Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency

Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency

عرض إصدارات أخرى (1)

Tetrahydrobiopterin (BH4) is a required cofactor for the synthesis of NO by endothelial nitric oxide synthase (eNOS), and endothelial BH4 bioavailability is a critical factor in regulating the balance between NO and superoxide production (eNOS coupling). Biosynthesis of BH4 is determined by the acti...

وصف كامل

التفاصيل البيبلوغرافية
المؤلفون الرئيسيون:	Crabtree, M, Hale, AB, Channon, K
التنسيق:	Journal article
اللغة:	English
منشور في:	2011

مواد مشابهة

Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency.
حسب: Crabtree, M, وآخرون
منشور في: (2011)

Integrated redox sensor and effector functions for tetrahydrobiopterin- and glutathionylation-dependent endothelial nitric-oxide synthase uncoupling.
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Critical role for tetrahydrobiopterin recycling by dihydrofolate reductase in regulation of endothelial nitric-oxide synthase coupling: relative importance of the de novo biopterin synthesis versus salvage pathways.
حسب: Crabtree, M, وآخرون
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Endothelial tetrahydrobiopterin deficiency accelerates atherosclerotic progression by nitric oxide synthase uncoupling
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Dihydrofolate reductase is required to maintain endothelial nitric oxide synthase coupling in vivo: Insights from methotrexate-treated BH4 deficient and GTPCH overexpressing mice
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Tetrahydrobiopterin Prevents Lung Ischemia/reperfusion-Induced Uncoupling of Endothelial Nitric Oxide Synthase
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Tetrahydrobiopterin: regulator of endothelial nitric oxide synthase in vascular disease.
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Recoupling the cardiac nitric oxide synthases: Tetrahydrobiopterin synthesis and recycling
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Dihydrofolate reductase and biopterin recycling in cardiovascular disease.
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Endothelial nitric oxide synthase dysfunction in diabetic mice: importance of tetrahydrobiopterin in eNOS dimerisation.
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Tetrahydrobiopterin protects against hypertrophic heart disease independent of myocardial nitric oxide synthase coupling
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Tetrahydrobiopterin Protects Against Hypertrophic Heart Disease Independent of Myocardial Nitric Oxide Synthase Coupling
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Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.
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Rapid, direct effects of statin treatment on arterial redox state and nitric oxide bioavailability in human atherosclerosis via tetrahydrobiopterin-mediated endothelial nitric oxide synthase coupling.
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Rapid, direct effects of statin treatment on arterial redox state and nitric oxide bioavailability in human atherosclerosis via tetrahydrobiopterin- mediated endothelial nitric oxide synthase coupling
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P683The role of nitric oxide synthase (NOS) and its essential cofactor tetrahydrobiopterin (BH4) in diabetic cardiomyopathy.
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Synthesis and recycling of tetrahydrobiopterin in endothelial function and vascular disease.
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Adenovirus-mediated GTP cyclohydrolase I gene delivery augments tetrahydrobiopterin and restores nitric oxide synthase function in hyperglycaemic human aortic endothelial cells
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Mulberry and its main components protect against oxidized low-density lipoprotein-induced endothelial nitric oxide synthase uncoupling
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Combined gene deletion of dihydrofolate reductase-thymidylate synthase and pteridine reductase in Leishmania infantum.
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Statin treatment improves vascular redox state through a tetrahydrobiopterin-mediated re-coupling of endothelial nitric oxide synthase, in human atherosclerosis
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Increased NOX2 expression in astrocytes leads to eNOS uncoupling through dihydrofolate reductase in endothelial cells after subarachnoid hemorrhage
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