ReviewEMBO reports2005
DNA polymerases and somatic hypermutation of immunoglobulin genes.
Review in EMBO reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 70 citations in OpenAlex.
- Human TLS DNA polymerase: saviors or threats under replication stress?Molecular and cellular biochemistry · 2025Review
- Regional mutational signature activities in cancer genomes.PLoS computational biology · 2022Article
- Tandem Substitutions in Somatic Hypermutation.Frontiers in immunology · 2021Article
- The pink salmon genome: Uncovering the genomic consequences of a two-year life cycle.PloS one · 2021Article
- Memory B Cells in Pregnancy Sensitization.Frontiers in immunology · 2021Review
- A high-resolution landscape of mutations in theProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mutating for Good: DNA Damage Responses During Somatic Hypermutation.Frontiers in immunology · 2019Review
- Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017Review
- Decreased mutation frequencies among immunoglobulin G variable region genes during viremic HIV-1 infection.PloS one · 2014Article
- Accumulation of the FACT complex, as well as histone H3.3, serves as a target marker for somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Mouse DNA polymerase kappa has a functional role in the repair of DNA strand breaks.DNA repair · 2013Article
- Leukotriene biosynthesis inhibitor MK886 impedes DNA polymerase activity.Chemical research in toxicology · 2013Article
- DNA polymerase POLQ and cellular defense against DNA damage.DNA repair · 2013Review
- REV1 and DNA polymerase zeta in DNA interstrand crosslink repair.Environmental and molecular mutagenesis · 2012Review
- DNA polymerase ζ generates tandem mutations in immunoglobulin variable regions.The Journal of experimental medicine · 2012Article
- Promiscuous DNA synthesis by human DNA polymerase θ.Nucleic acids research · 2012Article
- Directed evolution of mammalian anti-apoptosis proteins by somatic hypermutation.Protein engineering, design & selection : PEDS · 2012Article
- Gene Conversion-Like Events in the Diversification of Human Rearranged IGHV3-23*01 Gene Sequences.Frontiers in immunology · 2012Article
- DNA polymerases nu and theta are required for efficient immunoglobulin V gene diversification in chicken.The Journal of cell biology · 2010Article
- Optimization of DNA polymerase mutation rates during bacterial evolution.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Somatic hypermutation of immunoglobulin variable genes, which increases antibody diversity, is initiated by the activation-induced cytosine deaminase (AID) protein. The current DNA-deamination model posits that AID deaminates cytosine to uracil in DNA, and that mutations are generated by DNA polymerases during replication or repair of the uracil residue. Mutations could arise as follows: by DNA replicating past the uracil; by removing the uracil with a uracil glycosylase and replicating past the resulting abasic site with a low-fidelity polymerase; or by repairing the uracil and synthesizing a DNA-repair patch downstream using a low-fidelity polymerase. In this review, we summarize the biochemical properties of specialized DNA polymerases in mammalian cells and discuss their participation in the mechanisms of hypermutation. Many recent studies have examined mice deficient in the genes that encode various DNA polymerases, and have shown that DNA polymerase H (POLH) contributes to hypermutation, whereas POLI, POLK and several other enzymes do not have major roles. The low-fidelity enzyme POLQ has been proposed as another candidate polymerase because it can efficiently bypass abasic sites and recent evidence indicates that it might participate in hypermutation.
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.