ArticleOncotarget2016
Cell cycle-dependent resolution of DNA double-strand breaks.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed.
- XRCC1 deficiency drives telomeric chromatin leakage, inflammatory signalling and senescence.Redox biology · 2026Article
- Oxidative genomic or genotoxic stress in neurodegeneration: Mechanisms and therapeutic avenues.AIMS neuroscience · 2025Review
- Mitochondrial dysfunction and impaired DNA damage repair through PICT1 dysregulation in alveolar type II cells in emphysema.Cell communication and signaling : CCS · 2024Article
- Review
- Article
- High turnover and rescue effect of XRCC1 in response to heavy charged particle radiation.Biophysical journal · 2022Article
- Targeting Protein Arginine Methyltransferase 5 Suppresses Radiation-induced Neuroendocrine Differentiation and Sensitizes Prostate Cancer Cells to Radiation.Molecular cancer therapeutics · 2022Article
- Telomere shortening and DNA damage in culprit cells of different types of progressive fibrosing interstitial lung disease.ERJ open research · 2021Article
- Matrix metalloproteinase 9 (MMP9) limits reactive oxygen species (ROS) accumulation and DNA damage in colitis-associated cancer.Cell death & disease · 2020Article
- The genomic landscape of 8-oxodG reveals enrichment at specific inherently fragile promoters.Nucleic acids research · 2020Article
- Assessment of Nuclear and Mitochondrial DNA, Expression of Mitochondria-Related Genes in Different Brain Regions in Rats after Whole-Body X-ray Irradiation.International journal of molecular sciences · 2020Article
- A novel member of Prame family, Gm12794c, counteracts retinoic acid differentiation through the methyltransferase activity of PRC2.Cell death and differentiation · 2020Article
- DNA double-strand breaks: a potential therapeutic target for neurodegenerative diseases.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019Review
- Endoplasmic reticulum and Golgi stress in microcephaly.Cell stress · 2019Review
- Review
- Release of paused RNA polymerase II at specific loci favors DNA double-strand-break formation and promotes cancer translocations.Nature genetics · 2019Article
- Genome-wide mapping of 8-oxo-7,8-dihydro-2'-deoxyguanosine reveals accumulation of oxidatively-generated damage at DNA replication origins within transcribed long genes of mammalian cells.Nucleic acids research · 2019Article
- Dihydrocoumarin, an HDAC Inhibitor, Increases DNA Damage Sensitivity by Inhibiting Rad52.International journal of molecular sciences · 2017Article
- A meeting at risk: Unrepaired DSBs go for broke.Nucleus (Austin, Tex.) · 2017Review
- DNA Damage Induces a Secretory Program in the Quiescent TME that Fosters Adverse Cancer Phenotypes.Molecular cancer research : MCR · 2017Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double strand breaks (DSBs) elicit prompt activation of DNA damage response (DDR), which arrests cell-cycle either in G1/S or G2/M in order to avoid entering S and M phase with damaged DNAs. Since mammalian tissues contain both proliferating and quiescent cells, there might be fundamental difference in DDR between proliferating and quiescent cells (or G0-arrested). To investigate these differences, we studied recruitment of DSB repair factors and resolution of DNA lesions induced at site-specific DSBs in asynchronously proliferating, G0-, or G1-arrested cells. Strikingly, DSBs occurring in G0 quiescent cells are not repaired and maintain a sustained activation of the p53-pathway. Conversely, re-entry into cell cycle of damaged G0-arrested cells, occurs with a delayed clearance of DNA repair factors initially recruited to DSBs, indicating an inefficient repair when compared to DSBs induced in asynchronously proliferating or G1-synchronized cells. Moreover, we found that initial recognition of DSBs and assembly of DSB factors is largely similar in asynchronously proliferating, G0-, or G1-synchronized cells. Our study thereby demonstrates that repair and resolution of DSBs is strongly dependent on the cell-cycle state.
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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.