EC Number   |
Application |
Reference |
|---|
   3.5.3.18 | medicine |
hyperhomocysteinemia is induced in human DDAH1 transgenic mice and wild-type littermates using a high methionine/low folate diet. Plasma total homocysteine is elevated approximately 3fold in both wild-type and DDAH1 transgenic mice fed the high methionine/low folate diet compared with the control diet. Plasma asymmetrical dimethylarginine is approximately 40% lower in DDAH1 transgenic mice compared with wild-type mice irrespective of diet. Responses to 10 microM papaverine, a direct smooth muscle dilator, are impaired with the high methionine/low folate diet in wild-type mice but not DDAH1 transgenic mice. DDAH1 transgenic mice also are protected from hypertrophy of cerebral arterioles but not from accelerated carotid artery thrombosis induced by the high methionine/low folate diet |
711765 |
| 3.5.3.18 | medicine |
in a mouse model of severe malaria, Plasmodium berghei ANKA infection inactivates hepatic DDAH1 via a post-transcriptional mechanism as evidenced by stable mRNA transcript number, decreased DDAH1 protein concentration, decreased enzyme activity, elevated tissue asymmetric dimethylarginine, elevated asymmetric dimethylarginine/arginine ratio in plasma, and decreased whole blood nitrite concentration |
755203 |
| 3.5.3.18 | medicine |
in lung adenocarcinoma, isoform DDAH2 is expressed in fibroblasts of stroma of malignancies, with higher expression in minimally invasive adenocarcinoma and invasive adenocarcinoma than in adenocarcinoma in situ. Tumors with high stromal expression of DDAH2 have a poorer prognosis than those without |
755643 |
| 3.5.3.18 | medicine |
in patients with type 2 diabetes mellitus, the percentage of senescent endothelial progenitor cells increases while the expression of DDAH2 decreases concomitantly with an increase in the plasma levels of asymmetric dimethylarginine. Exogenous application of asymmetric dimethylarginine accelerates the senescence of cultured endothelial progenitor cells in a dose-dependent manner, and overexpression of DDAH2 inhibits high glucose-induced endothelial progenitor cells senescence. Resveratrol (activating silent information regulator SIRT1) inhibits high glucose-induced endothelial progenitor cells senescence by upregulating the expression of DDAH2 and decreasing the levels of asymmetric dimethylarginine |
752652 |
| 3.5.3.18 | medicine |
in vivo administration of DDAH inhibitors (2-amino-4-(NG-methyl-guanidino)butanoic acid and its analogues) increases plasma NG,NG-dimethyl-L-arginine levels, giving proof of concept that these can be used to probe the physiological effects of DDAH inhibition, with potential for pharmaceutical use of DDAH inhibitors in diseases where excess NO production is implicated |
669780 |
| 3.5.3.18 | medicine |
influence on atherosclerosis in experimental models by increased ADMA concentrations and reduced NO synthesis |
697831 |
| 3.5.3.18 | medicine |
novel therapeutic strategy for the treatment of chronic kidney disease |
699943 |
| 3.5.3.18 | medicine |
placental dysfunction of dimethylarginine dimethylaminohydrolase has been suggested as one of the initiating events in the development of preeclampsia |
686991 |
| 3.5.3.18 | medicine |
plasma asymmetric dimethylarginine/arginine ratios are elevated in children with acute severe malaria compared to 28-day follow-up values and compared to children with uncomplicated malaria or healthy children |
755203 |
| 3.5.3.18 | medicine |
protective effect of probucol on endothelium related to enhancement of DDAH activity |
668175 |
