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PMID:12176133

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Citation

Cai, S, Alp, NJ, McDonald, D, Smith, I, Kay, J, Canevari, L, Heales, S and Channon, KM (2002) GTP cyclohydrolase I gene transfer augments intracellular tetrahydrobiopterin in human endothelial cells: effects on nitric oxide synthase activity, protein levels and dimerisation. Cardiovasc. Res. 55:838-49

Abstract

Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase (eNOS) activity. BH4 levels are regulated by de novo biosynthesis; the rate-limiting enzyme is GTP cyclohydrolase I (GTPCH). BH4 activates and promotes homodimerisation of purified eNOS protein, but the intracellular mechanisms underlying BH4-mediated eNOS regulation in endothelial cells remain less clear. We aimed to investigate the role of BH4 levels in intracellular eNOS regulation, by targeting the BH4 synthetic pathway as a novel strategy to modulate intracellular BH4 levels.

Links

PubMed

Keywords

3T3 Cells; Adenoviridae/genetics; Animals; Biopterin/analogs & derivatives; Biopterin/metabolism; Cell Line; Dimerization; Endothelium, Vascular/metabolism; GTP Cyclohydrolase/genetics; GTP Cyclohydrolase/metabolism; Genetic Vectors/genetics; Humans; Intracellular Fluid/metabolism; Mice; Nitric Oxide Synthase/metabolism; Transfection/methods

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


See also

References

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