ReviewCell cycle (Georgetown, Tex.)2018
A new class of ultrafine anaphase bridges generated by homologous recombination.
Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 46 citations in OpenAlex.
- Distinct ways by which Srs2 helicase and Rrp1 translocase shape Rad51-DNA interactions in fission yeast.Nucleic acids research · 2026Article
- Towards a unified model of aneuploid karyotype dynamics.PLoS genetics · 2026Article
- Dual-site phosphorylation of SLX4 stabilizes the SLX4-MUS81 interface to promote mitotic SMX assembly and genome protection.Nucleic acids research · 2026Article
- A novel DNA repair-independent role for Gen nuclease in promoting unscheduled polyploidy cell proliferation.PLoS genetics · 2025Article
- RECQ4-MUS81 interaction contributes to telomere maintenance with implications to Rothmund-Thomson syndrome.Nature communications · 2025Article
- The interplay of the translocase activity and protein recruitment function of PICH in ultrafine anaphase bridge resolution and genomic stability.Nucleic acids research · 2025Article
- Molecular basis of FIGNL1 in dissociating RAD51 from DNA and chromatin.Science (New York, N.Y.) · 2025Article
- Cyclin F-EXO1 axis controls cell cycle-dependent execution of double-strand break repair.Science advances · 2024Article
- Molecular basis of FIGNL1 in dissociating RAD51 from DNA and chromatin.bioRxiv : the preprint server for biology · 2024Article
- Human AAA+ ATPase FIGNL1 suppresses RAD51-mediated ultra-fine bridge formation.Nucleic acids research · 2024Article
- DNA strand breaks at centromeres: Friend or foe?Seminars in cell & developmental biology · 2024Review
- The nuclear isoforms of the Fragile X mental retardation RNA-binding protein associate with genomic DNA bridges.Molecular biology of the cell · 2023Article
- Asymmetric Histone Inheritance: Establishment, Recognition, and Execution.Annual review of genetics · 2022Review
- Article
- Critical DNA damaging pathways in tumorigenesis.Seminars in cancer biology · 2022Review
- Processing DNA lesions during mitosis to prevent genomic instability.Biochemical Society transactions · 2022Review
- BLM Sumoylation Is Required for Replication Stability and Normal Fork Velocity During DNA Replication.Frontiers in molecular biosciences · 2022Article
- Regulation of mitotic chromosome architecture and resolution of ultrafine anaphase bridges by PICH.Cell cycle (Georgetown, Tex.) · 2021Article
- Structural Chromosome Instability: Types, Origins, Consequences, and Therapeutic Opportunities.Cancers · 2021Review
- A non-genetic, cell cycle-dependent mechanism of platinum resistance in lung adenocarcinoma.eLife · 2021Article
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
Abstract
Ultrafine anaphase bridges (UFBs) are a potential source of genome instability that is a hallmark of cancer. UFBs can arise from DNA catenanes at centromeres/rDNA loci, late replication intermediates induced by replication stress, and DNA linkages at telomeres. Recently, it was reported that DNA intertwinements generated by homologous recombination give rise to a new class of UFBs, which have been termed homologous recombination ultrafine bridges (HR-UFBs). HR-UFBs are decorated with PICH and BLM in anaphase, and are subsequently converted to RPA-coated, single-stranded DNA bridges. Breakage of these sister chromatid entanglements leads to DNA damage that can be repaired by non-homologous end joining in the next cell cycle, but the potential consequences include DNA rearrangements, chromosome translocations and fusions. Visualisation of these HR-UFBs, and knowledge of how they arise, provides a molecular basis to explain how upregulation of homologous recombination or failure to resolve recombination intermediates leads to the development of chromosomal instability observed in certain cancers.
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.