ReviewImmunologic research2013
The role of activation-induced deaminase in antibody diversification and genomic instability.
Review in Immunologic research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Detection of Genomic Uracil Patterns.International journal of molecular sciences · 2021Review
- HDAC inhibitors overcome immunotherapy resistance in B-cell lymphoma.Protein & cell · 2020Review
- Signaling control of antibody isotype switching.Advances in immunology · 2019Review
- Anti-double Stranded DNA Antibodies: Origin, Pathogenicity, and Targeted Therapies.Frontiers in immunology · 2019Review
- TRAF2 Deficiency in B Cells Impairs CD40-Induced Isotype Switching That Can Be Rescued by Restoring NF-κB1 Activation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Unexpected effects of different genetic backgrounds on identification of genomic rearrangements via whole-genome next generation sequencing.BMC genomics · 2016Article
- Imbalanced PTEN and PI3K Signaling Impairs Class Switch Recombination.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- AID-initiated DNA lesions are differentially processed in distinct B cell populations.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Generation and repair of AID-initiated DNA lesions in B lymphocytes.Frontiers of medicine · 2014Review
- DNA modifications and neurological disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- TET proteins: on the frenetic hunt for new cytosine modifications.Briefings in functional genomics · 2013Review
Corrections and comments
- Erratum issued
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
More than a decade ago, activation-induced deaminase (AID) was identified as the initiator for somatic hypermutation (SHM) and class switch recombination (CSR). Since then, tremendous progress has been achieved toward elucidating how AID functions. AID targets the highly repetitive switch regions of the immunoglobulin heavy chain (IgH) locus to induce DNA double-strand breaks (DSBs), which can be rejoined, leading to switch of constant regions of antibody. When targeting to variable region exons of IgH and IgL loci, AID predominantly induces point mutations, termed SHM, resulting in increased affinity of antibody for antigen. While SHM and CSR enhance antibody diversity, AID-initiated DSBs and mutations may predispose B cells to carcinogenesis. This review focuses on the mechanisms that provide the specificity of AID targeting to Ig loci and the role of AID in genomic instability.
Indexed as
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.