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Cytidine deaminase

Cytidine Deaminase, CdA, CDD
This gene encodes an enzyme involved in pyrimidine salvaging. The encoded protein forms a homotetramer that catalyzes the irreversible hydrolytic deamination of cytidine and deoxycytidine to uridine and deoxyuridine, respectively. It is one of several deaminases responsible for maintaining the cellular pyrimidine pool. Mutations in this gene are associated with decreased sensitivity to the cytosine nucleoside analogue cytosine arabinoside used in the treatment of certain childhood leukemias. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, V1a, APOBEC3G, IgM
Papers on Cytidine Deaminase
Multifunctional role of the transcription factor Blimp-1 in coordinating plasma cell differentiation.
New
Impact
Busslinger et al., Vienna, Austria. In Nat Immunol, Feb 2016
It directly repressed genes encoding several transcription factors and Aicda (which encodes the cytidine deaminase AID) and thus silenced B cell-specific gene expression, antigen presentation and class-switch recombination in plasmablasts.
Cry-like genes, in an uncommon gene configuration, produce a crystal that localizes within the exosporium when expressed in an acrystalliferous strain of Bacillus thuringiensis.
New
Rampersad et al., Edinburg, United States. In Fems Microbiol Lett, Feb 2016
Herein we show i) that five cry-like genes are present in the genome of Bt2-56, ii) that two pairs of these genes show organizational similarity to a relatively uncommon gene configuration that co-express a cry gene along with a gene whose product aids crystal formation and iii), that when one of these two gene pairs (cry21A-cdA) is expressed in an acrystalliferous strain of Bt, crystals are formed that localize within the exosporium.
Enzyme catalysis by entropy without Circe effect.
New
Åqvist et al., Uppsala, Sweden. In Proc Natl Acad Sci U S A, Feb 2016
The enzymatic reaction of cytidine deaminase appears to be a distinct example.
DNA Editing by APOBECs: A Genomic Preserver and Transformer.
Review
New
Levanon et al., Ramat Gan, Israel. In Trends Genet, Jan 2016
The unique AID (activation-induced cytidine deaminase)/APOBEC (apolipoprotein B mRNA editing enzyme, catalytic polypeptide) family comprises proteins that alter DNA sequences by converting deoxycytidines to deoxyuridines through deamination.
Dr Jekyll and Mr Hyde: a strange case of 5-ethynyl-2'-deoxyuridine and 5-ethynyl-2'-deoxycytidine.
New
Koberna et al., Praha, Czech Republic. In Open Biol, Jan 2016
The results of experiments with the targeted inhibition of the cytidine deaminase (CDD) and dCMP deaminase activities indicated that the dominant role in the conversion pathway of EdC to EdUTP is played by CDD in HeLa cells.
A subset of AID-dependent B-1a cells initiates hypersensitivity and pneumococcal pneumonia resistance.
Review
New
Ptak et al., Kraków, Poland. In Ann N Y Acad Sci, Dec 2015
Unlike conventional B-1a (cB-1a) cell-produced IgM natural Ab, IgM Ab produced by sB-1a cells has high Ag affinity owing to immunoglobulin V-region mutations induced by activation-induced cytidine deaminase (AID).
Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance.
New
Impact
Meffre et al., New Haven, United States. In Immunity, Dec 2015
Activation-induced cytidine deaminase (AID), the enzyme-mediating class-switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes, is essential for the removal of developing autoreactive B cells.
Orientation-specific joining of AID-initiated DNA breaks promotes antibody class switching.
New
Impact
Alt et al., Boston, United States. In Nature, Oct 2015
Activation-induced cytidine deaminase (AID) initiates CSR by promoting deamination lesions within Sμ and a downstream acceptor S region; these lesions are converted into DNA double-strand breaks (DSBs) by general DNA repair factors.
Safety and tolerability of guadecitabine (SGI-110) in patients with myelodysplastic syndrome and acute myeloid leukaemia: a multicentre, randomised, dose-escalation phase 1 study.
New
Impact
Kantarjian et al., Philadelphia, United States. In Lancet Oncol, Sep 2015
Guadecitabine (SGI-110) is a novel hypomethylating dinucleotide of decitabine and deoxyguanosine resistant to degradation by cytidine deaminase.
