SCUBA

DDAH2 — Dimethylarginine dimethylaminohydrolase 2

DDAH2 belongs to a gene co-expression module in 5 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

DDAH2's module in each cell type

Cell typeModuleShares the module with
CD19⁺ B cellsMembrane adhesion remodeling
migration & adhesion
ARL6IP5, ATP6V0E1, CAMK1D, CAST, CELF2, EMP3, FLNA, FXYD5 +6 moreView in SCUBA
EndothelialEndothelial NO Activation
Endothelial cell development
BCL6B, BLOC1S1, CD99, CDH13, COX5A, CREM, DDX46, EEA1 +8 moreView in SCUBA
FibroblastsElastin-Fibronectin ECM
ECM production
ABI3BP, ELN, FN1, LRIG3, S100A4, SERPINE2, SOD3, SSC5DView in SCUBA
Glial cellsGlial Identity Homeostasis
Housekeeping
ARPC1B, CMTM5, CPQ, FCGRT, METRN, PON2, S100B, SLC22A17 +2 moreView in SCUBA
Goblet cellsEpithelial Maintenance
Housekeeping
COX7A2L, IP6K2, LAPTM4A, MARCKS, METTL9, MKRN1, RNF44View in SCUBA

About the gene

SynonymsG6A
Chromosome6: 31727038-31730617
Predicted locationIntracellular
Essential geneNo
Protein classEnzymes, Metabolic proteins, Plasma proteins, Predicted intracellular proteins
Molecular functionHydrolase

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 (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.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.