Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0025202
Disease: melanoma
melanoma 		0.010 Biomarker disease BEFREE Clone 10d/BM28 (CDCL1), an early S-phase protein, is an important growth regulator of melanoma. 9371513 1997
CUI: C0007222
Disease: Cardiovascular Diseases
Cardiovascular Diseases 		0.030 GeneticVariation group BEFREE The discovery of a functional polymorphism within the DDAH2 promoter suggests that there may be common, individual differences in the ability to metabolise ADMA in vivo, that in turn, might underlie susceptibility to cardiovascular disease. 14550280 2003
CUI: C0036983
Disease: Septic Shock
Septic Shock 		0.010 GeneticVariation phenotype LHGDN Septic shock is correlated with asymmetrical dimethyl arginine levels, which may be influenced by a polymorphism in the dimethylarginine dimethylaminohydrolase II gene: a prospective observational study. 17002794 2006
CUI: C0010054
Disease: Coronary Arteriosclerosis
Coronary Arteriosclerosis 		0.330 Biomarker disease CTD_human Role of nitric oxide-producing and -degrading pathways in coronary endothelial dysfunction in chronic kidney disease. 17267746 2007
CUI: C1956346
Disease: Coronary Artery Disease
Coronary Artery Disease 		0.330 Biomarker disease CTD_human Role of nitric oxide-producing and -degrading pathways in coronary endothelial dysfunction in chronic kidney disease. 17267746 2007
CUI: C0856169
Disease: Endothelial dysfunction
Endothelial dysfunction 		0.040 Biomarker phenotype BEFREE In this review, the recent advances in the regulation and function of DDAH enzymes, their roles in the regulation of NO generation, and their possible contribution to endothelial dysfunction in patients with cardiovascular and kidney diseases are discussed. 17933965 2007
CUI: C0022658
Disease: Kidney Diseases
Kidney Diseases 		0.010 Biomarker group BEFREE In this review, the recent advances in the regulation and function of DDAH enzymes, their roles in the regulation of NO generation, and their possible contribution to endothelial dysfunction in patients with cardiovascular and kidney diseases are discussed. 17933965 2007
CUI: C0020538
Disease: Hypertensive disease
Hypertensive disease 		0.030 GeneticVariation group BEFREE The present study indicates that the -1151 A/C and -449 G/C polymorphisms in the DDAH2 promoter region are not related to plasma ADMA levels or measures of cardiac structure and function but are associated with an increased prevalence of hypertension. 19666123 2009
CUI: C0038454
Disease: Cerebrovascular accident
Cerebrovascular accident 		0.010 GeneticVariation group BEFREE No association was observed between the DDAH2 variant and atherothrombotic stroke. 19250061 2009
CUI: C0011860
Disease: Diabetes Mellitus, Non-Insulin-Dependent
Diabetes Mellitus, Non-Insulin-Dependent 		0.040 GeneticVariation disease BEFREE We sought to determine whether serum ADMA levels in type 2 diabetes are influenced by common polymorphisms in the DDAH1 and DDAH2 genes. 20209122 2010
CUI: C0856169
Disease: Endothelial dysfunction
Endothelial dysfunction 		0.040 AlteredExpression phenotype BEFREE DDAH2 overexpression not only improved endothelial dysfunction in diabetic aortas but also attenuated hyperglycemia-induced changes in DDAH/ADMA//NO pathway in endothelial cells. 19775692 2010
CUI: C0011849
Disease: Diabetes Mellitus
Diabetes Mellitus 		0.030 Biomarker group BEFREE The purposes of this study were to determine whether suppressed DDAH2 expression would implicate in endothelial dysfunction associated with diabetes mellitus and further to investigate whether adenovirus-mediated DDAH2 gene overexpression could improve the hyperglycemia-induced endothelial dysfunction. 19775692 2010
CUI: C0020456
Disease: Hyperglycemia
Hyperglycemia 		0.010 AlteredExpression disease BEFREE DDAH2 overexpression not only improved endothelial dysfunction in diabetic aortas but also attenuated hyperglycemia-induced changes in DDAH/ADMA//NO pathway in endothelial cells. 19775692 2010
