ArticleCell cycle (Georgetown, Tex.)2011
Give me a break, but not in mitosis: the mitotic DNA damage response marks DNA double-strand breaks with early signaling events.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Centromere protection requires strict mitotic inactivation of the Bloom syndrome helicase complex.Nature communications · 2025Article
- Article
- Mitotic DNA damage promotes chromokinesin-mediated missegregation of polar chromosomes in cancer cells.Molecular biology of the cell · 2023Article
- Revisiting the multisite phosphorylation that produces the M-phase supershift of key mitotic regulators.Molecular biology of the cell · 2022Article
- CIP2A Interacts with TopBP1 and Drives Basal-Like Breast Cancer Tumorigenesis.Cancer research · 2021Article
- Applicability of flow cytometry γH2AX assay in population studies: suitability of fresh and frozen whole blood samples.Archives of toxicology · 2021Article
- Chromosomal instability upregulates interferon in acute myeloid leukemia.Genes, chromosomes & cancer · 2020Article
- MDC1 Interacts with TOPBP1 to Maintain Chromosomal Stability during Mitosis.Molecular cell · 2019Article
- Repetitive Fragile Sites: Centromere Satellite DNA As a Source of Genome Instability in Human Diseases.Genes · 2018Review
- Active DNA end processing in micronuclei of ovarian cancer cells.BMC cancer · 2018Article
- The control of DNA repair by the cell cycle.Nature cell biology · 2016Review
- Chronic oxidative stress promotes H2AX protein degradation and enhances chemosensitivity in breast cancer patients.EMBO molecular medicine · 2016Article
- TopBP1-mediated DNA processing during mitosis.Cell cycle (Georgetown, Tex.) · 2016Article
- Adenovirus replaces mitotic checkpoint controls.Journal of virology · 2015Article
- Polo-like kinase 1 inhibits DNA damage response during mitosis.Cell cycle (Georgetown, Tex.) · 2015Article
- Article
- Mitosis, double strand break repair, and telomeres: a view from the end: how telomeres and the DNA damage response cooperate during mitosis to maintain genome stability.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- TPX2: of spindle assembly, DNA damage response, and cancer.Cellular and molecular life sciences : CMLS · 2014Review
- DNA double strand break repair in mitosis is suppressed by phosphorylation of XRCC4.PLoS genetics · 2014Article
- Dephosphorylation enables the recruitment of 53BP1 to double-strand DNA breaks.Molecular cell · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
: DNA double-strand breaks (DSBs) are extremely cytotoxic with a single unrepaired DSB being sufficient to induce cell death. A complex signalling cascade, termed the DNA damage response (DDR), is in place to deal with such DNA lesions and maintain genome stability. Recent work by us and others has found that the signalling cascade activated by DSBs in mitosis is truncated, displaying apical, but not downstream, components of the DDR. The E3 Ubiquitin ligases RNF8, RNF168 and BRCA1, along with the DDR mediator 53BP1, are not recruited to DSB sites in mitosis, and activation of downstream checkpoint kinases is also impaired. Here, we show that RNF8 and RNF168 are recruited to DNA damage foci in late mitosis, presumably to prime sites for 53BP1 recruitment in early G1. Interestingly, we show that, although RNF8, RNF168 and 53BP1 are excluded from DSB sites during most of mitosis, they associate with mitotic structures such as the kinetochore, suggesting roles for these DDR factors during mitotic cell division. We discuss these and other recent findings and suggest how these novel data collectively contribute to our understanding of mitosis and how cells deal with DNA damage during this crucial cell cycle stage.
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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.