EC Number |
General Information |
Reference |
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1.5.1.34 | malfunction |
enzyme inhibition results in a significant increase in transforming growth factor-beta1 expression |
724198 |
1.5.1.34 | malfunction |
tetrahydrobiopterin deficiency is associated with numerous metabolic syndromes and neuropsychological disorders |
742313 |
1.5.1.34 | malfunction |
the brain stem of intrauterine growth-restricted offspring show significant increase of L-tryptophan, 5-hydroxytryptamine, tryptophan-5-hydroxylase and also dihydropteridine activity in the brain stem in comparison to controls. Intrauterine growth restriction produces an increase of serotonin biosynthesis in the brain stem. This is accompanied by an increase in dihydropteridine activity that appears to be a compensatory mechanism to maintain sufficient tetrahydrobiopterin for the donation of electrons during the accelerated synthesis of brain serotonin in intrauterine growth-restricted rats |
712184 |
1.5.1.34 | metabolism |
enzyme catalyzes the last step of tetrahydrobiopterin recycling |
695339 |
1.5.1.34 | metabolism |
inhibition of de novo biosynthesis of tetrahydrobiopterin by preincubating the cells for 24 h with the GTP cyclohydrolase inhibitor DAHP (10 mM) diminishes L-citrulline formation. Addition of dihydrobiopterin fully restores L-citrulline formation. In addition to its effect on arginine-to-citrulline conversion, pretreatment of the cells with DAHP reduces A23187-induced cGMP accumulation. Addition of tetrahydrobiopterin or dihydrobiopterin not only antagonizes the inhibitory effect of DAHP but also increases cGMP accumulation. (6R)-5,6,7,8-Tetrahydro-L-biopterin availability regulates nitric oxide and superoxide formation by endothelial nitric oxide synthase (eNOS). At low tetrahydrobiopterin or low tetrahydrobiopterin to 7,8-dihydrobiopterin ratios the enzyme becomes uncoupled and generates superoxide at the expense of NO |
741864 |
1.5.1.34 | metabolism |
inhibition of de novo biosynthesis of tetrahydrobiopterin by preincubating the cells for 24 h with the GTP cyclohydrolase inhibitor dihydroxyacetone phosphate (10 mM) diminishes L-citrulline formation. Addition of dihydrobiopterin fully restores L-citrulline formation. In addition to its effect on arginine-to-citrulline conversion, pretreatment of the cells with dihydroxyacetone phosphate reduces A23187-induced cGMP accumulation. Addition of tetrahydrobiopterin or dihydrobiopterin not only antagonizes the inhibitory effect of dihydroxyacetone phosphate but also increases cGMP accumulation. (6R)-5,6,7,8-Tetrahydro-L-biopterin availability regulates nitric oxide and superoxide formation by endothelial nitric oxide synthase (eNOS). At low tetrahydrobiopterin or low tetrahydrobiopterin to 7,8-dihydrobiopterin ratios the enzyme becomes uncoupled and generates superoxide at the expense of NO |
741864 |
1.5.1.34 | metabolism |
the enzyme is involved in the De novo pathway and regeneration pathway of tetrahydrobiopterin biosynthesis |
742313 |
1.5.1.34 | physiological function |
enzyme in the regeneration pathway of tetrahydrobiopterin, expression is reduced in hypertensive rats compared to normotensive rats, tetrahydrobiopterin levels are attenuated in hypertensive rat aortic smooth muscle, tetrahydrobiopterin inhibits a serotonin-mediated vascular contraction increase |
701144 |
1.5.1.34 | physiological function |
the enzyme catalyzes (6R)-5,6,7,8-tetrahydro-L-biopterin recycling in endothelial cytosols |
741864 |
1.5.1.34 | physiological function |
the enzyme catalyzes (6R)-5,6,7,8-tetrahydro-L-biopterin recycling in endothelial cytosols with high affinity for dihydrobiopterin |
741864 |