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DDAHDimethylarginine Dimethylaminohydrolase
DDAHDesordem por Défice de Atenção com Hiperactividade (Portuguese: Attention Deficit Disorder with Hyperactivity)
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Asymmetric dimethylarginine causes hypertension and cardiac dysfunction in humans and is actively metabolized by dimethylarginine dimethylaminohydrolase.
33) Moreover, reductions in lipid, homocysteine, and triglyceride levels and insulin resistance enhance dimethylarginine dimethylaminohydrolase to enzymatically reduce asymmetric dimethylarginine and optimize nitric oxide synthase availability in nitric oxide production.
Lin KY, Ito A, Asagami T, Tsao PS, Adimoolam S, Kimoto M, Tsuji H, Reaven GM, Cooke JP Impaired nitric oxide synthase pathway in diabetes mellitus: role of asymmetric dimethylarginine and dimethylarginine dimethylaminohydrolase.
Regulation of nitric oxide synthesis by dimethylarginine dimethylaminohydrolase.
Dimethylarginine dimethylaminohydrolase overexpression enhances insulin sensitivity.
Cardiovascular biology of the asymmetric dimethylarginine: dimethylarginine dimethylaminohydrolase pathway.
Effects of overexpression of dimethylarginine dimethylaminohydrolase on tumor angiogenesis assessed by susceptibility magnetic resonance imaging.
Dimethylarginine dimethylaminohydrolase I enhances tumour growth and angiogenesis.
Novel mechanism for endothelial dysfunction: dysregulation of dimethylarginine dimethylaminohydrolase.
Inactivation of ADMA occurs via dimethylarginine dimethylaminohydrolase, and it has been hypothesized that this enzyme might be inhibited by homocysteine.
Glucose itself may suppress dimethylarginine dimethylaminohydrolases activity (7) and increase ADMA, but the mechanisms by which diabetes or insulin resistance may increase ADMA have yet to be elucidated (8).
Enzymatic hydrolysis by dimethylarginine dimethylaminohydrolases to dimethylamine and citrulline is the major pathway for elimination of ADMA (3).