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DDAH1 belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family. Additionally we are shipping DDAH1 Kits (15) and DDAH1 Proteins (13) and many more products for this protein.
Showing 10 out of 79 products:
Human Polyclonal DDAH1 Primary Antibody for ELISA, WB - ABIN268699
Pullamsetti, Kiss, Ghofrani, Voswinckel, Haredza, Klepetko, Aigner, Fink, Muyal, Weissmann, Grimminger, Seeger, Schermuly: Increased levels and reduced catabolism of asymmetric and symmetric dimethylarginines in pulmonary hypertension. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2005
Show all 2 Pubmed References
Human Polyclonal DDAH1 Primary Antibody for ICC, IF - ABIN4305227
Shao, Wang, Shrestha, Thakur, Borowski, Sweet, Thomas, Moravec, Hazen, Tang: Pulmonary hypertension associated with advanced systolic heart failure: dysregulated arginine metabolism and importance of compensatory dimethylarginine dimethylaminohydrolase-1. in Journal of the American College of Cardiology 2012
Cow (Bovine) Polyclonal DDAH1 Primary Antibody for IHC, WB - ABIN2785922
Deer, Krames, Hassenbusch, Burton, Caraway, Dupen, Eisenach, Erdek, Grigsby, Kim, Levy, McDowell, Mekhail, Panchal, Prager, Rauck, Saulino, Sitzman, Staats, Stanton-Hicks, Stearns, Dean Willis, Witt, Follett, Huntoon, Liem, Rathmell, Wallace, Buchser, Cou: Management of Intrathecal Catheter-Tip Inflammatory Masses: An Updated 2007 Consensus Statement From An Expert Panel. in Neuromodulation : journal of the International Neuromodulation Society 2011
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Cow (Bovine) Polyclonal DDAH1 Primary Antibody for IHC, WB - ABIN2785923
Kim, Park, Park, Jung, Pang, Ryu, Lee, Eom, Park: No association of the genetic polymorphisms of endothelial nitric oxide synthase, dimethylarginine dimethylaminohydrolase, and vascular endothelial growth factor with preeclampsia in Korean populations. in Twin research and human genetics : the official journal of the International Society for Twin Studies 2008
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Data demonstrate that DDAH1 deficiency promotes the epithelial to mesenchymal transition in renal proximal tubular epithelial cells and causes fibrosis, and oxidative stress in aging and diabetic kidneys. The study provides the first direct evidence that the DDAH1 has a marked effect on kidney fibrosis and oxidative stress induced (show SQSTM1 Antibodies) by aging or diabetes.
Results confirmed DDAH1 3'-UTR (show UTS2R Antibodies) as a target for miR (show MLXIP Antibodies)-21, and endogenous miR (show MLXIP Antibodies)-21 showed increased inhibitory effect on DDAH1-V3 transcript.
Inflammatory factors expressed in response to myocardial ischemia contributed to up-regulation of DDAH1.
DDAH1 plays dual roles in a particular matter-induced cell death in alveolar epithelial cells.
rs3087894 in DDAH1 was significantly associated with hypertension and showed conflicting results in different ethnic groups. This is therefore a candidate for further studies with the aim of helping to ascertain the mechanisms of hypertension in different populations.
results suggest that miR (show MLXIP Antibodies)-21 may regulate renal fibrosis by the Wnt (show WNT2 Antibodies) pathway via directly targeting DDAH1
The most significant associations were detected for PECAM1 (show PECAM1 Antibodies)*V/V + DDAH1*C (OR = 4.17 CI 1.56-11.15 Pperm = 0.005)
FoxO1 (show FOXO1 Antibodies) regulates asymmetric dimethylarginine via downregulation of dimethylaminohydrolase 1 in HUVECs and subjects with carotid atherosclerosis.
Inhibiting the expression of DDAH1, but not DDAH2 (show DDAH2 Antibodies), resulted in a significant increase in the sensitivity of the EVT cell line SGHPL-4 to tumour necrosis factor (show TNF Antibodies) related apoptosis inducing ligand (TRAIL) induced apoptosis
Genebased analyses revealed associations of the DDAH1 gene with longitudinal Blood Pressure phenotypes, associations with essential hypertension, Blood Pressure salt sensitivity, preeclampsia, or preclinical stages of atherosclerosis.
the ADMA/DDAH1 pathway has a marked effect on hepatic lipogenesis and steatosis induced by HFD feeding. Our findings suggest that strategies to increase DDAH1 activity in hepatocytes may provide a novel approach to attenuate NAFLD (show TSC2 Antibodies) development.
A time-dependent decrease in serum and tissue ADMA and increase in mRNA expression of DDAH-1 and PRMT-1 as well as higher rates of mRNA expression of CAT-1 and lower rates of CAT-2A and CAT-2B were found after 8-week MCD diet.
our results suggest that DDAH1 not only acts as an enzyme degrading ADMA but also controls cellular oxidative stress and apoptosis via a miR (show MLXIP Antibodies)-21-dependent pathway.
In mild CKD, dysregulation of the ADMA/DDAH (show DDAH2 Antibodies) pathway in adipose tissue triggers lipodystrophy-like phenotype changes, including ectopic fat depositions.
Endothelial deletion of DDAH1 profoundly impairs the angiogenic capacity of endothelial cells.
Our findings suggest that decreased expression of DDAH1 and DDAH2 (show DDAH2 Antibodies) in the lungs may contribute to allergic asthma and overexpression of DDAH1 attenuates allergen-induced airway inflammation through modulation of Th2 responses.
Overexpression of the ADMA degrading enzyme, DDAH1, did not ameliorate atherosclerosis in ApoE (show APOE Antibodies)-deficient subtotally nephrectomized mice.
DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis.
DDAH1 overexpression selectively decreased the sustained phase of hypoxic pulmonary vasoconstriction, partly via activation of the NO-cGMP pathway.
Pharmacological and genetic reduction of DDAH1 activity is protective against the vascular changes observed during endotoxic shock.
dimethylargininase-1 inhibited upon specific Cys (show DNAJC5 Antibodies)-S-nitrosylation.
High-resolution crystal structures of DDAH (show DDAH2 Antibodies) isoform 1 was presented.
Demonstrate a critical role for DDAH-1 and endogenous methylarginines in the pathogenesis of endothelial dysfunction.
DDAH-1 and DDAH-2 (show DDAH2 Antibodies) manifest their effects through different mechanisms, the former of which is largely ADMA-dependent and the latter ADMA-independent.
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.
, N(G),N(G)-dimethylarginine dimethylaminohydrolase 1
, NG, NG-dimethylarginine dimethylaminohydrolase
, NG,NG dimethylarginine dimethylaminohydrolase
, dimethylarginine dimethylaminohydrolase 1