Recombinant Human N (G),N (G)-dimethylarginine dimethylaminohydrolase 1 (DDAH1)

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Code CSB-EP006579HU
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Purity
Greater than 85% as determined by SDS-PAGE.
Target Names
DDAH1
Uniprot No.
Research Area
Cardiovascular
Alternative Names
DDAH; DDAH I; DDAH-1; DDAH1; DDAH1_HUMAN; DDAHI; Dimethylargininase 1; Dimethylargininase-1; Dimethylarginine dimethylaminohydrolase 1; N(G); N(G)-dimethylarginine dimethylaminohydrolase 1; NG NG dimethylarginine dimethylaminohydrolase
Species
Homo sapiens (Human)
Source
E.coli
Expression Region
2-285aa
Target Protein Sequence
AGLGHPAAFGRATHAVVRALPESLGQHALRSAKGEEVDVARAERQHQLYVGVLGSKLGLQVVELPADESLPDCVFVEDVAVVCEETALITRPGAPSRRKEVDMMKEALEKLQLNIVEMKDENATLDGGDVLFTGREFFVGLSKRTNQRGAEILADTFKDYAVSTVPVADGLHLKSFCSMAGPNLIAIGSSESAQKALKIMQQMSDHRYDKLTVPDDIAANCIYLNIPNKGHVLLHRTPEEYPESAKVYEKLKDHMLIPVSMSELEKVDGLLTCCSVLINKKVDS
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
38.4 kDa
Protein Length
Full Length of Mature Protein
Tag Info
N-terminal 10xHis-tagged and C-terminal Myc-tagged
Form
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer
Tris-based buffer,50% glycerol
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

