ArticleThe Journal of experimental medicine2009
Pol zeta ablation in B cells impairs the germinal center reaction, class switch recombination, DNA break repair, and genome stability.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
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Who cites it
45 citing papers in PubMed, 73 citations in OpenAlex.
- Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice.Nature structural & molecular biology · 2025Article
- Molecular mechanisms of DNA lesion and repair during antibody somatic hypermutation.Science China. Life sciences · 2024Review
- Shieldin and CST co-orchestrate DNA polymerase-dependent tailed-end joining reactions independently of 53BP1-governed repair pathway choice.bioRxiv : the preprint server for biology · 2023Article
- Senataxin and RNase H2 act redundantly to suppress genome instability during class switch recombination.eLife · 2022Article
- Identifying Novel Psoriatic Disease Drug Targets Using a Genetics-Based Priority Index Pipeline.Journal of psoriasis and psoriatic arthritis · 2021Article
- Disruption of DNA polymerase ζ engages an innate immune response.Cell reports · 2021Article
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- REV7 is required for processing AID initiated DNA lesions in activated B cells.Nature communications · 2020Article
- Site-specific proteolytic cleavage prevents ubiquitination and degradation of human REV3L, the catalytic subunit of DNA polymerase ζ.Nucleic acids research · 2020Article
- DNA polymerase ζ in DNA replication and repair.Nucleic acids research · 2019Review
- Mutating for Good: DNA Damage Responses During Somatic Hypermutation.Frontiers in immunology · 2019Review
- DNA polymerase ζ deficiency causes impaired wound healing and stress-induced skin pigmentation.Life science alliance · 2018Article
- Assessment of copy number variations in 120 patients with Poland syndrome.BMC medical genetics · 2016Article
- DNA polymerase ι functions in the generation of tandem mutations during somatic hypermutation of antibody genes.The Journal of experimental medicine · 2016Article
- The Polymerase Activity of Mammalian DNA Pol ζ Is Specifically Required for Cell and Embryonic Viability.PLoS genetics · 2016Article
- Expression Patterns of Circular RNAs from Primary Kinase Transcripts in the Mammary Glands of Lactating Rats.Journal of breast cancer · 2015Article
- Article
- REV7 is essential for DNA damage tolerance via two REV3L binding sites in mammalian DNA polymerase ζ.Nucleic acids research · 2015Article
- REV3L, a promising target in regulating the chemosensitivity of cervical cancer cells.PloS one · 2015Article
- Breakthrough for a DNA break-preventer.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Pol zeta is an error-prone DNA polymerase that is critical for embryonic development and maintenance of genome stability. To analyze its suggested role in somatic hypermutation (SHM) and possible contribution to DNA double-strand break (DSB) repair in class switch recombination (CSR), we ablated Rev3, the catalytic subunit of Pol zeta, selectively in mature B cells in vivo. The frequency of somatic mutation was reduced in the mutant cells but the pattern of SHM was unaffected. Rev3-deficient B cells also exhibited pronounced chromosomal instability and impaired proliferation capacity. Although the data thus argue against a direct role of Pol zeta in SHM, Pol zeta deficiency directly interfered with CSR in that activated Rev3-deficient B cells exhibited a reduced efficiency of CSR and an increased frequency of DNA breaks in the immunoglobulin H locus. Based on our results, we suggest a nonredundant role of Pol zeta in DNA DSB repair through nonhomologous end joining.
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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.