anti- ADA antibody

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935106861
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name
anti- ADA antibody
category
Primary Antibodies
provider
FineTest
reference
FNab00135
tested applications
ELISA, WB, IHC
Description
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.
Documents del producto
Instrucciones
Data sheet
Product specifications
Category | Primary Antibodies |
Immunogen Target | adenosine deaminase |
Host | Rabbit |
Reactivity | human,mouse |
Recommended Dilution | WB: 1:200-1:1000; IHC: 1:20-1:200 |
Clonality | polyclonal |
Conjugation | Unconjugated |
Isotype | IgG |
Observed MW | 45 kDa |
Purity | ≥95% as determined by SDS-PAGE |
Purification | Immunogen affinity purified |
Size 1 | 100µg |
Form | liquid |
Tested Applications | ELISA, WB, IHC |
Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3,-20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
UniProt ID | P00813 |
Gene ID | 100 |
Alias | Adenosine aminohydrolase |
Background | Antibody anti-ADA |
Status | RUO |
Note | This product is for research use only. |
Descripción
Adenosine deaminase (ADA) is an enzyme crucial in purine metabolism, responsible for catalyzing the irreversible deamination of adenosine and deoxyadenosine to inosine and deoxyinosine, respectively. ADA is predominantly found in lymphocytes, with high activity in tissues such as the thymus, spleen, and bone marrow. It is vital for the development and maintenance of the immune system, as its deficiency leads to the accumulation of toxic purine metabolites, which impair DNA synthesis and lymphocyte survival. Mutations in the ADA gene result in severe combined immunodeficiency (SCID), characterized by a lack of functional T, B, and NK cells. ADA is also widely studied as a marker of immune activation and inflammation in conditions like tuberculosis and rheumatoid arthritis. Therapeutic interventions for ADA deficiency include enzyme replacement therapy and gene therapy, both of which aim to restore immune function.
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