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. Impairment of DDAH causes ADMA accumulation and a reduction in cGMP generation. DDAH II, the predominant DDAH isoform in endothelial cells, facilitates the induction of nitric oxide synthesis by all-trans-Retinoic acid (atRA). DDAH proteins are highly expressed in colon, kidney, stomach and liver tissues.
Background References
1. Leiper J M et al. Identification of two human dimethylarginine dimethylaminohydrolases with distinct tissue distributions and homology with microbial arginine deiminases. Biochem J 343:209-214 (1999).
2. Cillero-Pastor B et al. Dimethylarginine dimethylaminohydrolase 2, a newly identified mitochondrial protein modulating nitric oxide synthesis in normal human chondrocytes. Arthritis Rheum 64:204-212 (2012).
Sequence Similarity
Belongs to the DDAH family.
Tissue Specificity
Detected in heart, placenta, lung, liver, skeletal muscle, kidney and pancreas, and at very low levels in brain.
Western blot analysis of DDAH2 on different lysates with Rabbit anti-DDAH2 antibody (ET7107-41) at 1/5,000 dilution.
Lane 1: MCF7 (Human breast cancer cell) cell lysate (15 µg/Lane) Lane 2: Mouse lung tissue lysate (30 µg/Lane) Lane 3: Rat lung tissue lysate (30 µg/Lane)
Exposure time: 20 seconds; ECL: K1802
Blocking: 5% NFDM/TBST, 1 hour at room temperature Primary antibody: ET7107-41, 1/5,000 in primary antibody dilution buffer (K1803), overnight at 4 ℃ Secondary antibody: Goat anti-Rabbit IgG-HRP (HA1001), 1/50,000 in 5% NFDM/TBST, 1 hour at room temperature
Predicted band size: 30 kDa Observed band size: 30 kDa
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