GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
PMID:15824199
| Citation |
Nandi, M, Miller, A, Stidwill, R, Jacques, TS, Lam, AA, Haworth, S, Heales, S and Vallance, P (2005) Pulmonary hypertension in a GTP-cyclohydrolase 1-deficient mouse. Circulation 111:2086-90 |
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| Abstract |
GTP-cyclohydrolase 1 (GTP-CH1) catalyzes the first step for the de novo production of tetrahydrobiopterin (BH4), a cofactor for nitric oxide synthase (NOS). The hyperphenylalaninemic mutant mouse (hph-1) displays a 90% reduction in GTP-CH1 activity. Reduced BH4 decreases NOS activity and may lead to endothelial dysfunction, and there is increasing evidence that a dysfunction of the NOS pathway may be implicated in pulmonary hypertension. The aim of the study was to investigate whether reduced BH4 in the hph-1 mouse results in a pulmonary hypertensive phenotype. |
| Links |
PubMed Online version:10.1161/01.CIR.0000163268.32638.F4 |
| Keywords |
Animals; Arteries/pathology; Biopterin/analogs & derivatives; Biopterin/deficiency; Biopterin/pharmacology; Biopterin/therapeutic use; Female; GTP Cyclohydrolase/deficiency; Hypertension, Pulmonary/drug therapy; Hypertension, Pulmonary/etiology; Hypertension, Pulmonary/pathology; Hypertrophy, Right Ventricular; Male; Mice; Mice, Mutant Strains; Muscle, Smooth, Vascular/pathology; Nitric Oxide/analysis; Pulmonary Circulation; Vascular Resistance |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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