ELISA/assay

Human Adenosine Deaminase ELISA Kit

MBS015277

96 Strip Wells

600 USD

ELISA Kit

Human Adenosine Deaminase ELISA Kit

Adenosine Deaminase

adenosine deaminase; Adenosine deaminase; adenosine deaminase; adenosine aminohydrolase; adenosine deaminase; Adenosine aminohydrolase

ADA

ADA; ADA; ADA1

ADA_HUMAN

Human

No significant cross-reactivity or interference between this analyte and analogues is observed.

Store all reagents at 2-8 degree C

Samples: Serum, Plasma and Tissue Homogenate. Detection Range: The detection range of this kit is 3.12U/L-100U/L.

Sensitivity: The sensitivity of this kit is 1.0U/L. Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100].

Background: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! This kit is intended to be used for determination the level of ADA (hereafter termed this analyte) in undiluted original Human serum, plasma and tissue homogenate samples.

47078295

NP_000013.2

NM_000022.2

P00813

40,764 Da

C-MYB Transcription Factor Network Pathway 138073!!Metabolism Pathway 477135!!Metabolism Of Nucleotides Pathway 106263!!Primary Immunodeficiency Pathway 83125!!Primary Immunodeficiency Pathway 537!!Purine Metabolism Pathway 82944!!Purine Metabolism Pathway 106265!!Purine Metabolism Pathway 307!!Purine Salvage Pathway 106273!!Adenine And Adenosine Salvage III Pathway 547495

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]

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.

96 Strip Wells

600 USD