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DDAH1 belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family. Additionally we are shipping DDAH1 Antibodies (79) and DDAH1 Proteins (13) and many more products for this protein.
Showing 4 out of 15 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
Human DDAH1 ELISA Kit for Sandwich ELISA - ABIN419628
El Assar, Angulo, Santos-Ruiz, Ruiz de Adana, Pindado, Sánchez-Ferrer, Hernández, Rodríguez-Mañas: Asymmetric dimethylarginine (ADMA) elevation and arginase up-regulation contribute to endothelial dysfunction related to insulin resistance in rats and morbidly obese humans. in The Journal of physiology 2016
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 ELISA Kits) by aging or diabetes.
Results confirmed DDAH1 3'-UTR (show UTS2R ELISA Kits) as a target for miR (show MLXIP ELISA Kits)-21, and endogenous miR (show MLXIP ELISA Kits)-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 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, 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
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 ELISA Kits) 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 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 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 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.
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