Recombinant Mouse N (G),N (G)-dimethylarginine dimethylaminohydrolase 1 (Ddah1)

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. PMID: 29892894
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. PMID: 28819685
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. PMID: 27565538
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. PMID: 27357826
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. PMID: 26806551
6. In mild CKD, dysregulation of the ADMA/DDAH pathway in adipose tissue triggers lipodystrophy-like phenotype changes, including ectopic fat depositions. PMID: 26516203
7. transgenic mice display attenuated cigarette smoke-induced lung inflammation PMID: 25913572
8. Endothelial deletion of DDAH1 profoundly impairs the angiogenic capacity of endothelial cells. PMID: 25910799
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. PMID: 24465497
10. Overexpression of the ADMA degrading enzyme, DDAH1, did not ameliorate atherosclerosis in ApoE-deficient subtotally nephrectomized mice. PMID: 24690995
11. DDAH1 deficiency attenuates endothelial cell cycle progression and angiogenesis. PMID: 24260221
12. DDAH1 overexpression selectively decreased the sustained phase of hypoxic pulmonary vasoconstriction, partly via activation of the NO-cGMP pathway. PMID: 23642043
13. Pharmacological and genetic reduction of DDAH1 activity is protective against the vascular changes observed during endotoxic shock. PMID: 22995517
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. PMID: 21677199
15. Indicate that DDAH1 is required for metabolizing asymmetrical dimethylarginine and N(omega)-monomethyl-L-arginine. PMID: 21493890
16. DDAH1 exerts a unique role in activating Akt that affects endothelial function independently of degrading endogenous nitirc oxide synthase inhibitors. PMID: 21212404
17. overexpression of DDAH1 reduces plaque formation in ApoE(-/-) mice by lowering ADMA PMID: 20348244
18. Dimethylarginine dimethylaminohydrolase-1 transgenic mice are not protected from ischemic stroke PMID: 19809508
19. Overexpression of DDAH-1 increases basal levels of vascular NO and protects against ADMA-induced endothelial dysfunction in the cerebral circulation. PMID: 18063827
20. Report tissue-specific downregulation of DDAH1 in hyperhomocysteinemia. PMID: 18567702
21. Results show that asymmetric methylarginine increases pulmonary endothelial permeability, and that its effects on permeability, Rac1 activation and VASP phosphorylation are prevented by overexpression of active DDAHI and DDAHII. PMID: 18923147
22. DDAH1 is highly expressed in vascular endothelium and that endothelial DDAH1 plays an important role in regulating blood pressure PMID: 19917889

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KEGG: mmu:69219

STRING: 10090.ENSMUSP00000029845

UniGene: Mm.234247