ArticleProceedings of the National Academy of Sciences of the United States of America2009
Aberrantly resolved RAG-mediated DNA breaks in Atm-deficient lymphocytes target chromosomal breakpoints in cis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed.
- Cardiac Tissue Engineering: Inclusion of Non-cardiomyocytes for Enhanced Features.Frontiers in cell and developmental biology · 2021Review
- DNA-PKcs phosphorylation at the T2609 cluster alters the repair pathway choice during immunoglobulin class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Epigenetic modifications of the VImmunology · 2017Article
- Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells.Nature communications · 2017Article
- RAG1/2 induces genomic insertions by mobilizing DNA into RAG1/2-independent breaks.The Journal of experimental medicine · 2017Article
- Mechanisms of human lymphoid chromosomal translocations.Nature reviews. Cancer · 2016Review
- Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Spatio-temporal regulation of RAG2 following genotoxic stress.DNA repair · 2015Article
- V(D)J Recombination: Mechanism, Errors, and Fidelity.Microbiology spectrum · 2014Review
- The ataxia telangiectasia mutated and cyclin D3 proteins cooperate to help enforce TCRβ and IgH allelic exclusion.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- End-joining, translocations and cancer.Nature reviews. Cancer · 2013Review
- Concurrent V(D)J recombination and DNA end instability increase interchromosomal trans-rearrangements in ATM-deficient thymocytes.Nucleic acids research · 2013Article
- 53BP1 alters the landscape of DNA rearrangements and suppresses AID-induced B cell lymphoma.Molecular cell · 2013Article
- Ikaros promotes rearrangement of TCR α genes in an Ikaros null thymoma cell line.European journal of immunology · 2013Article
- Review
- Mechanisms and impacts of chromosomal translocations in cancers.Frontiers of medicine · 2012Review
- Detection of early Abl kinase activation after ionizing radiation by using a peptide biosensor.Chembiochem : a European journal of chemical biology · 2012Article
- Spatial organization of the mouse genome and its role in recurrent chromosomal translocations.Cell · 2012Article
- Translocation capture sequencing: a method for high throughput mapping of chromosomal rearrangements.Journal of immunological methods · 2012Article
- The response to and repair of RAG-mediated DNA double-strand breaks.Annual review of immunology · 2012Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Canonical chromosomal translocations juxtaposing antigen receptor genes and oncogenes are a hallmark of many lymphoid malignancies. These translocations frequently form through the joining of DNA ends from double-strand breaks (DSBs) generated by the recombinase activating gene (RAG)-1 and -2 proteins at lymphocyte antigen receptor loci and breakpoint targets near oncogenes. Our understanding of chromosomal breakpoint target selection comes primarily from the analyses of these lesions, which are selected based on their transforming properties. RAG DSBs are rarely resolved aberrantly in wild-type developing lymphocytes. However, in ataxia telangiectasia mutated (ATM)-deficient lymphocytes, RAG breaks are frequently joined aberrantly, forming chromosomal lesions such as translocations that predispose (ATM)-deficient mice and humans to the development of lymphoid malignancies. Here, an approach that minimizes selection biases is used to isolate a large cohort of breakpoint targets of aberrantly resolved RAG DSBs in Atm-deficient lymphocytes. Analyses of this cohort revealed that frequently, the breakpoint targets for aberrantly resolved RAG breaks are other DSBs. Moreover, these nonselected lesions exhibit a bias for using breakpoints in cis, forming small chromosomal deletions, rather than breakpoints in trans, forming chromosomal translocations.
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