ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2009
Hijacked DNA repair proteins and unchained DNA polymerases.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Deep learning model of somatic hypermutation reveals importance of sequence context beyond hotspot targeting.iScience · 2022Article
- Structure and function relationships in mammalian DNA polymerases.Cellular and molecular life sciences : CMLS · 2020Review
- Chicken MBD4 Regulates Immunoglobulin Diversification by Somatic Hypermutation.Frontiers in immunology · 2019Article
- AID hits the jackpot when missing the target.Current opinion in immunology · 2016Review
- Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases.DNA repair · 2016Review
- Effects of Chronic Low-Dose Radiation on Human Neural Progenitor Cells.Scientific reports · 2016Article
- The histone methyltransferase MMSET regulates class switch recombination.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- DNA MMR systems, microsatellite instability and antioxidant activity variations in two species of wild bats: Myotis velifer and Desmodus rotundus, as possible factors associated with longevity.Age (Dordrecht, Netherlands) · 2012Article
- Three-dimensional architecture of the IgH locus facilitates class switch recombination.Annals of the New York Academy of Sciences · 2012Article
- AID targeting is dependent on RNA polymerase II pausing.Seminars in immunology · 2012Review
- DNA mismatch repair system: repercussions in cellular homeostasis and relationship with aging.Oxidative medicine and cellular longevity · 2012Review
- DNA polymerase eta and chemotherapeutic agents.Antioxidants & redox signaling · 2011Review
- Article
- AID: a riddle wrapped in a mystery inside an enigma.Immunologic research · 2011Review
- Error-prone DNA repair activity during somatic hypermutation in shark B lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Structure and mechanism of human DNA polymerase eta.Nature · 2010Article
- The RNF8/RNF168 ubiquitin ligase cascade facilitates class switch recombination.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
4 authors.
Funding
Abstract
Somatic hypermutation of immunoglobulin (Ig) genes occurs at a frequency that is a million times greater than the mutation in other genes. Mutations occur in variable genes to increase antibody affinity, and in switch regions before constant genes to cause switching from IgM to IgG. Hypermutation is initiated in activated B cells when the activation-induced deaminase protein deaminates cytosine in DNA to uracil. Uracils can be processed by either a mutagenic pathway to produce mutations or a non-mutagenic pathway to remove mutations. In the mutagenic pathway, we first studied the role of mismatch repair proteins, MSH2, MSH3, MSH6, PMS2 and MLH1, since they would recognize mismatches. The MSH2-MSH6 heterodimer is involved in hypermutation by binding to U:G and other mismatches generated during repair synthesis, but the other proteins are not necessary. Second, we analysed the role of low-fidelity DNA polymerases eta, iota and theta in synthesizing mutations, and conclude that polymerase eta is the dominant participant by generating mutations at A:T base pairs. In the non-mutagenic pathway, we examined the role of the Cockayne syndrome B protein that interacts with other repair proteins. Mice deficient in this protein had normal hypermutation and class switch recombination, showing that it is not involved.
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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.