金山科研平台，产品价格货期咨询微信：jinshanbio Source:E. coli-derived, Ala2-Ser285, with an N-terminal Met and 6-His tag Accession #:O94760 N-terminal Sequence Analysis:Inconclusive result, Met predicted. Protein identity confirmed by MS analysis of tryptic fragments. Purity:>95%, by SDS-PAGE under reducing conditions and visualized by Colloidal Coomassie® Blue stain at 5 µg per lane. Endotoxin Level: Predicted Molecular Mass:32 kDa SDS-PAGE:38 kDa, reducing conditions Activity:Measured by its ability to hydrolyze asymmetric dimethylarginine to L-citrulline and dimethylamine.The specific activity is >75 pmol/min/µg, as measured under the described conditions. Formulation:Supplied as a 0.2 µm filtered solution in Tris, NaCl, Glycerol and DTT.See Certificate of Analysis for details. Molecule Information: Dimethylarginine Dimethylaminohydrolase 1/DDAH1 Aliases: DDAHI; Dimethylargininase-1 Entrez Gene IDs: 23576 (Human) Background: DDAH1 Dimethylarginine Dimethylaminohydrolase (DDAH) metabolizes asymmetric dimethyl arginine (ADMA) to L-citrulline and dimethylamine, and N^G-monomethyl arginine (MMA) to L-citrulline and monomethylamine. 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. 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. 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. It has been observed that genetic variation in the DDAH1 and DDAH2 genes is significantly associated with serum ADMA levels.