ArticleProceedings of the National Academy of Sciences of the United States of America2018
DNA double-strand break response factors influence end-joining features of IgH class switch and general translocation junctions.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Simple Measurement of IgA Predicts Immunity and Mortality in Ataxia-Telangiectasia.Journal of clinical immunology · 2021Trial
- CFP1 promotes B cell class switch recombination through the regulation of S region germline transcription and proliferation.iScience · 2026Article
- 53BP1 orchestrates sequence feature of RAG targets to balance DNA repair outcomes during V(D)J recombination.Science advances · 2026Article
- Chromatin-intrinsic mechanisms determine orientation-specific class switch recombination.Nature communications · 2026Article
- Macrophages promote aberrant DNA repair in multiple myeloma via the CXCL5/8-CXCR2 axis.Haematologica · 2026Article
- Recombination junctions from antibody isotype switching classify immune and DNA repair dysfunction.Nature communications · 2025Article
- Polymerase theta repairs persistent G1-induced DNA breaks in S-phase during class switch recombination.Nature communications · 2025Article
- The LIM-domain-only protein LMO2 and its binding partner LDB1 are differentially required for class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ATM Expression and Activation in Ataxia Telangiectasia Patients with and without Class Switch Recombination Defects.Journal of clinical immunology · 2025Article
- Nucleotide level mapping of uracils in murine heavy chain switch regions shows correlation between uracilation and positions of switch junctions created during class-switch recombination.NAR molecular medicine · 2025Article
- Core enhancers of the 3'RR optimize IgH nuclear position and loop conformation for successful oriented class switch recombination.Nucleic acids research · 2024Article
- Ataxia Telangiectasia Mutated and MSH2 Control Blunt DNA End Joining in Ig Class Switch Recombination.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- SHLD1 is dispensable for 53BP1-dependent V(D)J recombination but critical for productive class switch recombination.Nature communications · 2022Article
- Alternative end-joining in BCR gene rearrangements and translocations.Acta biochimica et biophysica Sinica · 2022Review
- Article
- DNA Damage Response and Repair in Adaptive Immunity.Frontiers in cell and developmental biology · 2022Review
- Switch Tandem Repeats Influence the Choice of the Alternative End-Joining Pathway in Immunoglobulin Class Switch Recombination.Frontiers in immunology · 2022Article
- Genetic Risk Variants for Class Switching Recombination Defects in Ataxia-Telangiectasia Patients.Journal of clinical immunology · 2022Article
- FATC Domain Deletion Compromises ATM Protein Stability, Blocks Lymphocyte Development, and Promotes Lymphomagenesis.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Noncoding RNA processing by DIS3 regulates chromosomal architecture and somatic hypermutation in B cells.Nature genetics · 2021Article
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8 authors.
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Abstract
Ig heavy chain (IgH) class switch recombination (CSR) in B lymphocytes switches IgH constant regions to change antibody functions. CSR is initiated by DNA double-strand breaks (DSBs) within a donor IgH switch (S) region and a downstream acceptor S region. CSR is completed by fusing donor and acceptor S region DSB ends by classical nonhomologous end-joining (C-NHEJ) and, in its absence, by alternative end-joining that is more biased to use longer junctional microhomologies (MHs). Deficiency for DSB response (DSBR) factors, including ataxia telangiectasia-mutated (ATM) and 53BP1, variably impair CSR end-joining, with 53BP1 deficiency having the greatest impact. However, studies of potential impact of DSBR factor deficiencies on MH-mediated CSR end-joining have been technically limited. We now use a robust DSB joining assay to elucidate impacts of deficiencies for DSBR factors on CSR and chromosomal translocation junctions in primary mouse B cells and CH12F3 B-lymphoma cells. Compared with wild-type, CSR and c-myc to S region translocation junctions in the absence of 53BP1, and, to a lesser extent, other DSBR factors, have increased MH utilization; indeed, 53BP1-deficient MH profiles resemble those associated with C-NHEJ deficiency. However, translocation junctions between
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