Dimethylarginine Dimethylaminohydrolase 1 (DDAH1) ELISA Kits

DDAH1 belongs to the dimethylarginine dimethylaminohydrolase (DDAH) gene family. Additionally we are shipping DDAH1 Antibodies (90) and DDAH1 Proteins (13) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
DDAH1 23576 O94760
DDAH1 64157 O08557
DDAH1 69219 Q9CWS0
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Top DDAH1 ELISA Kits at antibodies-online.com

Showing 4 out of 18 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Supplier Delivery Price Details
Human 0.056 ng/mL 0.15 ng/mL - 10 ng/mL 96 Tests Log in to see 13 to 16 Days
Rat 9.75 pg/mL 39-2500 pg/mL Typical standard curve 96 Tests Log in to see 15 to 18 Days
Mouse < 0.086 ng/mL 0.156 ng/mL - 10 ng/mL   96 Tests Log in to see 11 to 18 Days
  96 Tests Log in to see 15 to 18 Days

Top referenced DDAH1 ELISA Kits

  1. 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 (PubMed)

  2. 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 (PubMed)

More ELISA Kits for DDAH1 Interaction Partners

Human Dimethylarginine Dimethylaminohydrolase 1 (DDAH1) interaction partners

  1. MiR-21-mediated DDAH1/ADMA/NO signal pathway.

  2. DDAH-1 expression is associated with promotion of angiogenesis stimulating factor VEGF.

  3. These findings suggest that DDAH1 functions as a tumor suppressor in gastric cancer (GC) and may be exploited as a diagnostic and prognostic biomarker for GC.

  4. 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 by aging or diabetes.

  5. Results confirmed DDAH1 3'-UTR as a target for miR-21, and endogenous miR-21 showed increased inhibitory effect on DDAH1-V3 transcript.

  6. Inflammatory factors expressed in response to myocardial ischemia contributed to up-regulation of DDAH1.

  7. DDAH1 plays dual roles in a particular matter-induced cell death in alveolar epithelial cells.

  8. 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.

  9. wild-type rs480414 was 92% sensitive and 53% specific for pulmonary hypertension in bronchopulmonary dysplasia

  10. results suggest that miR-21 may regulate renal fibrosis by the Wnt pathway via directly targeting DDAH1

  11. The most significant associations were detected for PECAM1*V/V + DDAH1*C (OR = 4.17 CI 1.56-11.15 Pperm = 0.005)

  12. FoxO1 regulates asymmetric dimethylarginine via downregulation of dimethylaminohydrolase 1 in HUVECs and subjects with carotid atherosclerosis.

  13. 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

  14. 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.

  15. increased ADMA levels in rheumatoid arthritis do not appear to relate to DDAH genetic polymorphisms

  16. DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis.

  17. the advanced glycation end products-receptor for advanced glycation end products-mediated reactive oxygen species generation could be involved in endothelial dysfunction in diabetic end-stage renal disease patients

  18. DDAH1 genotypes were closely related to asymmetric dimethylarginine levels, but not to measures of endothelium-dependent vasodilation in an elderly population.

  19. Only the DDAH1-V1 transcript is responsible for ADMA metabolism, and transcript specific primers are recommended to determine DDAH1 mRNA expression.

  20. Elevated asymmetric dimethylaginine is not a part of the proatherogenic risk profile in the young adult offspring of patients with premature Coronary artery disease.

Mouse (Murine) Dimethylarginine Dimethylaminohydrolase 1 (DDAH1) interaction partners

  1. DDAH1 in cardiomyocytes plays a vital role in attenuating left ventricular remodeling after acute myocardial infarction by regulating intracellular ROS levels and apoptosis sensitivity via a SOD2-dependent pathway.

  2. Cardiomyocyte DDAH1 activity is dispensable for cardiac function under basal conditions, but plays an important role in attenuating cardiac hypertrophy and ventricular remodeling under stress conditions, possibly through locally confined regulation of subcellular ADMA and NO signaling.

  3. 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 development.

  4. 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.

  5. our results suggest that DDAH1 not only acts as an enzyme degrading ADMA but also controls cellular oxidative stress and apoptosis via a miR-21-dependent pathway.

