ArticleHuman molecular genetics2010
Impaired replication dynamics at the FRA3B common fragile site.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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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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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Adaptive Replication Fork Acceleration by CDK1-Cyclin B1 Sustains Genome Duplication despite Impaired Origin Firing.bioRxiv : the preprint server for biology · 2026Article
- A Unifying Hypothesis for the Genome Dynamics Proposed to Underlie Neuropsychiatric Phenotypes.Genes · 2024Review
- Fragile sites, chromosomal lesions, tandem repeats, and disease.Frontiers in genetics · 2022Review
- New Era of Mapping and Understanding Common Fragile Sites: An Updated Review on Origin of Chromosome Fragility.Frontiers in genetics · 2022Review
- Efficiency and equity in origin licensing to ensure complete DNA replication.Biochemical Society transactions · 2021Review
- Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing.Cell research · 2020Article
- From R-Loops to G-Quadruplexes: Emerging New Threats for the Replication Fork.International journal of molecular sciences · 2020Review
- Common fragile sites: protection and repair.Cell & bioscience · 2020Review
- Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.International journal of molecular sciences · 2018Review
- Dormant origins as a built-in safeguard in eukaryotic DNA replication against genome instability and disease development.DNA repair · 2017Review
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- Evidence for chromosome fragility at the frataxin locus in Friedreich ataxia.Mutation research · 2015Article
- Interplay between genetic and epigenetic factors governs common fragile site instability in cancer.Cellular and molecular life sciences : CMLS · 2014Review
- Molecular characterization of common fragile sites as a strategy to discover cancer susceptibility genes.Cellular and molecular life sciences : CMLS · 2014Review
- Chromosome fragility and the abnormal replication of the FMR1 locus in fragile X syndrome.Human molecular genetics · 2014Article
- Impediments to replication fork movement: stabilisation, reactivation and genome instability.Chromosoma · 2013Review
- Genome instability at common fragile sites: searching for the cause of their instability.BioMed research international · 2013Review
- High-resolution whole-genome analysis of skull base chordomas implicates FHIT loss in chordoma pathogenesis.Neoplasia (New York, N.Y.) · 2012Article
- Chromatin changes in the development and pathology of the Fragile X-associated disorders and Friedreich ataxia.Biochimica et biophysica acta · 2012Review
- A genome-wide analysis of common fragile sites: what features determine chromosomal instability in the human genome?Genome research · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Chromosomal common fragile sites (CFSs) are genetically unstable regions of the genome that are induced by conditions that impair DNA replication. In this report, we show that treatment with the DNA polymerase inhibitor, aphidicolin (APH), slows the replication rate throughout S phase. To investigate the unusual sensitivity of CFSs to APH-induced replication stress, we examined replication dynamics within a 50 kb region of the most frequently expressed CFS, FRA3B. We mapped four origins of replication, ori 1-4, using two independent methods. In untreated cells, we detected significantly less newly replicated DNA at FRA3B ori 1-3, as compared with three control origins located within non-fragile regions (NCFSs). In APH-treated cells, all FRA3B and control origins tested were active; however, there was a significant increase of nascent strand DNA at the control origins and, to a lesser extent, at the FRA3B ori 1-3. On the basis of these observations and the theoretical modeling of the nascent strand abundance assay developed in this study, we hypothesize that CFS origins may be less efficient, and that APH treatment slows replication fork movement near these origins to a greater extent, resulting in impaired DNA replication and, ultimately, leading to the genetic instability characteristic of CFSs.
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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.