homo sapiens

Synonyms: NANOS1L, NOS-3, NOS3, Nanos homolog 3
 
 
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Disease relevance of NANOS3

  • The expression of the constitutive COX-1 and NOS-3 was negligible or weak in the glandular epithelium of proliferative and secretory endometrium and in endometrial cancer cells [1].
  • The mRNA steady-state levels of NOS-3, NOS-2, prostacyclin synthase, and COX- 1 were not altered by ischemia [2].
  • NOS-3 immunoreactivity increased in all pouchitis groups [3].
  • In osteomyelitis (OM), a chronic infection of the bone, homozygosity for the NOS3 (27-bp repeat, intron 4 polymorphism) 4 allele was significantly more frequent among the 80 patients than in 300 healthy controls (p=0.044) [4].
  • However, immunolabelling of osteoblasts for NOS3 in biopsy tissues did not correlate with the carriage of a determined NOS polymorphism but with the presence of bone inflammation [4].
 

High impact information on NANOS3

  • We find that ectopically produced Nanos2 protein rescues the Nanos3-null defects, because the germ cells fully develop in both sexes in the transgenic mice [5].
  • Nanos3 expression in the mouse embryo commences in the primordial germ cells (PGCs) just after their formation, and a loss of this protein results in the germ cell-less phenotype in both sexes [5].
  • The intensity of NOS2 and NOS3 gene expression observed in athlete's heart was similar to dilated cardiomyopathy with low LV diastolic stiffness-modulus and preserved LV stroke work [6].
  • The keratinocytes, which make up the bulk of the epidermis, constitutively express the neuronal isoform of NO synthase (NOS1), whereas the fibroblasts in the dermis and other cell types in the skin express the endothelial isoform (NOS3) [7].
  • Our laboratory has previously published that in salt-dependent hypertension there is an altered localization of NOS 3, with an increase in cytosolic expression [8].
 

Biological context of NANOS3

  • Endothelial NO synthase (NOS 3), which catalyses the formation of NO, is targeted to the plasma membrane by dual acylation [8].
  • We also determined whether plasma NO(x) or NOS 3 genotype predicted the risk of is chemic heart disease (IHD) [9].
  • Genotype frequencies were in Hardy-Weinberg equilibrium, and linkage disequilibrium was detected between all the NOS 3 polymorphismsstudied, with the strongest allelic association being detected between -922 A/G and -786 T/C polymorphisms in the gene promoter (Delta=0.90, P<0.001) [9].
  • We examined whether cholesterol, blood pressure, smoking status, and polymorphisms in the endothelial NO synthase gene (NOS 3) influence NO production (as assessed by the plasma levels of nitrogen oxides, NO(x)) in middle-aged men [9].
  • DNA samples were screened for 4 NOS 3 gene polymorphisms: -786 T/C, -922 A/G, 894 G/T (which predicts a Glu(298)-->Asp amino acid substitution in the mature protein), and a 27-bp tandem repeat in intron 4 (eNOS4a/4b) [9].
 

Anatomical context of NANOS3

  • NOS-1 is localised primarily to neuronal structures, where NO is a mediator of the inhibitory Non-Adrenergic Non-Cholinergic System and NOS-3 is present in endothelial cells [10].
  • Cytokines generate nitric oxide (NO) in osteoblasts and neutrophils through the induction of NO synthase isoforms, endothelial (NOS3) and inducible (NOS2), thereby producing bone loss [4].
  • These data support the hypothesis that the endothelial dysfunction observed in the blood vessels of smokers is related to reduced NO bioactivity but indicate that NOS 3 genotype does not influence significantly the level of plasma NO(x) or the risk of IHD in this population sample of middle-aged British men [9].
 

Other interactions of NANOS3

  • We report the cloning and the functional analyses of nanos2 and nanos3 in mice [11].
 

Analytical, diagnostic and therapeutic context of NANOS3

  • As compared to control groups there were significantly less NOS3 immunopositive EC in metastatic tumour vessels (45-50% and 1-3% in normal and tumour groups, respectively) [12].

References

  1. The expression of cyclooxygenase-1 and -2 in proliferative endometrium and endometrial adenocarcinoma. Uotila, P.J., Erkkola, R.U., Klemi, P.J. Ann. Med. (2002) [Pubmed]
  2. Serotonin-induced human coronary microvascular contraction during acute myocardial ischemia is blocked by COX-2 inhibition. Métais, C., Bianchi, C., Li, J., Li, J., Simons, M., Sellke, F.W. Basic Res. Cardiol. (2001) [Pubmed]
  3. Expression of inducible and endothelial nitric oxide synthases in pouchitis. Vento, P., Kiviluoto, T., Järvinen, H.J., Kärkkäinen, P., Kivilaakso, E., Soinila, S. Inflamm. Bowel Dis. (2001) [Pubmed]
  4. The NOS3 (27-bp repeat, intron 4) polymorphism is associated with susceptibility to osteomyelitis. Asensi, V., Montes, A.H., Valle, E., Oca??a, M.G., Astudillo, A., Alvarez, V., L??pez-Anglada, E., Sol??s, A., Coto, E., Meana, A., Gonzalez, P., Carton, J.A., Paz, J., Fierer, J., Celada, A. Nitric Oxide (2007) [Pubmed]
  5. Functional redundancy among Nanos proteins and a distinct role of Nanos2 during male germ cell development. Suzuki, A., Tsuda, M., Saga, Y. Development (2007) [Pubmed]
  6. Endomyocardial nitric oxide synthase and the hemodynamic phenotypes of human dilated cardiomyopathy and of athlete's heart. Bronzwaer, J.G., Zeitz, C., Visser, C.A., Paulus, W.J. Cardiovasc. Res. (2002) [Pubmed]
  7. Nitric oxide function in the skin. Cals-Grierson, M.M., Ormerod, A.D. Nitric Oxide (2004) [Pubmed]
  8. NOS 3 subcellular localization in the regulation of nitric oxide production. Sullivan, J.C., Pollock, J.S. Acta Physiol. Scand. (2003) [Pubmed]
  9. Genetic and environmental determinants of plasma nitrogen oxides and risk of ischemic heart disease. Jeerooburkhan, N., Jones, L.C., Bujac, S., Cooper, J.A., Miller, G.J., Vallance, P., Humphries, S.E., Hingorani, A.D. Hypertension (2001) [Pubmed]
  10. Mediators of asthma: nitric oxide. Fischer, A., Folkerts, G., Geppetti, P., Groneberg, D.A. Pulmonary pharmacology & therapeutics. (2002) [Pubmed]
  11. Conserved role of nanos proteins in germ cell development. Tsuda, M., Sasaoka, Y., Kiso, M., Abe, K., Haraguchi, S., Kobayashi, S., Saga, Y. Science (2003) [Pubmed]
  12. Increased expression of NOS and ET-1 immunoreactivity in human colorectal metastatic liver tumours is associated with selective depression of constitutive NOS immunoreactivity in vessel endothelium. Aliev, G., Smith, M.A., Seyidova, D., Neal, M.L., Shi, J., Loizidou, M., Turmaine, M., Friedland, R.P., Taylor, I., Burnstock, G., Perry, G., Lamanna, J.C. J. Submicrosc. Cytol. Pathol. (2002) [Pubmed]
 
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