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DDAH1 belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family. Additionally we are shipping DDAH1 Antibodies (69) and DDAH1 Proteins (16) and many more products for this protein.
Showing 4 out of 11 products:
Rat (Rattus) DDAH1 ELISA Kit for Sandwich ELISA - ABIN858752
Ferrigno, Rizzo, Bianchi, Di Pasqua, Berardo, Richelmi, Vairetti: Changes in ADMA/DDAH pathway after hepatic ischemia/reperfusion injury in rats: the role of bile. in BioMed research international 2014
results suggest that miR (show MLXIP ELISA Kits)-21 may regulate renal fibrosis by the Wnt (show WNT2 ELISA Kits) pathway via directly targeting DDAH1
The most significant associations were detected for PECAM1 (show PECAM1 ELISA Kits)*V/V + DDAH1*C (OR = 4.17 CI 1.56-11.15 Pperm = 0.005)
FoxO1 (show FOXO1 ELISA Kits) 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 ELISA Kits), 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
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 ELISA Kits) genetic polymorphisms
DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis.
the advanced glycation end products-receptor (show AGER ELISA Kits) 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.
dimethylargininase-1 inhibited upon specific Cys (show DNAJC5 ELISA Kits)-S-nitrosylation.
High-resolution crystal structures of DDAH (show DDAH2 ELISA Kits) 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 ELISA Kits) manifest their effects through different mechanisms, the former of which is largely ADMA-dependent and the latter ADMA-independent.
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 ELISA Kits)-21-dependent pathway.
In mild CKD, dysregulation of the ADMA/DDAH (show DDAH2 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)-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 ELISA Kits) inhibition reduces fibroblast-induced collagen deposition in an ADMA-independent manner and reduces abnormal epithelial proliferation in an ADMA-dependent manner.
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