SynthesisNucleic acids research2017
Meta-analysis of DNA double-strand break response kinetics.
Synthesis 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 39 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Article
- The NuRD chromatin remodeling complex contributes to repairing exogenous double-strand breaks in the Caenorhabditis elegans germline.Genetics · 2026Article
- Histone PARylation factor 1: a review of its role in the DNA damage response.Nucleic acids research · 2025Review
- NuRD chromatin remodeling is required to repair exogenous DSBs in thebioRxiv : the preprint server for biology · 2025Article
- Article
- CellTool: An Open-Source Software Combining Bio-Image Analysis and Mathematical Modeling for the Study of DNA Repair Dynamics.International journal of molecular sciences · 2023Article
- Genome-wide analysis of DNA-PK-bound MRN cleavage products supports a sequential model of DSB repair pathway choice.Nature communications · 2023Article
- Dissection of DNA damage and repair pathways in live cells by femtosecond laser microirradiation and free-electron modeling.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Live-cell tracking of γ-H2AX kinetics reveals the distinct modes of ATM and DNA-PK in the immediate response to DNA damage.Journal of cell science · 2023Article
- Recruitment of RBM6 to DNA Double-Strand Breaks Fosters Homologous Recombination Repair.Molecular and cellular biology · 2023Article
- Article
- Characterization of DNA-PK-Bound End Fragments Using GLASS-ChIP.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Automated modeling of protein accumulation at DNA damage sites using qFADD.py.Biological imaging · 2022Article
- The BRCT domain of PARP1 binds intact DNA and mediates intrastrand transfer.Molecular cell · 2021Article
- Reconsidering pathway choice: a sequential model of mammalian DNA double-strand break pathway decisions.Current opinion in genetics & development · 2021Review
- RBM6 splicing factor promotes homologous recombination repair of double-strand breaks and modulates sensitivity to chemotherapeutic drugs.Nucleic acids research · 2021Article
- DNArepairK: An Interactive Database for Exploring the Impact of Anticancer Drugs onto the Dynamics of DNA Repair Proteins.Biomedicines · 2021Article
- A simple microscopy setup for visualizing cellular responses to DNA damage at particle accelerator facilities.Scientific reports · 2021Article
- The Multifaceted Roles of Ku70/80.International journal of molecular sciences · 2021Review
- Super-resolution mapping of cellular double-strand break resection complexes during homologous recombination.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most proteins involved in the DNA double-strand break response (DSBR) accumulate at the damage sites, where they perform functions related to damage signaling, chromatin remodeling and repair. Over the last two decades, studying the accumulation of many DSBR proteins provided information about their functionality and underlying mechanisms of action. However, comparison and systemic interpretation of these data is challenging due to their scattered nature and differing experimental approaches. Here, we extracted, analyzed and compared the available results describing accumulation of 79 DSBR proteins at sites of DNA damage, which can be further explored using Cumulus (http://www.dna-repair.live/cumulus/)-the accompanying interactive online application. Despite large inter-study variability, our analysis revealed that the accumulation of most proteins starts immediately after damage induction, occurs in parallel and peaks within 15-20 min. Various DSBR pathways are characterized by distinct accumulation kinetics with major non-homologous end joining proteins being generally faster than those involved in homologous recombination, and signaling and chromatin remodeling factors accumulating with varying speeds. Our meta-analysis provides, for the first time, comprehensive overview of the temporal organization of the DSBR in mammalian cells and could serve as a reference for future mechanistic studies of this complex process.
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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.