ArticleProceedings of the National Academy of Sciences of the United States of America2010
Role of the translocation partner in protection against AID-dependent chromosomal translocations.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Competition for DNA binding between the genome protector replication protein A and the genome modifying APOBEC3 single-stranded DNA deaminases.Nucleic acids research · 2022Article
- Reframing Burkitt lymphoma: virology not epidemiology defines clinical variants.Annals of lymphoma · 2021Article
- ATM increases activation-induced cytidine deaminase activity at downstream S regions during class-switch recombination.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Checkpoint kinase 2 is required for efficient immunoglobulin diversification.Cell cycle (Georgetown, Tex.) · 2014Article
- Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers.Immune network · 2012Article
- Role of activation-induced cytidine deaminase in the progression of follicular lymphoma.Cancer science · 2012Article
- REG-γ associates with and modulates the abundance of nuclear activation-induced deaminase.The Journal of experimental medicine · 2011Article
- Article
- p53 represses class switch recombination to IgG2a through its antioxidant function.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Review
- Alternative end-joining catalyzes robust IgH locus deletions and translocations in the combined absence of ligase 4 and Ku70.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Chromosome translocations between Ig (Ig) and non-Ig genes are frequently associated with B-cell lymphomas in humans and mice. The best characterized of these is c-myc/IgH translocation, which is associated with Burkitt's lymphoma. These translocations are caused by activation-induced cytidine deaminase (AID), which produces double-strand DNA breaks in both genes. c-myc/IgH translocations are rare events, in part because ATM, p53, and p19 actively suppress them. To further define the mechanism of protection against the accumulation of cells that bear c-myc/IgH translocation, we assayed B cells from mice that carry mutations in cell-cycle and apoptosis regulator proteins that act downstream of p53. We find that PUMA, Bim, and PKCdelta are required for protection against c-myc/IgH translocation, whereas Bcl-XL and BAFF enhance c-myc/IgH translocation. Whether these effects are general or specific to c-myc/IgH translocation and whether AID produces dsDNA breaks in genes other than c-myc and Ig is not known. To examine these questions, we developed an assay for translocation between IgH and Igbeta, both of which are somatically mutated by AID. Igbeta/IgH, like c-myc/IgH translocations, are AID-dependent, and AID is responsible for lesions on IgH and the non-IgH translocation partners. However, ATM, p53, and p19 do not protect against Igbeta/IgH translocations. Instead, B cells are protected against Igbeta/IgH translocations by a BAFF- and PKCdelta-dependent pathway. We conclude that AID-induced double-strand breaks in non-Ig genes other than c-myc lead to their translocation, and that at least two nonoverlapping pathways protect against translocations in primary B cells.
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