| Post Translational Modifications | Phosphorylated by TBK1. Phosphorylation inhibits the translocation into the mitochondrion upon Sendai viral infection. |
| 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. 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. Similarly, enhances pancreatic insulin secretion through SP1-mediated transcriptional up-regulation of secretagogin/SCGN, an insulin vesicle docking protein. 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. |
| Protein Name | Putative Hydrolase Ddah2DdahiiInactive N(G -N(G-Dimethylarginine Dimethylaminohydrolase 2Ddah-2Inactive Dimethylarginine Dimethylaminohydrolase 2Protein G6aS-Phase Protein |
| Cellular Localisation | CytoplasmMitochondrionTranslocates From Cytosol To Mitochondrion Upon Il1b Stimulation In Chondrocytes(Microbial Infection) Translocates To The Mitochondrion Upon Sendai Viral Infection |
| Alternative Protein Names | Putative Hydrolase Ddah2 proteinDdahii proteinInactive N(G -N(G-Dimethylarginine Dimethylaminohydrolase 2 proteinDdah-2 proteinInactive Dimethylarginine Dimethylaminohydrolase 2 proteinProtein G6a proteinS-Phase Protein proteinDDAH2 proteinDDAH proteinG6A proteinNG30 protein |
Information sourced from Uniprot.org
