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DDAH1 belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family. Zusätzlich bieten wir Ihnen DDAH1 Kits (15) und DDAH1 Proteine (13) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 79 products:
Human Polyclonal DDAH1 Primary Antibody für 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
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Cow (Bovine) Polyclonal DDAH1 Primary Antibody für 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 für 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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Human Polyclonal DDAH1 Primary Antibody für 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
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 (zeige SQSTM1 Antikörper) by aging or diabetes.
Results confirmed DDAH1 3'-UTR (zeige UTS2R Antikörper) as a target for miR (zeige MLXIP Antikörper)-21, and endogenous miR (zeige MLXIP Antikörper)-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 (zeige MLXIP Antikörper)-21 may regulate renal fibrosis by the Wnt (zeige WNT2 Antikörper) pathway via directly targeting DDAH1
The most significant associations were detected for PECAM1 (zeige PECAM1 Antikörper)*V/V + DDAH1*C (OR = 4.17 CI 1.56-11.15 Pperm = 0.005)
FoxO1 (zeige FOXO1 Antikörper) regulates asymmetric dimethylarginine via downregulation of dimethylaminohydrolase 1 in HUVECs and subjects with carotid atherosclerosis.
Inhibiting the expression of DDAH1, but not DDAH2 (zeige DDAH2 Antikörper), resulted in a significant increase in the sensitivity of the EVT cell line SGHPL-4 to tumour necrosis factor (zeige TNF Antikörper) 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 (zeige TSC2 Antikörper) 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 (zeige MLXIP Antikörper)-21-dependent pathway.
In mild CKD, dysregulation of the ADMA/DDAH (zeige DDAH2 Antikörper) 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 (zeige DDAH2 Antikörper) 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 (zeige APOE Antikörper)-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 (zeige DNAJC5 Antikörper)-S-nitrosylation.
High-resolution crystal structures of DDAH (zeige DDAH2 Antikörper) 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 (zeige DDAH2 Antikörper) 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