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Adenosine deaminase

Adenosine Deaminase
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] (from NCBI)
Top mentioned proteins: CAN, HAD, ACID, V1a, AGE
Papers using Adenosine Deaminase antibodies
Restricting Zap70 Expression to CD4+CD8+ Thymocytes Reveals a T Cell Receptor–dependent Proofreading Mechanism Controlling the Completion of Positive Selection
Bosselut Rémy et al., In The Journal of Experimental Medicine, 1997
... A human adenosine deaminase (ADA)-based transgenic expression vector was constructed ...
Papers on Adenosine Deaminase
Hyperglycemia alters E-NTPDases, ecto-5'-nucleotidase, and ectosolic and cytosolic adenosine deaminase activities and expression from encephala of adult zebrafish (Danio rerio).
Da Silva et al., Porto Alegre, Brazil. In Purinergic Signal, Feb 2016
A significant increase in ecto-adenosine deaminase activity was observed in 111-mM glucose group, which remain elevated after 7 days of glucose withdrawal.
Neuroprotective effects of adenosine deaminase in the striatum.
Nibuya et al., Saitama, Japan. In J Cereb Blood Flow Metab, Feb 2016
UNASSIGNED: Adenosine deaminase (ADA) is a ubiquitous enzyme that catabolizes adenosine and deoxyadenosine.
Alveolar-like Stem Cell-derived Myb(neg) Macrophages Promote Recovery and Survival in Airway Disease.
Post et al., Toronto, Canada. In Am J Respir Crit Care Med, Feb 2016
RATIONALE: Abnormal alveolar macrophages (AM) are found in chronic obstructive pulmonary disease, asthma, cystic fibrosis and adenosine deaminase deficiency (ADA-/-).
To edit or not to edit: regulation of ADAR editing specificity and efficiency.
Hundley et al., Bloomington, United States. In Wiley Interdiscip Rev Rna, Jan 2016
Interestingly, during normal development, in specific cells, and in both neuropathological diseases and cancers, the extent of RNA editing does not directly correlate with levels of the substrate mRNA or the adenosine deaminase that act on RNA (ADAR) editing enzymes, implying that cellular factors are required for spatiotemporal regulation of A-to-I editing.
Aberrant purine metabolism in allergic asthma revealed by plasma metabolomics.
Zou et al., Beijing, China. In J Pharm Biomed Anal, Jan 2016
The increased level of inosine (P13) suggests that inflammatory cells induce adenosine triphosphate (ATP) breakdown, resulting in excessive expression of adenosine deaminase (ADA) in the formation of allergic asthma.
Genetic predisposition to bronchopulmonary dysplasia.
Ambalavanan et al., Birmingham, United States. In Semin Perinatol, Dec 2015
Pathway gene-set analysis in a North American cohort confirmed involvement of known pathways of lung development and repair (e.g., CD44 and phosphorus oxygen lyase activity) and indicated novel molecules and pathways (e.g., adenosine deaminase and targets of miR-219) involved in genetic predisposition to BPD.
The diagnosis of pleural effusions.
Lee et al., Lleida, Spain. In Expert Rev Respir Med, Dec 2015
Their precise etiological diagnosis depends on a combination of medical history, physical examination, imaging tests and pertinent pleural fluid analyses; including specific biomarkers (e.g., natriuretic peptides for heart failure, adenosine deaminase for tuberculosis, or mesothelin for mesothelioma).
Iron and Oxidative Stress in Parkinson's Disease: An Observational Study of Injury Biomarkers.
Fighera et al., Rio Grande, Brazil. In Plos One, Dec 2015
Forty PD patients and 46 controls were recruited to compare serum levels of iron, ferritin, transferrin, oxidative stress markers (superoxide dismutase (SOD), catalase (CAT), nitrosative stress marker (NOx), thiobarbituric acid reactive substances (TBARS), non-protein thiols (NPSH), advanced oxidation protein products (AOPP), ferric reducing ability of plasma (FRAP) and vitamin C) as well as inflammatory markers (NTPDases, ecto-5'-nucleotidase, adenosine deaminase (ADA), ischemic-modified albumin (IMA) and myeloperoxidase).
RNA editing by ADAR1 prevents MDA5 sensing of endogenous dsRNA as nonself.
