Adenosine Deaminase Enzyme | ADA enzyme

Adenosine Deaminase

Cat. Num. AAA653970

• Purity: Molecular Biology Grade
• Synonyms: Adenosine Deaminase; ADA enzyme

• Host: Calf spleen
• Purity/Purification: Molecular Biology Grade
• Form/Format: Supplied as a chromatographically purified, dialyzed, lyophilized powder.

• CAS Number: 9026-93-1
• Activity: 15units/mg
• Quality Control: SDS-PAGE
• Unit Definition: 1 unit converts 1µmole of adenosine to inosine per minute @ 25 degree C, pH 7.4.
• Preparation and Storage: Lyophilized powder may be stored at 4 degree C. Stable for 12 months at 4 degree C. Reconstitute immediately before use with sterile buffer. For maximum recovery of product, centrifuge the original vial prior to removing the cap.

Related Product Information for ADA enzyme

Adenosine deaminase (ADA) is a purine catabolic enzyme ubiquitous in mammalian tissue. In vitro it catalyzes deamination of both adenosine and 2'-deoxyadenosine to inosine and 2'-deoxyinosine respectively.

Product Categories/Family for ADA enzyme

Molecular Biology; MB-Enzymes

NCBI and Uniprot Product Information

• NCBI GI #: 47078295
• NCBI GeneID: 100
• NCBI Accession #: NP_000013.2
• NCBI GenBank Nucleotide #: NM_000022.2
• UniProt Accession #: P00813; Q53F92; Q6LA59
• Molecular Weight: 32.5kD
• NCBI Official Full Name: adenosine deaminase
• NCBI Official Synonym Full Names: adenosine deaminase
• NCBI Official Symbol: ADA
• NCBI Protein Information: adenosine deaminase; adenosine aminohydrolase
• UniProt Protein Name: Adenosine deaminase
• Protein Family: Adenosine deaminase
• UniProt Gene Name: ADA
• UniProt Synonym Gene Names: ADA1
• UniProt Entry Name: ADA_HUMAN

NCBI Description

This gene encodes an enzyme that catalyzes the hydrolysis of adenosine to inosine. Various mutations have been described for this gene and have been linked to human diseases. Deficiency in this enzyme causes a form of severe combined immunodeficiency disease (SCID), in which there is dysfunction of both B and T lymphocytes with impaired cellular immunity and decreased production of immunoglobulins, whereas elevated levels of this enzyme have been associated with congenital hemolytic anemia. [provided by RefSeq, Jul 2008]

Uniprot Description

Function: 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. Ref.13

Catalytic activity: Adenosine + H2O = inosine + NH3.

Cofactor: Binds 1 zinc ion per subunit. Ref.18

Subunit structure: Interacts with DPP4 (extracellular domain). Ref.10 Ref.11 Ref.12 Ref.14

Subcellular location: Cell membrane; Peripheral membrane protein; Extracellular side. Cell junction. Cytoplasmic vesicle lumen

By similarity. Cytoplasm

By similarity. Note: Colocalized with DPP4 at the cell junction in lymphocyte-epithelial cell adhesion. Ref.10 Ref.13

Tissue specificity: Found in all tissues, occurs in large amounts in T-lymphocytes and, at the time of weaning, in gastrointestinal tissues.

Polymorphism: There is a common allele, ADA*2, also known as the ADA 2 allozyme. It is associated with the reduced metabolism of adenosine to inosine. It specifically enhances deep sleep and slow-wave activity (SWA) during sleep.

Involvement in disease: Severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell-negative/NK-cell-negative due to adenosine deaminase deficiency (ADASCID) [MIM:102700]: An autosomal recessive disorder accounting for about 50% of non-X-linked SCIDs. 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 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.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.19 Ref.21 Ref.22 Ref.23 Ref.24 Ref.25 Ref.26 Ref.27 Ref.29 Ref.31

Sequence similarities: Belongs to the adenosine and AMP deaminases family.