ReviewDNA repair2016
Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases.
Review in DNA repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 57 citations in OpenAlex.
- Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.Nucleus (Austin, Tex.) · 2026Review
- Molecular mechanisms of DNA lesion and repair during antibody somatic hypermutation.Science China. Life sciences · 2024Review
- RPA guides UNG to uracil in ssDNA to facilitate antibody class switching and repair of mutagenic uracil at the replication fork.Nucleic acids research · 2024Article
- Genetic modifiers of repeat expansion disorders.Emerging topics in life sciences · 2023Article
- DNA repair mechanisms that promote insertion-deletion events during immunoglobulin gene diversification.Science immunology · 2023Article
- Review
- A Human MSH6 Germline Variant Associated With Systemic Lupus Erythematosus Induces Lupus-like Disease in Mice.ACR open rheumatology · 2022Article
- Contribution of rare mutational outcomes to broadly neutralizing antibodies.Acta biochimica et biophysica Sinica · 2022Review
- Unravelling the instability of mutational signatures extractionFrontiers in genetics · 2022Article
- The Role of DNA Repair in Immunological Diversity: From Molecular Mechanisms to Clinical Ramifications.Frontiers in immunology · 2022Review
- Article
- Decreased ATM Function Causes Delayed DNA Repair and Apoptosis in Common Variable Immunodeficiency Disorders.Journal of clinical immunology · 2021Article
- Mismatch Repair: From Preserving Genome Stability to Enabling Mutation Studies in Real-Time Single Cells.Cells · 2021Review
- DNA folds threaten genetic stability and can be leveraged for chemotherapy.RSC chemical biology · 2021Review
- DNA Mismatch Repair and its Role in Huntington's Disease.Journal of Huntington's disease · 2021Review
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
- AID Phosphorylation Regulates Mismatch Repair-Dependent Class Switch Recombination and Affinity Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- A high-resolution landscape of mutations in theProceedings of the National Academy of Sciences of the United States of America · 2019Article
- B cells from young and old mice switch isotypes with equal frequencies after ex vivo stimulation.Cellular immunology · 2019Article
- Genome-wide mapping of regions preferentially targeted by the human DNA-cytosine deaminase APOBEC3A using uracil-DNA pulldown and sequencing.The Journal of biological chemistry · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The enzyme activation-induced deaminase (AID) targets the immunoglobulin loci in activated B cells and creates DNA mutations in the antigen-binding variable region and DNA breaks in the switch region through processes known, respectively, as somatic hypermutation and class switch recombination. AID deaminates cytosine to uracil in DNA to create a U:G mismatch. During somatic hypermutation, the MutSα complex binds to the mismatch, and the error-prone DNA polymerase η generates mutations at A and T bases. During class switch recombination, both MutSα and MutLα complexes bind to the mismatch, resulting in double-strand break formation and end-joining. This review is centered on the mechanisms of how the MMR pathway is commandeered by B cells to generate antibody diversity.
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.