  6. In mild CKD, dysregulation of the ADMA/DDAH pathway in adipose tissue triggers lipodystrophy-like phenotype changes, including ectopic fat depositions.

  7. transgenic mice display attenuated cigarette smoke-induced lung inflammation

  8. Endothelial deletion of DDAH1 profoundly impairs the angiogenic capacity of endothelial cells.

  9. Our findings suggest that decreased expression of DDAH1 and DDAH2 in the lungs may contribute to allergic asthma and overexpression of DDAH1 attenuates allergen-induced airway inflammation through modulation of Th2 responses.

  10. Overexpression of the ADMA degrading enzyme, DDAH1, did not ameliorate atherosclerosis in ApoE-deficient subtotally nephrectomized mice.

  11. DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis.

  12. DDAH1 overexpression selectively decreased the sustained phase of hypoxic pulmonary vasoconstriction, partly via activation of the NO-cGMP pathway.

  13. Pharmacological and genetic reduction of DDAH1 activity is protective against the vascular changes observed during endotoxic shock.

  14. Data show that DDAH inhibition reduces fibroblast-induced collagen deposition in an ADMA-independent manner and reduces abnormal epithelial proliferation in an ADMA-dependent manner.

  15. Indicate that DDAH1 is required for metabolizing asymmetrical dimethylarginine and N(omega)-monomethyl-L-arginine.

  16. DDAH1 exerts a unique role in activating Akt that affects endothelial function independently of degrading endogenous nitirc oxide synthase inhibitors.

  17. overexpression of DDAH1 reduces plaque formation in ApoE(-/-) mice by lowering ADMA

  18. Dimethylarginine dimethylaminohydrolase-1 transgenic mice are not protected from ischemic stroke

  19. Overexpression of DDAH-1 increases basal levels of vascular NO and protects against ADMA-induced endothelial dysfunction in the cerebral circulation.

  20. Report tissue-specific downregulation of DDAH1 in hyperhomocysteinemia.

Cow (Bovine) Dimethylarginine Dimethylaminohydrolase 1 (DDAH1) interaction partners

  1. dimethylargininase-1 inhibited upon specific Cys-S-nitrosylation.

  2. High-resolution crystal structures of DDAH isoform 1 was presented.

  3. Demonstrate a critical role for DDAH-1 and endogenous methylarginines in the pathogenesis of endothelial dysfunction.

  4. DDAH-1 and DDAH-2 manifest their effects through different mechanisms, the former of which is largely ADMA-dependent and the latter ADMA-independent.

DDAH1 Antigen Profile

Antigen Summary

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.

Gene names and symbols associated with DDAH1

  • dimethylarginine dimethylaminohydrolase 1 (DDAH1) antibody
  • dimethylarginine dimethylaminohydrolase 1 (Ddah1) antibody
  • dimethylarginine dimethylaminohydrolase 1 L homeolog (ddah1.L) antibody
  • dimethylarginine dimethylaminohydrolase 1 (ddah1) antibody
  • 2410006N07Rik antibody
  • 2510015N06Rik antibody
  • AI987801 antibody
  • AW050362 antibody
  • DDAH antibody
  • DDAH1 antibody
  • wu:fc30c11 antibody
  • zgc:85829 antibody

Protein level used designations for DDAH1

DDAH-1 , DDAHI , N(G),N(G)-dimethylarginine dimethylaminohydrolase 1 , NG, NG-dimethylarginine dimethylaminohydrolase , dimethylargininase-1 , NG,NG dimethylarginine dimethylaminohydrolase , dimethylarginine dimethylaminohydrolase 1 , fc30c11

23576 Homo sapiens
64157 Rattus norvegicus
69219 Mus musculus
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380577 Xenopus laevis
537391 Bos taurus
711395 Macaca mulatta
736613 Pan troglodytes
100145661 Xenopus (Silurana) tropicalis
100339913 Oryctolagus cuniculus
490182 Canis lupus familiaris
100153814 Sus scrofa
406561 Danio rerio
100729503 Cavia porcellus
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