The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Specific activity is >40 units/mg, and is defined as the amount of enzyme that convert 1.0 umol of adenosine to inosine per minute at pH 7.5 at 25°C.
< 1.000 Eu/mg
% SDS-PAGE. No detergents such as urea, Triton or Tween were used to purify the proteins. Purified by using anion exchange chromatography (DEAE sepharose resin) and gel filtration chromatography (Sephacryl S 200) with 20mM Tris pH 7.5, 2mM EDTA.
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Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
pH: 8.00 Constituents: 0.32% Tris HCl, 20% Glycerol, 0.02% DTT
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Catalyzes the hydrolytic deamination of adenosine and 2-deoxyadenosine. Plays an important role in purine metabolism and in adenosine homeostasis. Modulates signaling by extracellular adenosine, and so contributes indirectly to cellular signaling events. Acts as a positive regulator of T-cell coactivation, by binding DPP4. Its interaction with DPP4 regulates lymphocyte-epithelial cell adhesion.
Found in all tissues, occurs in large amounts in T-lymphocytes and, at the time of weaning, in gastrointestinal tissues.
Defects in ADA are the cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-negative/NK-cell-negative due to adenosine deaminase deficiency (ADASCID) [MIM:102700]. SCID refers to a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients with SCID present in infancy with recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development. ADA-SCID is an autosomal recessive form accounting for about 50% of non-X-linked SCIDs. ADA deficiency has been diagnosed in chronically ill teenagers and adults (late or adult onset). Population and newborn screening programs have also identified several healthy individuals with normal immunity who have partial ADA deficiency.
Belongs to the adenosine and AMP deaminases family.
Cell membrane. Cell junction. Cytoplasmic vesicle lumen. Cytoplasm. Colocalized with DPP4 at the cell junction in lymphocyte-epithelial cell adhesion.