ReviewFrontiers in immunology2014
AIDing Chromatin and Transcription-Coupled Orchestration of Immunoglobulin Class-Switch Recombination.
Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 36 citations in OpenAlex.
- Genotoxic stressors mimicking synovial microenvironment modulate B cell fate in RA-FLS co-culture.Frontiers in immunology · 2026Article
- Transcription-Replication Conflicts: Unlocking New Frontiers in Cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Metabolic rewiring controlled by HIF-1α tunes IgA-producing B-cell differentiation and intestinal inflammation.Cellular & molecular immunology · 2025Article
- BRD2 promotes antibody class switch recombination by facilitating DNA repair in collaboration with NIPBL.Nucleic acids research · 2024Article
- A Germinal Center Checkpoint of AIRE in B Cells Limits Antibody Diversification.bioRxiv : the preprint server for biology · 2024Article
- Article
- How the Signaling Crosstalk of B Cell Receptor (BCR) and Co-Receptors Regulates Antibody Class Switch Recombination: A New Perspective of Checkpoints of BCR Signaling.Frontiers in immunology · 2021Review
- TRAF3 Acts as a Checkpoint of B Cell Receptor Signaling to Control Antibody Class Switch Recombination and Anergy.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Current insights into the mechanism of mammalian immunoglobulin class switch recombination.Critical reviews in biochemistry and molecular biology · 2019Review
- The B Cell Activation-Induced miR-183 Cluster Plays a Minimal Role in Canonical Primary Humoral Responses.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Signaling control of antibody isotype switching.Advances in immunology · 2019Review
- A licensing step links AID to transcription elongation for mutagenesis in B cells.Nature communications · 2018Article
- Transcription factor YY1 can control AID-mediated mutagenesis in mice.European journal of immunology · 2018Article
- Article
- AID/APOBEC-network reconstruction identifies pathways associated with survival in ovarian cancer.BMC genomics · 2016Article
- Non-canonical uracil processing in DNA gives rise to double-strand breaks and deletions: relevance to class switch recombination.Nucleic acids research · 2016Article
- The MRX Complex Ensures NHEJ Fidelity through Multiple Pathways Including Xrs2-FHA-Dependent Tel1 Activation.PLoS genetics · 2016Article
- Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.Nature reviews. Immunology · 2016Review
- AID targeting: old mysteries and new challenges.Trends in immunology · 2015Review
- Elucidation of IgH 3' region regulatory role during class switch recombination via germline deletion.Nature communications · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Secondary diversification of the antibody repertoire upon antigenic challenge, in the form of immunoglobulin heavy chain (IgH) class-switch recombination (CSR) endows mature, naïve B cells in peripheral lymphoid organs with a limitless ability to mount an optimal humoral immune response, thus expediting pathogen elimination. CSR replaces the default constant (CH) region exons (Cμ) of IgH with any of the downstream CH exons (Cγ, Cε, or Cα), thereby altering effector functions of the antibody molecule. This process depends on, and is orchestrated by, activation-induced deaminase (AID), a DNA cytidine deaminase that acts on single-stranded DNA exposed during transcription of switch (S) region sequences at the IgH locus. DNA lesions thus generated are processed by components of several general DNA repair pathways to drive CSR. Given that AID can instigate DNA lesions and genomic instability, stringent checks are imposed that constrain and restrict its mutagenic potential. In this review, we will discuss how AID expression and substrate specificity and activity is rigorously enforced at the transcriptional, post-transcriptional, post-translational, and epigenetic levels, and how the DNA-damage response is choreographed with precision to permit targeted activity while limiting bystander catastrophe.
Indexed as
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.