ArticleNucleic acids research2015
53BP1 promotes microhomology-mediated end-joining in G1-phase cells.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- Persistent TOP1 cleavage complexes in drug-tolerant cells drive adaptive resistance to EGFR-targeted therapies in lung cancer.Science advances · 2026Article
- Activation of Pol theta-mediated end joining begins during mitotic commitment.bioRxiv : the preprint server for biology · 2026Article
- Roles for the 3D genome in the cell cycle, DNA replication, and double strand break repair.Frontiers in cell and developmental biology · 2025Review
- Computational advances in the design and discovery of artemis inhibitors for radiosensitization in cancer therapy.Frontiers in chemistry · 2025Article
- Increased DNA Damage and Insufficient DNA Repair in Euthyroid Patients With Nodular Goiter Analyzed by γ-H2AX and 53BP1 Foci Assay.Journal of clinical practice and research · 2024Article
- Gene expression of non-homologous end-joining pathways in the prognosis of ovarian cancer.iScience · 2023Article
- Enhancing Precision and Efficiency of Cas9-Mediated Knockin Through Combinatorial Fusions of DNA Repair Proteins.The CRISPR journal · 2023Article
- GAPDH facilitates homologous recombination repair by stabilizing RAD51 in an HDAC1-dependent manner.EMBO reports · 2023Article
- The contribution of DNA repair pathways to genome editing and evolution in filamentous pathogens.FEMS microbiology reviews · 2022Review
- Contribution of Microhomology to Genome Instability: Connection between DNA Repair and Replication Stress.International journal of molecular sciences · 2022Review
- Potential Molecular Mechanisms behind the Ultra-High Dose Rate "FLASH" Effect.International journal of molecular sciences · 2022Review
- Article
- Targeting PARP proteins in acute leukemia: DNA damage response inhibition and therapeutic strategies.Journal of hematology & oncology · 2022Review
- DNA End Joining: G0-ing to the Core.Biomolecules · 2021Review
- Review
- Replicated chromatin curtails 53BP1 recruitment in BRCA1-proficient and BRCA1-deficient cells.Life science alliance · 2021Article
- Thermodynamic analysis of DNA hybridization signatures near mitochondrial DNA deletion breakpoints.iScience · 2021Article
- Alternative Non-Homologous End-Joining: Error-Prone DNA Repair as Cancer's Achilles' Heel.Cancers · 2021Review
- Somatic Mutations in Oncogenes Are in Chronic Myeloid Leukemia AcquiredFrontiers in oncology · 2021Article
- To Join or Not to Join: Decision Points Along the Pathway to Double-Strand Break Repair vs. Chromosome End Protection.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Alternative non-homologous end joining (alt-NHEJ) was originally identified as a backup repair mechanism in the absence of classical NHEJ (c-NHEJ) factors but recent studies have demonstrated that alt-NHEJ is active even when c-NHEJ as well as homologous recombination is available. The functions of 53BP1 in NHEJ processes are not well understood. Here, we report that 53BP1 promotes DNA double-strand break (DSB) repair and genomic stability not only in c-NHEJ-proficient but also -deficient human G1-phase cells. Using an array of repair substrates we show that these effects of 53BP1 are correlated with a promotion of microhomology-mediated end-joining (MMEJ), a subtype of alt-NHEJ, in G1-phase. Consistent with a specific role in MMEJ we confirm that 53BP1 status does not affect c-NHEJ. 53BP1 supports sequence deletion during MMEJ consistent with a putative role in facilitating end-resection. Interestingly, promotion of MMEJ by 53BP1 in G1-phase cells is only observed in the presence of functional BRCA1. Depletion of both 53BP1 and BRCA1 increases repair needing microhomology usage and augments loss of DNA sequence, suggesting that MMEJ is a highly regulated DSB repair process. Together, these findings significantly expand our understanding of the cell-cycle-dependent roles of 53BP1 in DSB repair.
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Registered trials
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.