CUI: C0010054
Disease: Coronary Arteriosclerosis
Coronary Arteriosclerosis 		0.330 GeneticVariation disease BEFREE Association study of dimethylarginine dimethylaminohydrolase 2 gene polymorphisms and coronary heart disease. 22923027 2012
CUI: C1956346
Disease: Coronary Artery Disease
Coronary Artery Disease 		0.330 GeneticVariation disease BEFREE Association study of dimethylarginine dimethylaminohydrolase 2 gene polymorphisms and coronary heart disease. 22923027 2012
CUI: C0032914
Disease: Pre-Eclampsia
Pre-Eclampsia 		0.300 Biomarker phenotype CTD_human In pre-eclampsia, we found only weak correlations between maternal ADMA levels and DDAH 1 (r=-0.41; p=0.22) and DDAH 2 expressions (r=-0.45; p=0.17) but a slightly stronger correlation between DDAH 2 expression and feto-maternal ADMA gradient (r=0.60; p=0.07). 22285683 2012
CUI: C0011860
Disease: Diabetes Mellitus, Non-Insulin-Dependent
Diabetes Mellitus, Non-Insulin-Dependent 		0.040 GeneticVariation disease BEFREE In the present study, we found that SNP rs2272592 in DDAH2 is associated with type 2 diabetes but SNP rs805304 in DDAH2 is not. 22579530 2012
CUI: C0011860
Disease: Diabetes Mellitus, Non-Insulin-Dependent
Diabetes Mellitus, Non-Insulin-Dependent 		0.040 GeneticVariation disease BEFREE Examining data from the DIAGRAM+ (Diabetes Genetics Replication And Meta-analysis), we identified a variant (rs9267551) in the DDAH2 gene nominally associated with type 2 diabetes (P = 3 × 10(-5)). 22558392 2012
CUI: C0856169
Disease: Endothelial dysfunction
Endothelial dysfunction 		0.040 AlteredExpression phenotype BEFREE These results indicate that suppression of DDAH2 expression is a culprit for homocysteine-induced impairments of DDAH/ADMA/NOS/NO pathway in endothelial cells, and therapeutic manipulation of DDAH2 expression may be a promising strategy for preventing endothelial dysfunction and cardiovascular diseases associated with hyperhomocysteinemia. 23171931 2012
CUI: C0007222
Disease: Cardiovascular Diseases
Cardiovascular Diseases 		0.030 AlteredExpression group BEFREE These results indicate that suppression of DDAH2 expression is a culprit for homocysteine-induced impairments of DDAH/ADMA/NOS/NO pathway in endothelial cells, and therapeutic manipulation of DDAH2 expression may be a promising strategy for preventing endothelial dysfunction and cardiovascular diseases associated with hyperhomocysteinemia. 23171931 2012
CUI: C0010068
Disease: Coronary heart disease
Coronary heart disease 		0.030 GeneticVariation disease BEFREE Association study of dimethylarginine dimethylaminohydrolase 2 gene polymorphisms and coronary heart disease. 22923027 2012
CUI: C0020538
Disease: Hypertensive disease
Hypertensive disease 		0.030 GeneticVariation group BEFREE Both SNP rs805304 and rs2272592 in DDAH2 were not significantly associated with hypertension. 22579530 2012
CUI: C0036690
Disease: Septicemia
Septicemia 		0.020 GeneticVariation disease BEFREE We sought to determine whether functional polymorphisms in DDAH2, which metabolizes the NO synthase inhibitor asymmetric dimethylarginine (ADMA), are associated with susceptibility to sepsis, plasma ADMA, distinct hemodynamic states, and vasopressor requirements in pediatric septic shock. 22428028 2012
CUI: C0243026
Disease: Sepsis
Sepsis 		0.020 GeneticVariation disease BEFREE We sought to determine whether functional polymorphisms in DDAH2, which metabolizes the NO synthase inhibitor asymmetric dimethylarginine (ADMA), are associated with susceptibility to sepsis, plasma ADMA, distinct hemodynamic states, and vasopressor requirements in pediatric septic shock. 22428028 2012
CUI: C0011854
Disease: Diabetes Mellitus, Insulin-Dependent
Diabetes Mellitus, Insulin-Dependent 		0.010 GeneticVariation disease BEFREE We found limited evidence that genetic polymorphisms in DDAH genes influence serum ADMA levels in individuals with T1DM. 22521321 2012