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DDAH2 belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family.
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genetic variations in the DDAH2 gene may influence the ADMA concentration and erythropoietin (show EPO ELISA Kits) resistance in MHD patients
The main finding from this study was that it demonstrated that the C-allele of rs3087894 in DDAH1 is a risk factor for hypertension in the Kazakh group but a protective factor in the Uygur group. In addition, we did not find any genotype of DDAH1 and DDAH2 associated with hypertension in the Han group.
Exogenous human DDAH2 gene promotes differentiation of rabbit bone marrow-derived endothelial progenitor cells into mature endothelial cells.
expression of DDAH2 is associated with invasiveness of lung adenocarcinoma via tumor angiogenesis
Inhibiting the expression of DDAH1 (show DDAH1 ELISA Kits), but not DDAH2, resulted in a significant increase in the sensitivity of the EVT cell line SGHPL-4 to tumour necrosis factor (show TNF ELISA Kits) related apoptosis inducing ligand (TRAIL) induced apoptosis
increased ADMA levels in rheumatoid arthritis do not appear to relate to DDAH genetic polymorphisms
The percentage of senescent endothelial progenitor cells increased while the expression of DDAH2 decreased concomitantly with an increase in the plasma levels of asymmetric dimethylarginine in patients with type 2 diabetes mellitus.
DDAH-1 (show DDAH1 ELISA Kits) is a specific molecular target for portal pressure reduction, through actions on ADMA-mediated regulation of eNOS (show NOS3 ELISA Kits) activity.
Our results suggest that the rs805304 C allele of the DDAH gene was associated with decreased risk of myocardial infarction and decreased risk of obesity.
Homocysteine disrupts EPCs function via inducing the hypermethylation of DDAH2 promoter, suggesting a key role of epigenetic mechanism in the progression of atherosclerosis
We conclude that pp60(Src (show SRC ELISA Kits)) can directly inhibit DDAH II and this is involved in the increased ADMA levels that enhance eNOS (show NOS3 ELISA Kits) uncoupling during the development of acute lung injury (ALI).
In mild CKD, dysregulation of the ADMA/DDAH pathway in adipose tissue triggers lipodystrophy-like phenotype changes, including ectopic fat depositions.
The Sirt1 (show SIRT1 ELISA Kits)/DDAH2/secretagogin (show SCGN ELISA Kits) pathway is a novel regulator of glucose-stimulated insulin (show INS ELISA Kits) secretion.
DDAH2/ADMA pathway can be a novel therapeutic target for vasculopathy in the ADMA or angiotensin II-induced pathophysiological conditions
Report tissue-specific downregulation of DDAH2 in hyperhomocysteinemia.
Results show that asymmetric methylarginine increases pulmonary endothelial permeability, and that its effects on permeability, Rac1 activation and VASP (show VASP ELISA Kits) phosphorylation are prevented by overexpression of active DDAHI (show DDAH1 ELISA Kits) and DDAHII.
ADMA and nitrosative stress are related to increased expression of protein-arginine methyltransferase-2 (show PRMT2 ELISA Kits), an ADMA-synthesizing enzyme, and reduced expression of dimethylarginine dimethylaminohydrolase-2, an ADMA-degrading enzyme, in bronchial epithelia
This gene belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family. The encoded enzyme plays a role in nitric oxide generation by regulating cellular concentrations of methylarginines, which in turn inhibit nitric oxide synthase activity.
NG,NG-dimethylarginine dimethylaminohydrolase 2
, dimethylarginine dimethylaminohydrolase 2
, N(G),N(G)-dimethylarginine dimethylaminohydrolase 2
, NG-dimethylarginine dimethylamino hydrolase homolog
, S-phase protein
, alternative name: NG30, G6a
, dimethylarginine dimethylaminohydrolase II
, protein G6a
, Clone 7u