ArticleNucleic acids research2017
Microhomology-mediated end joining is activated in irradiated human cells due to phosphorylation-dependent formation of the XRCC1 repair complex.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 84 citations in OpenAlex.
- Radiation-induced lymphopenia during chemoradiation therapy for non-small cell lung cancer is linked with age, lung V5, and XRCC1 rs25487 genotypes in lymphocytes.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2021Trial
- DNA-PKcs and PARP1 at the interface between DNA damage responses and cGAS-STING signaling: context-dependent roles and therapeutic implications.Cancer biology & therapy · 2026Review
- Defective microhomology-mediated end joining inScience advances · 2026Article
- Invas: an inversion-aware method for transcriptome assembly.Nature communications · 2026Article
- BRCA1-A and LIG4 complexes mediate ecDNA biogenesis and cancer drug resistance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- HP1β recruits RING1A to ubiquitinate histone H2A for BRCA1-mediated resection of double-stand breaks.iScience · 2026Article
- Hepatitis B viral DNA integration occurs within three days of infection and is enhanced by ATR inhibition.Tumour virus research · 2025Article
- Defective Microhomology-Mediated End-joining in SMARCB1-Deficient Tumors.bioRxiv : the preprint server for biology · 2025Article
- Influence of PARP1 on CRISPR/Cas9 induced double strand break repair in proliferating cells.Computational and structural biotechnology journal · 2025Article
- How to use CRISPR/Cas9 in plants: from target site selection to DNA repair.Journal of experimental botany · 2024Review
- High-complexity of DNA double-strand breaks is key for alternative end-joining choice.Communications biology · 2024Article
- Review
- PARG is essential for Polθ-mediated DNA end-joining by removing repressive poly-ADP-ribose marks.Nature communications · 2024Article
- XRCC1: a potential prognostic and immunological biomarker in LGG based on systematic pan-cancer analysis.Aging · 2024Article
- Mammalian DNA ligases; roles in maintaining genome integrity.Journal of molecular biology · 2024Review
- A goldilocks computational protocol for inhibitor discovery targeting DNA damage responses including replication-repair functions.Frontiers in molecular biosciences · 2024Article
- Novobiocin blocks nucleic acid binding to Polθ and inhibits stimulation of its ATPase activity.Nucleic acids research · 2023Article
- Overexpression of XRCC1 is Associated with Poor Survival in Patients with Head and Neck Squamous Carcinoma and Has Potential to Be Used as Targeted Therapy by Synthetic Lethality.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- The APE2 nuclease is essential for DNA double-strand break repair by microhomology-mediated end joining.Molecular cell · 2023Article
- PARP-1: a critical regulator in radioprotection and radiotherapy-mechanisms, challenges, and therapeutic opportunities.Frontiers in pharmacology · 2023Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
Microhomology-mediated end joining (MMEJ), an error-prone pathway for DNA double-strand break (DSB) repair, is implicated in genomic rearrangement and oncogenic transformation; however, its contribution to repair of radiation-induced DSBs has not been characterized. We used recircularization of a linearized plasmid with 3΄-P-blocked termini, mimicking those at X-ray-induced strand breaks, to recapitulate DSB repair via MMEJ or nonhomologous end-joining (NHEJ). Sequence analysis of the circularized plasmids allowed measurement of relative activity of MMEJ versus NHEJ. While we predictably observed NHEJ to be the predominant pathway for DSB repair in our assay, MMEJ was significantly enhanced in preirradiated cells, independent of their radiation-induced arrest in the G2/M phase. MMEJ activation was dependent on XRCC1 phosphorylation by casein kinase 2 (CK2), enhancing XRCC1's interaction with the end resection enzymes MRE11 and CtIP. Both endonuclease and exonuclease activities of MRE11 were required for MMEJ, as has been observed for homology-directed DSB repair (HDR). Furthermore, the XRCC1 co-immunoprecipitate complex (IP) displayed MMEJ activity in vitro, which was significantly elevated after irradiation. Our studies thus suggest that radiation-mediated enhancement of MMEJ in cells surviving radiation therapy may contribute to their radioresistance and could be therapeutically targeted.
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