Human Dimethylarginine Dimethylaminohydrolase 1/DDAH1 Antibody
Human Dimethylarginine Dimethylaminohydrolase 1/DDAH1 Antibody Summary
Accession # O94760
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Dimethylarginine Dimethylaminohydrolase 1/DDAH1 in Human Brain. Dimethylarginine Dimethylaminohydrolase 1/ DDAH1 was detected in immersion fixed paraffin-embedded sections of human brain using Sheep Anti-Human Dimethylarginine Dimethylaminohydrolase 1/DDAH1 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF6530) at 3 µg/mL overnight at 4 °C. Before incubation with the primary antibody, tissue was subjected to heat-induced epitope retrieval using Antigen Retrieval Reagent-Basic (Catalog # CTS013). Tissue was stained using the Anti-Sheep HRP-DAB Cell & Tissue Staining Kit (brown; Catalog # CTS019) and counter-stained with hematoxylin (blue). Specific staining was localized to neuronal cell bodies and processes. View our protocol for Chromogenic IHC Staining of Paraffin-embedded Tissue Sections.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: Dimethylarginine Dimethylaminohydrolase 1/DDAH1
Dimethylarginine Dimethylaminohydrolase (DDAH) metabolizes asymmetric dimethyl arginine (ADMA) to L-citrulline and dimethylamine, and NG-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).
- Tadashi, O. et al. (1989) J. Biol. Chem. 264:10205.
- Tran, C. T. et al. (2000) Genomics 68:101.
- Tran, C. T. et al. (2003) Atheroscler. Suppl. 4:33.
- Leiper, J. et al. (2007) Nat. Med. 13:198.
- Abhary, S. et al. (2010) PNAS PLoS One. 5:e9462.
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