ReviewChromosoma2017
Transcription-replication conflicts at chromosomal fragile sites-consequences in M phase and beyond.
Review in Chromosoma, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 21 citations in OpenAlex.
- Transcription-replication conflict resolution by nuclear RNA interference.Molecular cell · 2025Article
- Chromoanasynthesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Modification of Seurat v4 for the Development of a Phase Assignment Tool Able to Distinguish between G2 and Mitotic Cells.International journal of molecular sciences · 2024Article
- XPF interacts with TOP2B for R-loop processing and DNA looping on actively transcribed genes.Science advances · 2023Article
- Consequences and Resolution of Transcription-Replication Conflicts.Life (Basel, Switzerland) · 2021Review
- Sites of chromosomal instability in the context of nuclear architecture and function.Cellular and molecular life sciences : CMLS · 2021Review
- Large Intronic Deletion of the Fragile Site GeneFrontiers in genetics · 2021Article
- TriTag: an integrative tool to correlate chromatin dynamics and gene expression in living cells.Nucleic acids research · 2020Article
- A distinct role for recombination repair factors in an early cellular response to transcription-replication conflicts.Nucleic acids research · 2020Article
- Transcription-replication conflicts as a source of common fragile site instability caused by BMI1-RNF2 deficiency.PLoS genetics · 2020Article
- Transcription-mediated replication hindrance: a major driver of genome instability.Genes & development · 2019Review
- The processivity factor Pol32 mediates nuclear localization of DNA polymerase delta and prevents chromosomal fragile site formation in Drosophila development.PLoS genetics · 2019Article
- Review
- R-loops: targets for nuclease cleavage and repeat instability.Current genetics · 2018Review
- Translesion and Repair DNA Polymerases: Diverse Structure and Mechanism.Annual review of biochemistry · 2018Review
- FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells.Nucleic acids research · 2018Article
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
Collision between the molecular machineries responsible for transcription and replication is an important source of genome instability. Certain transcribed regions known as chromosomal fragile sites are particularly prone to recombine and mutate in a manner that correlates with specific transcription and replication patterns. At the same time, these chromosomal fragile sites engage in aberrant DNA structures in mitosis. Here, we discuss the mechanistic details of transcription-replication conflicts including putative scenarios for R-loop-induced replication inhibition to understand how transcription-replication conflicts transition from S phase into various aberrant DNA structures in mitosis.
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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.