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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Aicda activation-induced cytidine deaminase

activation-induced cytidine deaminase
Top mentioned proteins: CAN, IgM, IgA, IgM, POLYMERASE
Papers on activation-induced cytidine deaminase
The DNA Ligase IV Syndrome R278H Mutation Impairs B Lymphopoiesis via Error-Prone Nonhomologous End-Joining.
Yan et al., Boston, United States. In J Immunol, Feb 2016
Activated Lig4(R/R)HL B cells consistently accumulated high frequencies of activation-induced cytidine deaminase-dependent IgH locus chromosomal breaks and translocations and were more prone to apoptosis, effects that appeared to be p53-independent, as p53 deficiency did not markedly influence these events.
DNA Editing by APOBECs: A Genomic Preserver and Transformer.
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.
A subset of AID-dependent B-1a cells initiates hypersensitivity and pneumococcal pneumonia resistance.
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).
MCM3AP and POMP Mutations Cause a DNA-Repair and DNA-Damage-Signaling Defect in an Immunodeficient Child.
Wiesmüller et al., Ulm, Germany. In Hum Mutat, Dec 2015
GANP was previously described to promote B-cell maturation by nuclear targeting of activation-induced cytidine deaminase (AID) and to control AID-dependent hyperrecombination.
Associations between activation-induced cytidine deaminase/apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like cytidine deaminase expression, hepatitis B virus (HBV) replication and HBV-associated liver disease (Review).
Gao et al., Changchun, China. In Mol Med Report, Nov 2015
The activation‑induced cytidine deaminase (AID)/apolipoprotein B mRNA editing enzyme, catalytic polypeptide‑like (APOBEC) family of cytidine deaminases is significant in innate immunity, as it restricts numerous viruses, including HBV, through hypermutation‑dependent and ‑independent mechanisms.
Autosomal recessive hyper IgM syndrome associated with activation-induced cytidine deaminase gene in three Turkish siblings presented with tuberculosis lymphadenitis - Case report.
Unal et al., Kayseri, Turkey. In Acta Microbiol Immunol Hung, Sep 2015
Herein, we describe three Turkish siblings with HIGM syndrome who had a homozygous missense mutation (c.70C>T, p.Arg24Trp) in the activation-induced cytidine deaminase gene which results in autosomal recessive HIGM syndrome.
Plasmodium Infection Promotes Genomic Instability and AID-Dependent B Cell Lymphoma.
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.
AID, p53 and MLH1 expression in early gastric neoplasms and the correlation with the background mucosa.
Murawaki et al., Yonago, Japan. In Oncol Lett, Aug 2015
The expression of activation-induced cytidine deaminase (AID), p53 and MLH1 in 151 early gastric neoplasms [22 gastric adenomas, 92 intramucosal carcinomas (MCs), and 37 submucosal carcinomas (SMCs)] was examined immunohistochemically and compared with that of the corresponding background mucosal condition.
Non-coding RNA Generated following Lariat Debranching Mediates Targeting of AID to DNA.
Chaudhuri et al., New York City, United States. In Cell, Jun 2015
Likewise, recruitment of activation-induced cytidine deaminase (AID) to S regions is critical for CSR; however, the underlying mechanism has not been fully elucidated.
B cell super-enhancers and regulatory clusters recruit AID tumorigenic activity.
Casellas et al., Bethesda, United States. In Cell, 2015
The antibody gene mutator activation-induced cytidine deaminase (AID) promiscuously damages oncogenes, leading to chromosomal translocations and tumorigenesis.
Diversification of the Primary Antibody Repertoire by AID-Mediated Gene Conversion.
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.
Epigenetics of Peripheral B-Cell Differentiation and the Antibody Response.
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.
Whole-genome sequencing reveals activation-induced cytidine deaminase signatures during indolent chronic lymphocytic leukaemia evolution.
Brown et al., Boston, United States. In Nat Commun, 2014
The most commonly mutated gene in our cohort, IGLL5, shows a mutational pattern suggestive of activation-induced cytidine deaminase (AID) activity.
Noncoding RNA transcription targets AID to divergently transcribed loci in B cells.
Basu et al., New York City, United States. In Nature, 2014
Exosc3-deficient B cells lack the ability to undergo normal levels of class switch recombination and somatic hypermutation, two mutagenic DNA processes used to generate antibody diversity via the B-cell mutator protein activation-induced cytidine deaminase (AID).
A DNA break- and phosphorylation-dependent positive feedback loop promotes immunoglobulin class-switch recombination.
Chaudhuri et al., New York City, United States. In Nat Immunol, 2013
The ability of activation-induced cytidine deaminase (AID) to efficiently mediate class-switch recombination (CSR) is dependent on its phosphorylation at Ser38; however, the trigger that induces AID phosphorylation and the mechanism by which phosphorylated AID drives CSR have not been elucidated.
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