ArticleLife science alliance2021
Replicated chromatin curtails 53BP1 recruitment in BRCA1-proficient and BRCA1-deficient cells.
Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- Nuclear and genome dynamics underlying DNA double-strand break repair.Nature reviews. Molecular cell biology · 2025Review
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- RAD18 directs DNA double-strand break repair by homologous recombination to post-replicative chromatin.Nucleic acids research · 2024Article
- Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.Aging cell · 2024Article
- DNA Double Strand Break and Response Fluorescent Assays: Choices and Interpretation.International journal of molecular sciences · 2024Review
- Decline of DNA damage response along with myogenic differentiation.Life science alliance · 2024Article
- ZMYM2 restricts 53BP1 at DNA double-strand breaks to favor BRCA1 loading and homologous recombination.Nucleic acids research · 2022Article
- Laser Microirradiation and Real-time Recruitment Assays Using an Engineered Biosensor.Bio-protocol · 2022Article
- Heterogeneity of Organization of Subcompartments in DSB Repair Foci.Frontiers in genetics · 2022Article
- When the RAP (80) fades out, you can hear BRCA1 RING.EMBO reports · 2021Article
- Revisiting the BRCA-pathway through the lens of replication gap suppression: "Gaps determine therapy response in BRCA mutant cancer".DNA repair · 2021Review
- Review
- Sex-specific differences in DNA double-strand break repair of cycling human lymphocytes during aging.Aging · 2021Article
- Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency.Molecular cell · 2021Article
- Cell-cycle dependent inhibition of BRCA1 signaling by the lysine methyltransferase SET8.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
DNA double-strand breaks can be repaired by non-homologous end-joining or homologous recombination. Which pathway is used depends on the balance between the tumor suppressors 53BP1 and BRCA1 and on the availability of an undamaged template DNA for homology-directed repair. How cells switch from a 53BP1-dominated to a BRCA1-governed homologous recombination response as they progress through the cell cycle is incompletely understood. Here we reveal, using high-throughput microscopy and applying single cell normalization to control for increased genome size as cells replicate their DNA, that 53BP1 recruitment to damaged replicated chromatin is inefficient in both BRCA1-proficient and BRCA1-deficient cells. Our results substantiate a dual switch model from a 53BP1-dominated response in unreplicated chromatin to a BRCA1-BARD1-dominated response in replicated chromatin, in which replication-coupled dilution of 53BP1's binding mark H4K20me2 functionally cooperates with BRCA1-BARD1-mediated suppression of 53BP1 binding. More generally, we suggest that appropriate normalization of single cell data, for example, to DNA content, provides additional layers of information, which can be critical for quantifying and interpreting cellular phenotypes.
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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.