ArticleMolecular and cellular biology2014
KAP-1 promotes resection of broken DNA ends not protected by γ-H2AX and 53BP1 in G₁-phase lymphocytes.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Senataxin and DNA-PKcs redundantly promote non-homologous end joining repair of DNA double strand breaks during V(D)J recombination.Science advances · 2025Article
- THE GID COMPLEX REGULATES DNA END PROCESSING DURING DNA DOUBLE-STRAND BREAK REPAIR BY NONHOMOLOGOUS END JOINING.Transactions of the American Clinical and Climatological Association · 2025Article
- ATM and 53BP1 regulate alternative end joining-mediated V(D)J recombination.Science advances · 2024Article
- MYSM1 attenuates DNA damage signals triggered by physiologic and genotoxic DNA breaks.The Journal of allergy and clinical immunology · 2024Article
- Nuclease-independent functions of RAG1 direct distinct DNA damage responses in B cells.EMBO reports · 2023Article
- DNA polymerase η promotes nonhomologous end joining upon etoposide exposure dependent on the scaffolding protein Kap1.The Journal of biological chemistry · 2022Article
- The regulation of DNA end resection by chromatin response to DNA double strand breaks.Frontiers in cell and developmental biology · 2022Review
- A Whole Genome CRISPR/Cas9 Screening Approach for Identifying Genes Encoding DNA End-Processing Proteins.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Assessing DNA Damage Responses Using B Lymphocyte Cultures.Methods in molecular biology (Clifton, N.J.) · 2022Article
- The RNF8 and RNF168 Ubiquitin Ligases Regulate Pro- and Anti-Resection Activities at Broken DNA Ends During Non-Homologous End Joining.DNA repair · 2021Article
- Article
- RAG enhances BCR-ABL1-positive leukemic cell growth through its endonuclease activity in vitro and in vivo.Cancer science · 2021Article
- The (Lack of) DNA Double-Strand Break Repair Pathway Choice During V(D)J Recombination.Frontiers in genetics · 2021Review
- Homology-Directed Repair and the Role of BRCA1, BRCA2, and Related Proteins in Genome Integrity and Cancer.Annual review of cancer biology · 2018Article
- Bromodomain proteins: repairing DNA damage within chromatin.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- ATM loss leads to synthetic lethality in BRCA1 BRCT mutant mice associated with exacerbated defects in homology-directed repair.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Deficiency of XLF and PAXX prevents DNA double-strand break repair by non-homologous end joining in lymphocytes.Cell cycle (Georgetown, Tex.) · 2017Article
- RAG2 and XLF/Cernunnos interplay reveals a novel role for the RAG complex in DNA repair.Nature communications · 2016Article
- Analysis of the ways and methods of signaling pathways in regulating cell cycle of NIH3T3 at transcriptional level.BMC cell biology · 2015Article
- HCoDES reveals chromosomal DNA end structures with single-nucleotide resolution.Molecular cell · 2014Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The resection of broken DNA ends is required for DNA double-strand break (DSB) repair by homologous recombination (HR) but can inhibit normal repair by nonhomologous end joining (NHEJ), the main DSB repair pathway in G1-phase cells. Antigen receptor gene assembly proceeds through DNA DSB intermediates generated in G1-phase lymphocytes by the RAG endonuclease. These DSBs activate ATM, which phosphorylates H2AX, forming γ-H2AX in flanking chromatin. γ-H2AX prevents CtIP from initiating resection of RAG DSBs. Whether there are additional proteins required to promote resection of these DNA ends is not known. KRAB-associated protein 1 (KAP-1) (TRIM28) is a transcriptional repressor that modulates chromatin structure and has been implicated in the repair of DNA DSBs in heterochromatin. Here, we show that in murine G1-phase lymphocytes, KAP-1 promotes resection of DSBs that are not protected by H2AX and its downstream effector 53BP1. In these murine cells, KAP-1 activity in DNA end resection is attenuated by a single-amino-acid change that reflects a KAP-1 polymorphism between primates and other mammalian species. These findings establish KAP-1 as a component of the machinery that can resect DNA ends in G1-phase cells and suggest that there may be species-specific features to this activity.
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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.