DDAH2 Antibody
Rabbit mAb
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, IP |
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Primary Accession | O95865 |
Reactivity | Rat |
Clonality | Monoclonal |
Other Names | DDAH; DDAH II; DDAH2; DDAHII; Dimethylargininase 2; G6a; |
Isotype | Rabbit IgG |
Host | Rabbit |
Calculated MW | 29644 Da |
Dilution | WB 1:500~1:2000 IP 1:50 |
---|---|
Purification | Affinity-chromatography |
Immunogen | A synthesized peptide derived from human DDAH2 |
Description | 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. |
Storage Condition and Buffer | Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at +4°C short term. Store at -20°C long term. Avoid freeze / thaw cycle. |
Name | DDAH2 (HGNC:2716) |
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Synonyms | DDAH, G6A, NG30 |
Function | Putative hydrolase with unknown substrate (Probable). Does not hydrolyze N(G),N(G)-dimethyl-L-arginine (ADMA) which acts as an inhibitor of NOS (PubMed:21493890, PubMed:37296100). In endothelial cells, induces expression of vascular endothelial growth factor (VEGF) via phosphorylation of the transcription factor SP1 by PKA in a process that is independent of NO and NO synthase (By similarity). Similarly, enhances pancreatic insulin secretion through SP1-mediated transcriptional up-regulation of secretagogin/SCGN, an insulin vesicle docking protein (By similarity). Upon viral infection, relocates to mitochondria where it promotes mitochondrial fission through activation of DNM1L leading to the inhibition of innate response activation mediated by MAVS (PubMed:33850055). |
Cellular Location | Cytoplasm. Mitochondrion Note=Translocates from cytosol to mitochondrion upon IL1B stimulation in chondrocytes |
Tissue Location | Detected in heart, placenta, lung, liver, skeletal muscle, kidney and pancreas, and at very low levels in brain |

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