Dimethylarginine Dimethylaminohydrolase 2 (DDAH2) ELISA Kits

Human Dimethylarginine Dimethylaminohydrolase 2 (DDAH2) interaction partners

1. genetic variations in the DDAH2 gene may influence the ADMA concentration and erythropoietin resistance in MHD patients

2. 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.

3. Exogenous human DDAH2 gene promotes differentiation of rabbit bone marrow-derived endothelial progenitor cells into mature endothelial cells.

4. expression of DDAH2 is associated with invasiveness of lung adenocarcinoma via tumor angiogenesis

5. Inhibiting the expression of DDAH1, but not DDAH2, resulted in a significant increase in the sensitivity of the EVT cell line SGHPL-4 to tumour necrosis factor related apoptosis inducing ligand (TRAIL) induced apoptosis

6. increased ADMA levels in rheumatoid arthritis do not appear to relate to DDAH genetic polymorphisms

7. 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.

8. DDAH-1 is a specific molecular target for portal pressure reduction, through actions on ADMA-mediated regulation of eNOS activity.

9. 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.

10. Homocysteine disrupts EPCs function via inducing the hypermethylation of DDAH2 promoter, suggesting a key role of epigenetic mechanism in the progression of atherosclerosis

11. -476 to -469 of the DDAH2 promoter was a NF-kB responsive element and is important for the transactivation of DDAH2.

12. The rs9267551 functional variant of the DDAH2 gene is associated with chronic kidney disease with carriers of the C allele having a lower risk of renal dysfunction independently from several confounders

13. Our approaches revealed signature candidates of differentially hypermethylated genes of DDAH2 and DUSP1 which can be further developed as potential biomarkers for OSCC as diagnostic, prognostic and therapeutic targets in the future.

14. Enhancing pulmonary DDAH II activity attenuates LPS-mediated lung leak in acute lung injury.

15. There is a significant difference in distribution of DDAH2 gene polymorphism among hemodialysis patients compared to healthy individuals.

16. DDAH2-1151 A/C polymorphism is associated with Chronic renal impairment in type 2 diabetes.

17. Glucose-stimulated insulin secretion is increased in Ddah2-transgenic pancreatic islets by 33%, compared to its levels in wild-type mice.

18. Suppression of DDAH2 expression is a culprit for homocysteine-induced impairments of DDAH/ADMA/NOS/NO pathway in endothelial cells.

19. Found that SNP rs2272592 in DDAH2 is associated with type 2 diabetes but SNP rs805304 in DDAH2 is not. DDAH2 SNP rs2272592 AG+GG genotypes are associated with genetic susceptibility to type 2 diabetes in Korean population.

20. No association was observed between the DDAH2 polymorphisms at rs805305 and rs2272592 and coronary heart disease.

Mouse (Murine) Dimethylarginine Dimethylaminohydrolase 2 (DDAH2) interaction partners

1. the overexpression of DDAH2 attenuates myocardial fibrosis and protects against Diabetic cardiomyopathy DCM through activation of the DDAH/ADMA/NOS/NO pathway

2. We conclude that pp60(Src) can directly inhibit DDAH II and this is involved in the increased ADMA levels that enhance eNOS uncoupling during the development of acute lung injury (ALI).

3. In mild CKD, dysregulation of the ADMA/DDAH pathway in adipose tissue triggers lipodystrophy-like phenotype changes, including ectopic fat depositions.

4. The Sirt1/DDAH2/secretagogin pathway is a novel regulator of glucose-stimulated insulin secretion.

5. DDAH2/ADMA pathway can be a novel therapeutic target for vasculopathy in the ADMA or angiotensin II-induced pathophysiological conditions

6. Report tissue-specific downregulation of DDAH2 in hyperhomocysteinemia.

7. Results show that asymmetric methylarginine increases pulmonary endothelial permeability, and that its effects on permeability, Rac1 activation and VASP phosphorylation are prevented by overexpression of active DDAHI and DDAHII.

8. ADMA and nitrosative stress are related to increased expression of protein-arginine methyltransferase-2, an ADMA-synthesizing enzyme, and reduced expression of dimethylarginine dimethylaminohydrolase-2, an ADMA-degrading enzyme, in bronchial epithelia