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Validated All-in-One™ qPCR Primer for ADA(NM_000022.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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.
Gene References into function
- Clustered charged amino acids of human adenosine deaminase comprise a functional epitope for binding the adenosine deaminase complexing protein CD26/dipeptidyl peptidase IV
- Relationship between plasma malondialdehyde levels and adenosine deaminase activities in preeclampsia.
- serum adenosine deaminase-2 (but not adenosine deaminase-1) and cytidine deaminase levels were significantly higher in systemic lupus erythematosus patients
- In humans, ADA1 was mainly purified concomitant with ADA-binding protein and dipeptidyl peptidase IV, was not adsorbed in adenosine-Sepharose, but was adsorbed in IgG anti-ADA1-Sepharose column; properties compared with chicken ADA1
- The activity of this enzyme was studied in tissues, erythrocytes, and blood plasma of patients with peptic ulcer both in its uncomplicated course and in the development of complications.
- The activity of ADA was determined in lymphocytes, esoinophils and blood serum in patients with bronchial asthma.
- ADA was analyzed by linkage disequilibrium and no correlation was found between hot spots of equal and unequal homologous recombination.
- Adenosine deaminase binding is diminished by mutation of ADA residues known to interact with CD26.
- adenosine-related gene variants do not appear to alter susceptibility to the disease in this group of essential hypertensives
- adenosine deaminase contributes to the clinical manifestations of type 2 diabetes and probably also have a marginal influence on susceptibility to the disease
- The adenosine deaminase (ADA) gene was highly up-regulated in Ara-C-resistant cells, while equilibrative nucleoside transporter 1 (ENT1) and several cell-cycle-related genes were down-regulated.
- ADA colocalizing with adenosine receptors on dendritic cells interact with CD26 expressed on lymphocytes.
- Adenosine deaminase activity was abnormal in active nephrotic syndrome, and lymphocyte ADA demonstrated change both in active as well as remission stage of the disease.
- We tested whether p63 is implicated in transcriptional events related to sustaining cell proliferation by transactivation of antiapoptotic and cell survival target genes such as Adenosine Deaminase (ADA), an important gene involved in cell proliferation.
- During acute hypoxia associated with vascular leakage and excessive inflammation, ADA inhibition may serve as therapeutic strategy.
- Findings suggest a possible role for a low-activity genotype of adenosine deaminase in the pathogenesis of mild mental retardation. No significant differences were found when comparing the group with moderate or severe mental retardation and controls.
- the ADA c7C/T mutation was estimated to be approximately 7,100 years old
- Increased adenosine deaminase is associated with hydatidiform mole
- ADA*2 allele may decrease genetic susceptibility to coronary artery disease.
- G22A polymorphism plays a minimal role in susceptibility to autism in North American families
- The measurement of adenosine deaminase activity in ascites represents a diagnostic advance in tuberculous peritonitis among end-stage renal failure patients.
- the transition-state structures of PfADA, HsADA, and bovine ADA (BtADA) solved using competitive kinetic isotope effects (KIE) and density functional calculations
- This study shows that adenosine elimination on human airway epithelia is mediated by ADA1, CNT2, and CNT3, which constitute important regulators of adenosine-mediated inflammation.
- CD4(+) T cells from ADA-severe combined immunodeficiency patients have severely compromised T cell receptor/CD28-driven proliferation and cytokine production, both at the transcriptional and protein levels.
- Results describe the activities of ectonucleotide pyrophosphatase/phosphodiesterase and adenosine deaminase in patients with uterine cervix neoplasia.
- the primary mechanism in men with ischemic stroke might involve the reduction of ADA1 activity
- Suggest that adenosine deaminase can be used to distinguish between tuberculous and malignant pleural effusions.
- Negative association between coronary artery disease and ADA*2 allele is only present in males
- the increased level of ADA activity in the subararachnoid hemorrhage patients with the poor clinical and consciousness level may have resulted from the ischemic cerebral insult
- Human ADA, apart from reducing the adenosine concentration and thus preventing A(1)R desensitization, binds to A(1)R behaving as an allosteric effector that markedly enhances agonist affinity and increases receptor functionality.
- Zygotes with low adenosine deaminase locus 1 activity and low F activity may experience the most favourable intrauterine conditions for a balanced development of the feto-placental unit.
- heterozygosity for the 22G>A variant of ADA, although reducing catalytic activity, does not enhance forearm reactive hyperaemia
