ArticleThe Journal of experimental medicine2011
XRCC1 suppresses somatic hypermutation and promotes alternative nonhomologous end joining in Igh genes.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Ubiquitylation of DNA polymerase β via atypical K27 chains signals a DNA damage response.Nucleic acids research · 2026Article
- RECQL4 requires PARP1 for recruitment to DNA damage, and PARG dePARylation facilitates its associated role in end joining.Experimental & molecular medicine · 2025Article
- Mechanism and regulation of secondary immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2023Review
- APE2 Promotes AID-Dependent Somatic Hypermutation in Primary B Cell Cultures That Is Suppressed by APE1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- IL-23 Promotes a Coordinated B Cell Germinal Center Program for Class-Switch Recombination to IgG2b in BXD2 Mice.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- AID Phosphorylation Regulates Mismatch Repair-Dependent Class Switch Recombination and Affinity Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- DNA Breaks in Ig V Regions Are Predominantly Single Stranded and Are Generated by UNG and MSH6 DNA Repair Pathways.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Characterization of the APLF FHA-XRCC1 phosphopeptide interaction and its structural and functional implications.Nucleic acids research · 2017Article
- Coordination of DNA single strand break repair.Free radical biology & medicine · 2017Review
- Microhomology-mediated end joining is activated in irradiated human cells due to phosphorylation-dependent formation of the XRCC1 repair complex.Nucleic acids research · 2017Article
- DNA polymerase ι functions in the generation of tandem mutations during somatic hypermutation of antibody genes.The Journal of experimental medicine · 2016Article
- Hsp90: A New Player in DNA Repair?Biomolecules · 2015Review
- The R280H X-ray cross-complementing 1 germline variant induces genomic instability and cellular transformation.DNA repair · 2015Article
- Identification of novel radiosensitizers in a high-throughput, cell-based screen for DSB repair inhibitors.Molecular cancer therapeutics · 2015Article
- ATAD5 deficiency decreases B cell division and Igh recombination.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Base excision repair capacity in informing healthspan.Carcinogenesis · 2014Review
- HSP90 regulates DNA repair via the interaction between XRCC1 and DNA polymerase β.Nature communications · 2014Article
- Refining the Neuberger model: Uracil processing by activated B cells.European journal of immunology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 4 countries.
Funding
Abstract
Activation-induced deaminase (AID) deaminates cytosine to uracil in immunoglobulin genes. Uracils in DNA can be recognized by uracil DNA glycosylase and abasic endonuclease to produce single-strand breaks. The breaks are repaired either faithfully by DNA base excision repair (BER) or mutagenically to produce somatic hypermutation (SHM) and class switch recombination (CSR). To unravel the interplay between repair and mutagenesis, we decreased the level of x-ray cross-complementing 1 (XRCC1), a scaffold protein involved in BER. Mice heterozygous for XRCC1 showed a significant increase in the frequencies of SHM in Igh variable regions in Peyer's patch cells, and of double-strand breaks in the switch regions during CSR. Although the frequency of CSR was normal in Xrcc1(+/-) splenic B cells, the length of microhomology at the switch junctions decreased, suggesting that XRCC1 also participates in alternative nonhomologous end joining. Furthermore, Xrcc1(+/-) B cells had reduced Igh/c-myc translocations during CSR, supporting a role for XRCC1 in microhomology-mediated joining. Our results imply that AID-induced single-strand breaks in Igh variable and switch regions become substrates simultaneously for BER and mutagenesis pathways.
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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.