Plasmodium Infection Promotes Genomic Instability and AID-Dependent B Cell Lymphoma.
New
Impact
Nussenzweig et al., New York City, United States. In Cell, Sep 2015
Pc induces prolonged expansion of germinal centers (GCs), unique compartments in which B cells undergo rapid clonal expansion and express activation-induced cytidine deaminase (AID), a DNA mutator.
Zinc enhancement of cytidine deaminase activity highlights a potential allosteric role of loop-3 in regulating APOBEC3 enzymes.
Alian et al., Haifa, Israel. In Sci Rep, 2014
We suggest that loop-3 may play a general role in allosterically tuning the activity of zinc-dependent cytidine deaminase family members.
Chemoprotection of murine hematopoietic cells by combined gene transfer of cytidine deaminase (CDD) and multidrug resistance 1 gene (MDR1).
Moritz et al., Hannover, Germany. In J Exp Clin Cancer Res, 2014
To apply this concept in the context of acute myeloid leukemia and myelodysplasia, we have investigated the overexpression of the multidrug resistance 1 (MDR1) and the cytidine deaminase (CDD) gene conferring resistance to anthracyclines and cytarabine (Ara-C), the two most important drugs in the treatment of these diseases.
Diversification of the Primary Antibody Repertoire by AID-Mediated Gene Conversion.
Review
Knight et al., Maywood, United States. In Results Probl Cell Differ, 2014
Gene conversion, mediated by activation-induced cytidine deaminase (AID), has been found to contribute to generation of the primary antibody repertoire in several vertebrate species.
Fibrinogen-Related Proteins (FREPs) in Mollusks.
Review
Adema, Albuquerque, United States. In Results Probl Cell Differ, 2014
Somatic mutation may result from sequence exchange among tandemly arranged FREP genes in the genome, and analysis of sequence variants also suggests involvement of cytidine deaminase-like activity or epigenetic regulation.
Epigenetics of Peripheral B-Cell Differentiation and the Antibody Response.
Review
Casali et al., San Antonio, United States. In Front Immunol, 2014
Inducible histone modifications, together with DNA methylation and miRNAs modulate the transcriptome, particularly the expression of activation-induced cytidine deaminase, which is essential for CSR and SHM, and factors central to plasma cell differentiation, such as B lymphocyte-induced maturation protein-1.
High incidence of severe neutropenia after gemcitabine-based chemotherapy in Chinese cancer patients with CDA 79A>C mutation.
GeneRIF
Cai et al., Shanghai, China. In Clin Chim Acta, 2012
Chinese patients carrying A79C variant C allele of CDA were found to be at higher risk of developing severe neutropenia after gemcitabine-based chemotherapy.
Correlation of cytidine deaminase polymorphisms and activity with clinical outcome in gemcitabine-/platinum-treated advanced non-small-cell lung cancer patients.
GeneRIF
Peters et al., Livorno, Italy. In Ann Oncol, 2012
cytidine deaminase enzymatic activity appears to be the strongest candidate biomarker of activity and efficacy of platinum-gemcitabine-based chemotherapy in advanced non-small-cell lung cancer patients
Cytidine deaminase genetic variants influence RNA expression and cytarabine cytotoxicity in acute myeloid leukemia.
GeneRIF
Balasubramanian et al., Vellore, India. In Pharmacogenomics, 2012
CDA RNA expression as well as Ara-C IC showed wide variation in AML samples and normal controls.
Association of cytidine deaminase and xeroderma pigmentosum group D polymorphisms with response, toxicity, and survival in cisplatin/gemcitabine-treated advanced non-small cell lung cancer patients.
GeneRIF
Crinò et al., Perugia, Italy. In J Thorac Oncol, 2011
Cytidine deaminase (CDA) 435 T/T genotype was significantly associated with better response to treatment and the CDA 435 C/T genotype was associated with a significantly increased risk of nonhematological toxicity.
Mechanisms of resistance to decitabine in the myelodysplastic syndrome.
GeneRIF
Issa et al., Houston, United States. In Plos One, 2010
Data show that the CDA/DCK ratio was 3 fold higher in non-responders than responders (P<.05), suggesting that this could be a mechanism of primary resistance.
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