ReviewChromosoma2013
Impediments to replication fork movement: stabilisation, reactivation and genome instability.
Review in Chromosoma, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 95 citations in OpenAlex.
- Canonical and noncanonical forms of G4 DNA at cluster III of the BCL6 breakpoint region could lead to chromosomal translocation in DLBCL.The Journal of biological chemistry · 2026Article
- Replication Stress in Cancer: Mechanistic Insights and Therapeutic Opportunities for Radiosensitization.Current issues in molecular biology · 2026Review
- Overcoming natural replication barriers formed by DNA structures and the role of repositioning to the nuclear periphery.DNA repair · 2025Review
- Review
- Joint Efforts of Replicative Helicase and SSB Ensure Inherent Replicative Tolerance of G-Quadruplex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The nucleolar protein GNL3 prevents resection of stalled replication forks.EMBO reports · 2023Article
- Article
- An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress.Nature communications · 2023Article
- The organizer of chromatin topology RIF1 ensures cellular resilience to DNA replication stress.Life science alliance · 2023Article
- Rad52's DNA annealing activity drives template switching associated with restarted DNA replication.Nature communications · 2022Article
- Confined migration induces heterochromatin formation and alters chromatin accessibility.iScience · 2022Article
- RecA and RecB: probing complexes of DNA repair proteins with mitomycin C in liveJournal of the Royal Society, Interface · 2022Article
- SLX4-XPF mediates DNA damage responses to replication stress induced by DNA-protein interactions.The Journal of cell biology · 2021Article
- The Replication Stress Response on a Narrow Path Between Genomic Instability and Inflammation.Frontiers in cell and developmental biology · 2021Review
- Approaching Protein Barriers: Emerging Mechanisms of Replication Pausing in Eukaryotes.Frontiers in cell and developmental biology · 2021Review
- Deletion of the GAPDH gene contributes to genome stability in Saccharomyces cerevisiae.Scientific reports · 2020Article
- Time for remodeling: SNF2-family DNA translocases in replication fork metabolism and human disease.DNA repair · 2020Review
- Review
- Review
- Article
4 more citing papers are in PubMed but not listed here.
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 2 institutions in 2 countries.
Funding
Abstract
Maintaining genome stability is essential for the accurate transmission of genetic material. Genetic instability is associated with human genome disorders and is a near-universal hallmark of cancer cells. Genetic variation is also the driving force of evolution, and a genome must therefore display adequate plasticity to evolve while remaining sufficiently stable to prevent mutations and chromosome rearrangements leading to a fitness disadvantage. A primary source of genome instability are errors that occur during chromosome replication. More specifically, obstacles to the movement of replication forks are known to underlie many of the gross chromosomal rearrangements seen both in human cells and in model organisms. Obstacles to replication fork progression destabilize the replisome (replication protein complex) and impact on the integrity of forked DNA structures. Therefore, to ensure the successful progression of a replication fork along with its associated replisome, several distinct strategies have evolved. First, there are well-orchestrated mechanisms that promote continued movement of forks through potential obstacles. Second, dedicated replisome and fork DNA stabilization pathways prevent the dysfunction of the replisome if its progress is halted. Third, should stabilisation fail, there are mechanisms to ensure damaged forks are accurately fused with a converging fork or, when necessary, re-associated with the replication proteins to continue replication. Here, we review what is known about potential barriers to replication fork progression, how these are tolerated and their impact on genome instability.
Indexed as
Identifiers
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.