Walkley et al., Australia. In Science, Oct 2015
Adenosine-to-inosine (A-to-I) editing is a highly prevalent posttranscriptional modification of RNA, mediated by ADAR (adenosine deaminase acting on RNA) enzymes.
Novel immunotherapeutic approaches in targeting dendritic cells with virus vectors.
Fraefel et al., Zürich, Switzerland. In Discov Med, Sep 2015
In fact, the first human gene therapy trial performed involved the implantation of autologous bone marrow cells transduced ex vivo with gamma retrovirus vectors expressing adenosine deaminase in a patient with severe combined immunodeficiency.
[Adenosine deaminase in experimental trypanosomiasis: future implications].
Rondón-Mercado et al., In Invest Clin, Sep 2015
The adenosine deaminase represents a control point in the regulation of extracellular adenosine levels, thus playing a critical role in the modulation of purinergic responses to certain pathophysiological events.
Early-onset stroke and vasculopathy associated with mutations in ADA2.
Aksentijevich et al., Aş Şanamayn, Syria. In N Engl J Med, 2014
RESULTS: All nine patients carried recessively inherited mutations in CECR1 (cat eye syndrome chromosome region, candidate 1), encoding adenosine deaminase 2 (ADA2), that were predicted to be deleterious; these mutations were rare or absent in healthy controls.
Mutant adenosine deaminase 2 in a polyarteritis nodosa vasculopathy.
Levy-Lahad et al., Aş Şanamayn, Syria. In N Engl J Med, 2014
RESULTS: In all the families, vasculitis was caused by recessive mutations in CECR1, the gene encoding adenosine deaminase 2 (ADA2).
Recoding RNA editing of AZIN1 predisposes to hepatocellular carcinoma.
Guan et al., Hong Kong, Hong Kong. In Nat Med, 2013
A→I editing of AZIN1 transcripts, specifically regulated by ADAR1 (encoding adenosine deaminase acting on RNA-1), results in a serine-to-glycine substitution at residue 367 of AZIN1, located in β-strand 15 (β15) and predicted to cause a conformational change, induced a cytoplasmic-to-nuclear translocation and conferred gain-of-function phenotypes that were manifested by augmented tumor-initiating potential and more aggressive behavior.
Evaluation of cerebrospinal fluid adenosine deaminase activity for the differential diagnosis of tuberculous and nontuberculous meningitis.
Zhu et al., Shanghai, China. In Am J Med Sci, 2012
cutoff value of 9.5 U/L in CSF is a useful aid for the differential diagnosis of tuberculous meningitis and non-tuberculous meningitis
Role of ascites adenosine deaminase in differentiating between tuberculous peritonitis and peritoneal carcinomatosis.
Song et al., Seoul, South Korea. In World J Gastroenterol, 2012
Ascitic fluid ADA measurement is helpful in the differential diagnosis of tuberculous peritonitis and peritoneal carcinomatosis.
Comprehensive analysis of RNA-Seq data reveals extensive RNA editing in a human transcriptome.
Wang et al., Shenzhen, China. In Nat Biotechnol, 2012
Most changes (∼93%) converted A to I(G), consistent with known editing mechanisms based on adenosine deaminase acting on RNA (ADAR).
Alterations in the adenosine metabolism and CD39/CD73 adenosinergic machinery cause loss of Treg cell function and autoimmunity in ADA-deficient SCID.
Aiuti et al., Milano, Italy. In Blood, 2012
Data show that the alterations in the CD39/CD73 adenosinergic machinery and loss of function in ADA-deficient Tregs provide insights into a predisposition to autoimmunity and the underlying mechanisms causing defective peripheral tolerance in ADA-SCID.
Role of the purinergic system in patients with cervical intraepithelial neoplasia and uterine cancer.
Schetinger et al., Santa Maria, Brazil. In Biomed Pharmacother, 2012
ADA1 was found to be the ADA isoenzyme present in platelets of healthy people
Lack of association of the G22A polymorphism of the ADA gene in patients with ankylosing spondylitis.
Mattos et al., Ribeirão Preto, Brazil. In Genet Mol Res, 2011
results indicate that the G22A polymorphism of ADA in isolation or together with HLA-B*27 is not associated with ankylosing spondylitis
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