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DDAH1 belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family. Additionally we are shipping DDAH1 Proteins (16) and DDAH1 Kits (10) and many more products for this protein.
Showing 10 out of 64 products:
Chicken Polyclonal DDAH1 Primary Antibody for IHC, WB - ABIN2785923
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
Show all 2 references for ABIN2785923
Chicken Polyclonal DDAH1 Primary Antibody for IHC, WB - ABIN2785922
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
Show all 2 references for ABIN2785922
Cow (Bovine) Polyclonal DDAH1 Primary Antibody for WB - ABIN374149
Kimoto, Miyatake, Sasagawa, Yamashita, Okita, Oka, Ogawa, Tsuji: Purification, cDNA cloning and expression of human NG,NG-dimethylarginine dimethylaminohydrolase. in European journal of biochemistry / FEBS 1999
Human Polyclonal DDAH1 Primary Antibody for FACS, IF - ABIN389434
Ellger, Richir, van Leeuwen, Debaveye, Langouche, Vanhorebeek, Teerlink, Van den Berghe: Glycemic control modulates arginine and asymmetrical-dimethylarginine levels during critical illness by preserving dimethylarginine-dimethylaminohydrolase activity. in Endocrinology 2008
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.
increased ADMA levels in rheumatoid arthritis do not appear to relate to DDAH (show DDAH2 Antibodies) genetic polymorphisms
DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis.
the advanced glycation end products-receptor (show AGER Antibodies) for advanced glycation end products-mediated reactive oxygen species generation could be involved in endothelial dysfunction in diabetic end-stage renal disease patients
DDAH1 genotypes were closely related to asymmetric dimethylarginine levels, but not to measures of endothelium-dependent vasodilation in an elderly population.
Only the DDAH1-V1 transcript is responsible for ADMA metabolism, and transcript specific primers are recommended to determine DDAH1 mRNA expression.
Data suggest that estradiol alone has no effect on DDAH (show DDAH2 Antibodies)/asymmetric dimethylarginine/nitric oxide pathway in arterial endothelium, but rather counters oxidized LDL; estradiol restores DDAH (show DDAH2 Antibodies) activity and prevents loss of eNOS (show NOS3 Antibodies) (nitric oxide synthase (show NOS Antibodies) 3).
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.
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 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.
Data show that DDAH (show DDAH2 Antibodies) inhibition reduces fibroblast-induced collagen deposition in an ADMA-independent manner and reduces abnormal epithelial proliferation in an ADMA-dependent manner.
Indicate that DDAH1 is required for metabolizing asymmetrical dimethylarginine and N(omega)-monomethyl-L-arginine (show GATM Antibodies).
DDAH1 exerts a unique role in activating Akt (show AKT1 Antibodies) that affects endothelial function independently of degrading endogenous nitirc oxide synthase inhibitors.
overexpression of DDAH1 reduces plaque formation in ApoE (show APOE Antibodies)(-/-) mice by lowering ADMA
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.
dimethylarginine dimethylaminohydrolase 1
, N(G),N(G)-dimethylarginine dimethylaminohydrolase 1
, NG, NG-dimethylarginine dimethylaminohydrolase
, NG,NG dimethylarginine dimethylaminohydrolase