ArticleNucleic acids research2019
AT-dinucleotide rich sequences drive fragile site formation.
Article in Nucleic acids research, 2019. 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.
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
33 citing papers in PubMed, 63 citations in OpenAlex.
- Determinants of dicentric chromosome breakage inbioRxiv : the preprint server for biology · 2026Article
- Clustering of inverted triplications in centromeric and subtelomeric chromosomal regions ofMicrobiology spectrum · 2026Article
- Computational tools for tandem repeat detection using long-read sequencing.Briefings in bioinformatics · 2026Review
- Thermodynamic Determinants in Antibody-Free Nucleic Acid Lateral Flow Assays (AF-NALFA): Lessons from Molecular Detection ofBiomolecules · 2025Article
- Dinucleotide preferences underlie apparent codon preference reversals in theProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanistic study ofFrontiers in genetics · 2025Article
- Downstream transcription promotes human recurrent CNV associated AT-rich sequence mediated genome rearrangements in yeast.iScience · 2024Article
- Running the gauntlet: challenges to genome integrity in spermiogenesis.Nucleus (Austin, Tex.) · 2024Review
- Microsatellite density landscapes illustrate short tandem repeats aggregation in the complete reference human genome.BMC genomics · 2024Article
- Replication of [AT/TA]Biochemistry · 2024Article
- MutSβ protects common fragile sites by facilitating homology-directed repair at DNA double-strand breaks with secondary structures.Nucleic acids research · 2024Article
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- Transcription-Replication Conflicts as a Source of Genome Instability.Annual review of genetics · 2023Review
- Replication of [AT/TA]bioRxiv : the preprint server for biology · 2023Article
- Characterization of the immunoglobulin lambda chain locus from diverse populations reveals extensive genetic variation.Genes and immunity · 2023Article
- The progress in our understanding of CIN in breast cancer research.Frontiers in oncology · 2023Review
- 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
- Article
- Structural Chromosome Instability: Types, Origins, Consequences, and Therapeutic Opportunities.Cancers · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Common fragile sites (CFSs) are genomic regions prone to breakage under replication stress conditions recurrently rearranged in cancer. Many CFSs are enriched with AT-dinucleotide rich sequences (AT-DRSs) which have the potential to form stable secondary structures upon unwinding the double helix during DNA replication. These stable structures can potentially perturb DNA replication progression, leading to genomic instability. Using site-specific targeting system, we show that targeted integration of a 3.4 kb AT-DRS derived from the human CFS FRA16C into a chromosomally stable region within the human genome is able to drive fragile site formation under conditions of replication stress. Analysis of >1300 X chromosomes integrated with the 3.4 kb AT-DRS revealed recurrent gaps and breaks at the integration site. DNA sequences derived from the integrated AT-DRS showed in vitro a significantly increased tendency to fold into branched secondary structures, supporting the predicted mechanism of instability. Our findings clearly indicate that intrinsic DNA features, such as complexed repeated sequence motifs, predispose the human genome to chromosomal instability.
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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.