ReviewAnnals of the New York Academy of Sciences2005
DNA lesions and repair in immunoglobulin class switch recombination and somatic hypermutation.
Review in Annals of the New York Academy of Sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
34 citing papers in PubMed, 51 citations in OpenAlex.
- B cell TET2 recruits OGT for nuclear TET2 and H2B O-GlcNAcylation to drive AID and BLIMP-1 expression and maturation of the antibody response.Cell reports · 2026Article
- B-cell immunodeficiency associated with polynucleotide kinase 3'-phosphatase (PNKP) deficiency.The journal of allergy and clinical immunology. Global · 2025Article
- Hallmarks of Cancers: Primary Antibody DeficiencyFrontiers in immunology · 2021Review
- Integrative transcriptome and chromatin landscape analysis reveals distinct epigenetic regulations in human memory B cells.Nature communications · 2020Article
- HMCES Functions in the Alternative End-Joining Pathway of the DNA DSB Repair during Class Switch Recombination in B Cells.Molecular cell · 2020Article
- Relevance of PSGL-1 Expression in B Cell Development and Activation.Frontiers in immunology · 2020Article
- Immunodeficiency in Bloom's Syndrome.Journal of clinical immunology · 2018Article
- Identification of CVID Patients With Defects in Immune Repertoire Formation or Specification.Frontiers in immunology · 2018Article
- Review
- Review
- The regulatory network of B-cell differentiation: a focused view of early B-cell factor 1 function.Immunological reviews · 2014Review
- Scaffold functions of 14-3-3 adaptors in B cell immunoglobulin class switch DNA recombination.PloS one · 2013Article
- Nijmegen breakage syndrome (NBS).Orphanet journal of rare diseases · 2012Review
- Article
- Mismatch-mediated error prone repair at the immunoglobulin genes.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2011Review
- Endonuclease G plays a role in immunoglobulin class switch DNA recombination by introducing double-strand breaks in switch regions.Molecular immunology · 2011Article
- Estrogen receptors bind to and activate the HOXC4/HoxC4 promoter to potentiate HoxC4-mediated activation-induced cytosine deaminase induction, immunoglobulin class switch DNA recombination, and somatic hypermutation.The Journal of biological chemistry · 2010Article
- Mobile elements reveal small population size in the ancient ancestors of Homo sapiens.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- HoxC4 binds to the promoter of the cytidine deaminase AID gene to induce AID expression, class-switch DNA recombination and somatic hypermutation.Nature immunology · 2009Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Immunoglobulin (Ig) gene somatic hypermutation (SHM) and class switch DNA recombination (CSR) are critical for the maturation of the antibody response. These processes endow antibodies with increased antigen-binding affinity and acquisition of new biological effector functions, thereby underlying the generation of memory B cells and plasma cells. They are dependent on the generation of specific DNA lesions and the intervention of activation-induced cytidine deaminase as well as newly identified translesion DNA polymerases, which are expressed in germinal center B cells. DNA lesions include mismatches, abasic sites, nicks, single-strand breaks, and double-strand breaks (DSBs). DSBs in the switch (S) region DNA are critical for CSR, but they also occur in V(D)J regions and possibly contribute to the events that lead to SHM. The nature of the DSBs in the Ig locus, their generation, and the repair processes that they trigger and that are responsible for their regulation remain poorly understood. Aberrant regulation of these events can result in chromosomal breaks and translocations, which are significant steps in B-cell neoplastic transformation.
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Identifiers
What OpenQuestion holds
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.