ArticleGenome research2006
Common fragile sites are conserved features of human and mouse chromosomes and relate to large active genes.
Article in Genome research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 102 citations in OpenAlex.
- Multiomic characterization of DNA released after airway exposure to allergens and nanoparticles reveals selective export of repetitive and fragile site DNA.Physiological genomics · 2026Article
- Early replication fragile sites are associated with cancer-related CNVs and SNVs in human embryonic stem cells.Stem cell reports · 2026Article
- Microsatellite density landscapes illustrate short tandem repeats aggregation in the complete reference human genome.BMC genomics · 2024Article
- Cell-Free Genic Extrachromosomal Circular DNA Profiles of DNase Knockouts Associated with Systemic Lupus Erythematosus and Relation with Common Fragile Sites.Biomedicines · 2023Article
- Review
- Article
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- UBE2T resolves transcription-replication conflicts and protects common fragile sites in primordial germ cells.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Breaking the paradigm: early insights from mammalian DNA breakomes.The FEBS journal · 2022Review
- Genomic patterns of transcription-replication interactions in mouse primary B cells.Nucleic acids research · 2022Article
- Article
- Consequences and Resolution of Transcription-Replication Conflicts.Life (Basel, Switzerland) · 2021Review
- Genomic Instability Profiles at the Single Cell Level in Mouse Colorectal Cancers of Defined Genotypes.Cancers · 2021Article
- Sites of chromosomal instability in the context of nuclear architecture and function.Cellular and molecular life sciences : CMLS · 2021Review
- Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing.Cell research · 2020Article
- Small RNAs, Big Diseases.International journal of molecular sciences · 2020Review
- Transcription-replication conflicts as a source of common fragile site instability caused by BMI1-RNF2 deficiency.PLoS genetics · 2020Article
- A P53-Independent DNA Damage Response Suppresses Oncogenic Proliferation and Genome Instability.Cell reports · 2020Article
- Visualizing locus-specific sister chromatid exchange reveals differential patterns of replication stress-induced fragile site breakage.Oncogene · 2020Article
2 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites (CFSs) are seen as chromosomal gaps and breaks brought about by inhibition of replication, and it is thought that they cluster with tumor breakpoints. This study presents a comprehensive analysis using conventional and molecular cytogenetic mapping of CFSs and their expression frequencies in two mouse strains, BALB/c and C57BL/6, and in human probands. Here we show that induced mouse CFSs relate to sites of spontaneous gaps and breaks and that CFS expression levels in chromosome bands are conserved between the two mouse strains and between syntenic mouse and human DNA segments. Furthermore, four additional mouse CFSs were found to be homologous to human CFSs on the molecular cytogenetic level (Fra2D-FRA2G, Fra4C2-FRA9E, Fra6A3.1-FRA7G, and Fra6B1-FRA7H), increasing the number of such CFSs already described in the literature to eight. Contrary to previous reports, DNA helix flexibility is not increased in the 15 human and eight mouse CFSs molecularly defined so far, compared to large nonfragile control regions. Our findings suggest that the mechanisms that provoke instability at CFSs are evolutionarily conserved. The role that large transcriptionally active genes may play in CFS expression is discussed.
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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.