Localization of brain nitric oxide synthase (NOS) to human chromosome 12

Kishimoto, Jiro; Spurr, Nigel K.; Liao, Martha; Liu, Lizhi; Emson, Piers C.; Xu, Weiming

doi:10.1016/s0888-7543(05)80192-2

Cited by 70 publications

(17 citation statements)

References 18 publications

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“…In the cell, NO can be generated from L-arginine via either one of three nitric oxide synthases: eNOS, iNOS, and neuronal NOS, whereby the latter is specifically expressed in brain tissue and skeletal muscle (Schmidt et al, 1992;Kishimoto et al, 1992;Silvagno et al, 1996;Gath et al, 1996) and was therefore not investigated here. Although the effects seen by NO in this study could be reasonably explained by the activation of particular downstream targets, supplementation with a fixed concentration of an NO donor is a rather indiscriminate way of mimicking the levels of NO produced in a healthy cell.…”

Section: Discussionmentioning

confidence: 99%

Exogenous nitric oxide enhances calcification in embryonic stem cell-derived osteogenic cultures

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Exogenous nitric oxide enhances calcification in embryonic stem cell-derived osteogenic cultures

et al. 2015

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“…Nitric oxide synthase (NOS) has three genetically distinct isoforms: neuronal NOS encoded by NOS1 (12q24-q24.3), 1 macrophage-derived isoforms encoded by genes on chromosome 17 (NOS2A, 2B and 2C), 2 and an endothelial-derived isoform encoded by NOS3 (7q36). 3 Endothelial NOS is constitutively expressed in the human outflow pathway and ciliary muscle where it may modulate outflow facility.…”

Section: Introductionmentioning

confidence: 99%

Endothelial Nitric Oxide Synthase Gene Variants and Primary Open-Angle Glaucoma: Interactions with Sex and Postmenopausal Hormone Use

Kang

Wiggs

Rosner

et al. 2010

Invest. Ophthalmol. Vis. Sci.

107

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Purpose To evaluate the association between nitric oxide synthase gene (NOS3) variants and primary open-angle glaucoma (POAG). Methods Two functional single nucleotide polymorphisms (SNPs)( T-786C: rs2070744, Glu298Asp: rs1799983) and three tagging SNPs (rs7830; rs3918188; rs1800779) were evaluated in nested case-control studies from the Nurses’ Health Study (followed 1980 – 2002) and the Health Professionals’ Follow-up Study (followed 1986 – 2002). Participants were aged ≥ 40 years and Caucasian. We included 527 incident cases and 1543 controls, matched on cohort, age and eye exam at the matched cases’ diagnosis dates. Cohort–specific relative risks (RR) were estimated using multivariable conditional logistic regression and pooled with meta-analysis. Results No NOS3 polymorphism was significantly associated with overall POAG. For high tension POAG (HTPOAG), rs3918188 was significantly inversely associated among women (AA vs. CC genotype: RR = 0.48; 95% CI=0.28, 0.82) but not among men (p-heterogeneity by gender= 0.02). The minor alleles of T-786C and rs1800779 showed positive associations with high tension POAG (p-trend<0.02) in women only, but the p-heterogeneity was not significant. In women, four of the five NOS3 SNPs showed significant interactions with postmenopausal hormone (PMH) use in relation to HTPOAG: e.g., among women with TT genotype in T-786C, PMH use was inversely associated (RR = 0.41; 95% CI = 0.22, 0.76), but among carriers of the minor allele, PMH use was not associated. Conclusions Interactions were observed between NOS3 SNPs and gender and postmenopausal hormone use in women in relation to HTPOAG. These findings should be confirmed in populations with different racial/ethnic groups.

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“…The human nNOS gene has been located on chromosome 1q24 [9]. A recent genetic study has determined an association between a single nucleotide polymorphism of the nNOS gene [C → T transition located 276 base pairs (bp) downstream from the translation termination site] and schizophrenia [10].…”

Section: Introductionmentioning

confidence: 99%

Association Analysis for Neuronal Nitric Oxide Synthase Gene Polymorphism with Major Depression and Fluoxetine Response

Yu¹,

Chen

Wang

et al. 2003

Neuropsychobiology

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Nitric oxide (NO) is produced from its precursor L-arginine by the enzyme NO synthase (NOS), which includes at least three distinct isoforms – neuronal (nNOS), endothelial, and inducible NOS. Recent studies have implicated NOS in the mechanism that underlies the therapeutic efficacy of antidepressant medication. In addition, major depressive disorder (MDD) patients were found to have significantly higher plasma nitrate concentrations than normal subjects, an index of NO production, in comparison to normal subjects. In a population-based association study, we tested the hypothesis that the nNOS C276T polymorphism confers susceptibility to MDD. We also examined the association between this polymorphism and therapeutic fluoxetine response in 114 MDD patients who underwent a 4-week fluoxetine treatment. The results demonstrate that the nNOS variants are found at similar frequencies in MDD patients and healthy control subjects. Further, we did not discover any genetic variants that influenced the fluoxetine response in MDD patients treated with fluoxetine. Our findings suggest that this nNOS C276T polymorphism does not play a major role in the susceptibility to, or fluoxetine response in, MDD. However, the association between other NOS variants and MDD or antidepressant response, including sexual dysfunction, may warrant further investigation.

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Localization of brain nitric oxide synthase (NOS) to human chromosome 12

Cited by 70 publications

References 18 publications

Exogenous nitric oxide enhances calcification in embryonic stem cell-derived osteogenic cultures

Exogenous nitric oxide enhances calcification in embryonic stem cell-derived osteogenic cultures

Endothelial Nitric Oxide Synthase Gene Variants and Primary Open-Angle Glaucoma: Interactions with Sex and Postmenopausal Hormone Use

Association Analysis for Neuronal Nitric Oxide Synthase Gene Polymorphism with Major Depression and Fluoxetine Response

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