ReviewF1000Research2017
The "enemies within": regions of the genome that are inherently difficult to replicate.
Review in F1000Research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
19 citing papers in PubMed, 33 citations in OpenAlex.
- The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ.Nature communications · 2025Article
- CDK-driven phosphorylation of TRAIP is essential for mitotic replisome disassembly and MiDAS.Nucleic acids research · 2025Article
- Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells.Nucleic acids research · 2024Article
- Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells.Nature communications · 2023Article
- A moving target for drug discovery: Structure activity relationship and many genome (de)stabilizing functions of the RAD52 protein.DNA repair · 2022Review
- Break-induced replication: unraveling each step.Trends in genetics : TIG · 2022Review
- Break-induced replication mechanisms in yeast and mammals.Current opinion in genetics & development · 2021Review
- Review
- Repair of DNA Breaks by Break-Induced Replication.Annual review of biochemistry · 2021Review
- The epigenetic regulator LSH maintains fork protection and genomic stability via MacroH2A deposition and RAD51 filament formation.Nature communications · 2021Article
- High-resolution mapping of mitotic DNA synthesis regions and common fragile sites in the human genome through direct sequencing.Cell research · 2020Article
- Mechanisms of eukaryotic replisome disassembly.Biochemical Society transactions · 2020Review
- TRAIP drives replisome disassembly and mitotic DNA repair synthesis at sites of incomplete DNA replication.eLife · 2019Article
- EXD2 Protects Stressed Replication Forks and Is Required for Cell Viability in the Absence of BRCA1/2.Molecular cell · 2019Article
- Mitotic replisome disassembly depends on TRAIP ubiquitin ligase activity.Life science alliance · 2019Article
- Mitotic CDK Promotes Replisome Disassembly, Fork Breakage, and Complex DNA Rearrangements.Molecular cell · 2019Article
- Break-Induced Replication: The Where, The Why, and The How.Trends in genetics : TIG · 2018Review
- Pathways for maintenance of telomeres and common fragile sites during DNA replication stress.Open biology · 2018Review
- DNA replication stress and cancer chemotherapy.Cancer science · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An unusual feature of many eukaryotic genomes is the presence of regions that appear intrinsically difficult to copy during the process of DNA replication. Curiously, the location of these difficult-to-replicate regions is often conserved between species, implying a valuable role in some aspect of genome organization or maintenance. The most prominent class of these regions in mammalian cells is defined as chromosome fragile sites, which acquired their name because of a propensity to form visible gaps/breaks on otherwise-condensed chromosomes in mitosis. This fragility is particularly apparent following perturbation of DNA replication-a phenomenon often referred to as "replication stress". Here, we review recent data on the molecular basis for chromosome fragility and the role of fragile sites in the etiology of cancer. In particular, we highlight how studies on fragile sites have provided unexpected insights into how the DNA repair machinery assists in the completion of DNA replication.
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What OpenQuestion holds
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.