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Target Background

Function
Hydrolyzes N(G),N(G)-dimethyl-L-arginine (ADMA) and N(G)-monomethyl-L-arginine (MMA) which act as inhibitors of NOS. Has therefore a role in the regulation of nitric oxide generation.
Gene References into Functions
  1. MiR-21-mediated DDAH1/ADMA/NO signal pathway. PMID: 29682517
  2. DDAH-1 expression is associated with promotion of angiogenesis stimulating factor VEGF. PMID: 28741166
  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. PMID: 28580735
  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. PMID: 28594240
  5. Results confirmed DDAH1 3'-UTR as a target for miR-21, and endogenous miR-21 showed increased inhibitory effect on DDAH1-V3 transcript. PMID: 27663503
  6. Inflammatory factors expressed in response to myocardial ischemia contributed to up-regulation of DDAH1. PMID: 28145161
  7. DDAH1 plays dual roles in a particular matter-induced cell death in alveolar epithelial cells. PMID: 26996393
  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. PMID: 26786611
  9. wild-type rs480414 was 92% sensitive and 53% specific for pulmonary hypertension in bronchopulmonary dysplasia PMID: 26663142
  10. results suggest that miR-21 may regulate renal fibrosis by the Wnt pathway via directly targeting DDAH1 PMID: 26455824
  11. The most significant associations were detected for PECAM1*V/V + DDAH1*C (OR = 4.17 CI 1.56-11.15 Pperm = 0.005) PMID: 26662939
  12. FoxO1 regulates asymmetric dimethylarginine via downregulation of dimethylaminohydrolase 1 in HUVECs and subjects with carotid atherosclerosis. PMID: 26226438
  13. 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. PMID: 25424718
  14. DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis. PMID: 24260221
  15. 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 PMID: 23766377
  16. DDAH1 genotypes were closely related to asymmetric dimethylarginine levels, but not to measures of endothelium-dependent vasodilation in an elderly population. PMID: 23892448
  17. Only the DDAH1-V1 transcript is responsible for ADMA metabolism, and transcript specific primers are recommended to determine DDAH1 mRNA expression. PMID: 23864585
  18. Elevated asymmetric dimethylaginine is not a part of the proatherogenic risk profile in the young adult offspring of patients with premature Coronary artery disease. PMID: 23022711
  19. A significant decrease in asymmetric dimethylarginine levels was found in ex-extremely low birth weight young adults compared to term birth weight young adults. PMID: 21420186
  20. Data suggest that estradiol alone has no effect on DDAH/asymmetric dimethylarginine/nitric oxide pathway in arterial endothelium, but rather counters oxidized LDL; estradiol restores DDAH activity and prevents loss of eNOS (nitric oxide synthase 3). PMID: 22982060
  21. DDAH1 gene DNA methylation is impoetant in the pathogenesis of idiopathic pulmonary fibrosis. PMID: 22700861
  22. Genetic polymorphisms in DDAH genes influence serum ADMA levels in individuals with T1 diabetes mellitus. PMID: 22521321
  23. High DDAH1 is associated with pediatric diffuse intrinsic pontine glioma. PMID: 22492959
  24. Non-diabetic hypertensive subjects with a hypertensive response to exercise compared to those with normal response were characterized by augmented asymmetric dimethylarginine and osteoprotegerin levels. PMID: 21975354
  25. did not find evidence for association with pre-eclampsia PMID: 21174581
  26. In acute congestive heart failure acute renal impairment function and the modulation of metabolism and extracellular transport by the DDAH-1/CAT-1 system determine high ADMA and SDMA levels after therapy for acute congestive heart failure. PMID: 21722652
  27. 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. PMID: 21677199
  28. HDL significantly increased the attenuated endothelial cell NO production induced by ox-LDL, which was attributed to its effect on DDAH/ADMA pathway PMID: 21264497
  29. Indicate that DDAH1 is required for metabolizing asymmetrical dimethylarginine and N(omega)-monomethyl-L-arginine. PMID: 21493890
  30. Results provide evidence that SNP rs1241321 in DDAH1 is associated with type 2 diabetes and its long-term outcome. PMID: 21303562
  31. DDAH1 exerts a unique role in activating Akt that affects endothelial function independently of degrading endogenous nitirc oxide synthase inhibitors. PMID: 21212404
  32. Recent studies in this review suggest that DDAH may regulate endothelial nitric oxide activity and endothelial function through both asymmetric dimethylarginine-dependent and -independent mechanisms. PMID: 19682581
  33. Expression of hDDAH1 messenger RNA is found in all organs of DDAH1 transgenic mice investigated, whereas human DDAH1 is absent in wild-type littermates. PMID: 19666120
  34. Circulating methylarginine levels and the decline in renal function in patients with chronic kidney disease are modulated by DDAH1 polymorphisms. PMID: 20010544
  35. Results suggest that the DDAH1 loss-of-function polymorphism is associated with both increased risk of thrombosis stroke and coronary artery disease in the Chinese Han population. PMID: 20167924
  36. Recombinant human DDAH1 overexpression protects transgenic mice from adverse structural and functional changes in cerebral arterioles in hyperhomocysteinemia but not from accelerated carotid artery thrombosis induced by the HM/LF diet. PMID: 20019334
  37. hydrolyzes methylated inhibitors of nitric oxide synthase is present in circulating human red blood cells PMID: 11811522
  38. The first evidence of the importance of DDAH1 polymorphisms in pre-eclampsia susceptibility was provided. PMID: 15501905
  39. By increasing the synthesis of the proangiogenic factor nitric oxide, DDAH promotes postnatal angiogenesis and arteriogenesis. PMID: 15781754
  40. DDAH-1 and DDAH-2 messenger RNA and protein were demonstrated in first trimester placental tissue, primary extravillous trophoblasts and extravillous trophoblast-derived cell lines. PMID: 16920729
  41. it is concluded that L-arginine regulates asymmetric dimethylarginine (ADMA) metabolism dose-dependently by competing for DDAH thus maintaining the metabolic balance of L-arginine and ADMA, and endothelial NO homeostasis PMID: 17075694
  42. DDAH-1 activity leads to accumulation of asymmetric dimethylarginine and reduction in nitric oxide signaling. PMID: 17273169
  43. Demonstrate a critical role for DDAH-1 and endogenous methylarginines in the pathogenesis of endothelial dysfunction. PMID: 17881609
  44. human dimethylarginine dimethylaminohydrolase-1 is inhibited by S-nitroso-L-homocysteine and hydrogen peroxide PMID: 17895252
  45. maintenance of normoglycemia and not glycemia-independent actions of insulin maintained dimethylarginine tissue levels by preserving physiological DDAH activity. PMID: 18292189

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Protein Families
DDAH family
Tissue Specificity
Detected in brain, liver, kidney and pancreas, and at low levels in skeletal muscle.
Database Links

HGNC: 2715

OMIM: 604743

KEGG: hsa:23576

STRING: 9606.ENSP00000284031

UniGene: Hs.713411

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