Adenosine Desaminase (ADA) deficiency, is a purine metabolic disorder that cause severe combined immunodeficiency (SCID) due to the accumulation of toxic metabolites that primarily affects development, differentiation and function of T and B lymphocytes. Adenosine deaminase is a polymorphic enzyme that has an important role in immune functions and in the regulation of intracellular and extracellular concentrations of adenosine and adenosine receptor activity. ADA activity might be considered as a useful diagnostic tool among the other markers in these diseases. Genetic variability of ADA activity may have, therefore, an important role in resistance to malaria. Adenosine Deaminase (ADA) deficiency is an autosomal recessive variant of severe combined immunodeficiency (SCID) caused by systemic accumulation of ADA substrates.
Pack Size | Availability | Price/USD | Quantity |
---|---|---|---|
50 μg | 5 days | $ 600.00 |
Description | Adenosine Desaminase (ADA) deficiency, is a purine metabolic disorder that cause severe combined immunodeficiency (SCID) due to the accumulation of toxic metabolites that primarily affects development, differentiation and function of T and B lymphocytes. Adenosine deaminase is a polymorphic enzyme that has an important role in immune functions and in the regulation of intracellular and extracellular concentrations of adenosine and adenosine receptor activity. ADA activity might be considered as a useful diagnostic tool among the other markers in these diseases. Genetic variability of ADA activity may have, therefore, an important role in resistance to malaria. Adenosine Deaminase (ADA) deficiency is an autosomal recessive variant of severe combined immunodeficiency (SCID) caused by systemic accumulation of ADA substrates. |
Species | Human |
Expression System | Baculovirus-Insect Cells |
Tag | His |
Accession Number | P00813 |
Synonyms | ADA1, adenosine deaminase, ADA |
Construction | A DNA sequence encoding the human ADA (P00813) (Met1-Leu363) was expressed with a C-terminal polyhistidine tag. |
Protein Purity | > 95 % as determined by SDS-PAGE |
Molecular Weight | Approxiamtely 42.1 kDa |
Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method |
Formulation | Lyophilized from sterile 20 mM Tris, 500 mM NaCl, 10% glycerol, pH 7.4. Please contact us for any concerns or special requirements. Normally 5 % - 8 % trehalose, mannitol and 0. 01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the hard copy of CoA. |
Reconstitution | A hardcopy of datasheet with reconstitution instructions is sent along with the products. Please refer to it for detailed information. |
Stability & Storage |
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles. |
Shipping |
In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise. |
Research Background | Adenosine Desaminase (ADA) deficiency, is a purine metabolic disorder that cause severe combined immunodeficiency (SCID) due to the accumulation of toxic metabolites that primarily affects development, differentiation and function of T and B lymphocytes. Adenosine deaminase is a polymorphic enzyme that has an important role in immune functions and in the regulation of intracellular and extracellular concentrations of adenosine and adenosine receptor activity. ADA activity might be considered as a useful diagnostic tool among the other markers in these diseases. Genetic variability of ADA activity may have, therefore, an important role in resistance to malaria. Adenosine Deaminase (ADA) deficiency is an autosomal recessive variant of severe combined immunodeficiency (SCID) caused by systemic accumulation of ADA substrates. |
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