Recombinant Human DDAH1 Protein, CF

Dimethylarginine Dimethylaminohydrolase (DDAH) metabolizes asymmetric dimethyl arginine (ADMA) to L-citrulline and dimethylamine, and N^G-monomethyl arginine (MMA) to L-citrulline and monomethylamine (1). Two members of the DDAH family have been identified in humans. DDAH1 is widely expressed, especially in liver and kidney. DDAH2 predominates in vascular endothelium and expressed selectively in kidney (2). It is also expressed in immune tissues including spleen, thymus, peripheral leukocytes, lymph nodes, and bone marrow. Over 90 % of endogenous ADMA is metabolized by DDAH with the remainder excreted (3). ADMA and MMA are endogenous inhibitors of nitric oxide synthase (NOS). Thus, enzymes of the DDAH family play a key role in vascular function through the turnover of methylated arginine (4). It has been observed that genetic variation in the DDAH1 and DDAH2 genes is significantly associated with serum ADMA levels (5).