Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Nos3. (This text reflects annotations as of Thursday, July 24, 2014.)

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] Nitric oxide is a reactive free radical which acts as a biologic mediator in several processes, including neurotransmission and antimicrobial and antitumoral activities. Nitric oxide is synthesized from L-arginine by nitric oxide synthases. Variations in this gene are associated with susceptibility to coronary spasm. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, May 2009]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Nos3
  • is located in the following cellular components:
    • cytoplasm ^[5]
    • nucleus ^[5]
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Nos3
  • participates in the following biological processes:
    • angiogenesis ^[2]
    • blood vessel remodeling ^[6]
    • in utero embryonic development ^[5]
    • lipopolysaccharide-mediated signaling pathway ^[1]
    • lung development ^[2]
    • negative regulation of calcium ion transport ^[8]
    • negative regulation of cell proliferation ^[6]
    • negative regulation of hydrolase activity ^[8]
    • negative regulation of muscle hyperplasia ^[6]
    • negative regulation of potassium ion transport ^[8]
    • nitric oxide biosynthetic process ^[1]
    • ovulation from ovarian follicle ^[3]
    • oxidation-reduction process ^[1]
    • positive regulation of angiogenesis ^[4]
    • regulation of blood vessel size ^[6]
    • regulation of sodium ion transport ^[8]
    • smooth muscle hyperplasia ^[6]
  • performs the following molecular functions:
    • nitric-oxide synthase activity ^[1]
• Researchers have inferred, based on genetic interactions, that the gene product of Nos3
  • participates in the following biological processes:
    • regulation of the force of heart contraction by chemical signal based on interactions with Cav1 ^[7]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Nos3:
  • participates in the following biological processes:
    • arginine catabolic process
    • cellular response to mechanical stimulus
    • cellular response to transforming growth factor beta stimulus
    • endothelial cell migration
    • negative regulation of blood pressure
    • negative regulation of smooth muscle cell proliferation
    • nitric oxide biosynthetic process
    • nitric oxide mediated signal transduction
    • positive regulation of apoptotic process
    • positive regulation of guanylate cyclase activity
    • positive regulation of vasodilation
    • regulation of systemic arterial blood pressure by endothelin
    • response to estradiol
    • signal transduction
  • performs the following molecular functions:
    • actin binding
    • actin monomer binding
    • arginine binding
    • beta-catenin binding
    • cadherin binding
    • calmodulin binding
    • heme binding
    • Hsp90 protein binding
    • NADPH-hemoprotein reductase activity
    • nitric-oxide synthase activity
    • nitric-oxide synthase binding
    • scaffold protein binding
    • tetrahydrobiopterin binding
  • is located in the following cellular components:
    • apical part of cell
    • caveola
    • cytoplasm
    • cytosol
    • Golgi apparatus
    • membrane raft
    • mitochondrion
    • nucleolus
    • nucleus
    • plasma membrane
    • sarcolemma
    • vesicle membrane

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Summary text based on GO annotations supported by structural data

• Nos3 encodes a protein or proteins that contain the following InterPro domains: FAD-binding, type 1, Ferredoxin reductase-type FAD-binding domain, Flavodoxin, Flavodoxin/nitric oxide synthase, Flavoprotein pyridine nucleotide cytochrome reductase, NADPH-cytochrome p450 reductase, FAD-binding, alpha-helical domain-3, Nitric oxide synthase, oxygenase domain, Nitric-oxide synthase, metazoa, Oxidoreductase FAD/NAD(P)-binding, Riboflavin synthase-like beta-barrel, indicating that the gene product:
  • performs the following molecular functions:
    • flavin adenine dinucleotide binding
    • FMN binding
    • iron ion binding
    • NADP binding
    • oxidoreductase activity

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Nos3 indicates that it:
  • performs the following molecular functions:
    • metal ion binding
    • oxidoreductase activity
  • is located in the following cellular components:
    • cytoskeleton
    • membrane

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References

1. Connelly L et al. (2005) Resistance to endotoxic shock in endothelial nitric-oxide synthase (eNOS) knock-out mice: a pro-inflammatory role for eNOS-derived no in vivo. J Biol Chem, 280:10040-6. (PubMed:15647265)
2. Han RN et al. (2004) Defective lung vascular development and fatal respiratory distress in endothelial NO synthase-deficient mice: a model of alveolar capillary dysplasia? Circ Res, 94:1115-23. (PubMed:15016731)
3. Hefler LA et al. (2002) Inducible and endothelial nitric oxide synthase: genetic background affects ovulation in mice. Fertil Steril, 77:147-51. (PubMed:11779605)
4. Murohara T et al. (1998) Nitric oxide synthase modulates angiogenesis in response to tissue ischemia. J Clin Invest, 101:2567-78. (PubMed:9616228)
5. Nishikimi A et al. (2001) Localization of nitric oxide synthase activity in unfertilized oocytes and fertilized embryos during preimplantation development in mice. Reproduction, 122:957-63. (PubMed:11732991)
6. Rudic RD et al. (1998) Direct evidence for the importance of endothelium-derived nitric oxide in vascular remodeling. J Clin Invest, 101:731-6. (PubMed:9466966)
7. Wunderlich C et al. (2008) Nitric oxide synthases are crucially involved in the development of the severe cardiomyopathy of caveolin-1 knockout mice. Biochem Biophys Res Commun, 377:769-74. (PubMed:18951881)
8. Zhou L et al. (2002) Lack of nitric oxide synthase depresses ion transporting enzyme function in cardiac muscle. Biochem Biophys Res Commun, 294:1030-5. (PubMed:12074580)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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