GTP cyclohydrolase I deficiency results in oxidative stress and pulmonary hypertension

GTP cyclohydrolase I deficiency results in oxidative stress and pulmonary hypertension

Detaylı Bibliyografya
Asıl Yazarlar:	Khoo, J, Zhao, L, Alp, N, Bendall, J, Nicoll, T, Wilkins, MR, Channon, K
Materyal Türü:	Conference item
Baskı/Yayın Bilgisi:	2004

Benzer Materyaller

Endothelial-targeted GTP cyclohydrolase I overexpression increases endothelial tetrahydrobiopterin levels and preserves eNOS coupling in eNOS overexpressing mice
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GTP cyclohydrolase I expression, protein, and activity determine intracellular tetrahydrobiopterin levels, independent of GTP cyclohydrolase feedback regulatory protein expression.
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Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I over-expression
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Endotoxemia-related acute kidney injury in transgenic mice with endothelial overexpression of GTP cyclohydrolase-1.
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Prevention of hypoxia-induced pulmonary hypertension and vascular remodelling by targeting endothelial tetrahydrobiopterin-dependent nitric oxide synthase regulation
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GTP cyclohydrolase as a novel mechanism for tumour growth
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Pivotal role for endothelial tetrahydrobiopterin in pulmonary hypertension.
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GTP cyclohydrolase I gene transfer reverses tetrahydrobiopterin deficiency and increases nitric oxide synthesis in endothelial cells and isolated vessels from diabetic rats.
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