Background of the antigen
DDAH, a dimethylarginine dimethylaminohydrolase, hydrolyzes dimethyl arginine (ADMA) and monomethyl arginine (MMA), both inhibitors of nitric oxide synthases, and may be involved in in-vivo modulation of nitric oxide production (1,2). Impairment of DDAH causes ADMA accumulation and a reduction in cGMP generation (3). DDAH II, the predominant DDAH isoform in endothelial cells, facilitates the induction of nitric oxide synthesis by all-trans-Retinoic acid (atRA) (4). DDAH proteins are highly expressed in colon, kidney, stomach and liver tissues (1).