EC Number   |
Application |
Reference |
|---|
   3.5.3.18 | analysis |
use of inhibitor N-(but-3-yn-1-yl)-2-chloroethanimidamide as a broad-specificity probe for labeling endogenous DDAH isoforms and enzymes with similar pharmacophores. Inhibitor labels the active fraction of DDAH-1 in intact mammalian cells and can be blocked by the presence of competitive reversible and irreversible inhibitors. Incorporation of the alkyne tag allows to derivatize with a variety of reagents after in vivo tagging |
712238 |
| 3.5.3.18 | medicine |
2-chloroacetamidine may potentially find wide applicability as a general pharmacophore, useful in delineating characteristics of the amidinotransferase superfamily |
664074 |
| 3.5.3.18 | medicine |
DDAH activity and elevated endogenous asymmetric dimethylarginine is implicated in endothelial dysfunction exposed to glycosylated bovine serum albumin, aminoguanidine can protect endothelium against injury induced by glycosylated bovine serum albumin both in vitro and in vivo |
667365 |
| 3.5.3.18 | medicine |
DDAH influences insulin sensitivity by regulating the endogenous nitric oxide synthase inhibitor asymmetrical dimethylarginine |
695944 |
| 3.5.3.18 | medicine |
decreased DDAH-1 expression may cause accumulation of endogenous inhibitors of enothelial NO synthase, thereby contributing to endothelial dysfunction in the failing heart |
667155 |
| 3.5.3.18 | medicine |
endogenous nitric oxide synthase inhibitor asymmetrical dimethylarginine (hydrolyzed by DDAH) is elevated in many patients and may contribute to the initiation and progression of their disease |
667159 |
| 3.5.3.18 | medicine |
epoetin beta and darbepoetin alpha posttranslationally impair DDAH activity via increased oxidative stress, causing NG,NG-dimethyl-L-arginine as an important cardiovascular risk factor to accumulate and inhibit NO-synthesis |
669059 |
| 3.5.3.18 | medicine |
expression and secretion of the vascular endothelial growth factor is not increased in DDAH1-transfected cells |
667355 |
| 3.5.3.18 | medicine |
global knockout of Ddah2 results in elevated blood pressure during periods of activity and changes in vascular responsiveness mediated by changes in methylarginine concentration, and systemic nitric oxide concentrations. In a model of severe polymicrobial sepsis, Ddah2 knockout affects outcome. Monocyte-specific deletion of Ddah2 results in a similar pattern of increased severity to that seen in globally deficient animals |
752613 |
| 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 |
