ReviewGenes2018
The Unresolved Problem of DNA Bridging.
Review in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 50 citations in OpenAlex.
- ESCRT-III assembles around mis-segregated DNA to protect genome stability.Nature structural & molecular biology · 2026Article
- RECQ4 arginine methylation suppresses single-stranded DNA gap accumulation at replication forks.Nucleic acids research · 2026Article
- Dual-site phosphorylation of SLX4 stabilizes the SLX4-MUS81 interface to promote mitotic SMX assembly and genome protection.Nucleic acids research · 2026Article
- A MOPD II-associated Pericentrin variant disrupts PACT domain dimerization and pericentriolar material recruitment.bioRxiv : the preprint server for biology · 2026Article
- Local heterochromatin enrichment promotes telomere clustering and PML nuclear body assembly at telomeres.Cell reports · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Article
- Integrated Assessment of Silver Nanoparticles on Plant Growth and Cytogenotoxicity UsingJournal of xenobiotics · 2025Article
- Centromere protection requires strict mitotic inactivation of the Bloom syndrome helicase complex.Nature communications · 2025Article
- SRBD1 facilitates chromosome segregation by promoting topoisomerase IIα localization to mitotic chromosomes.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
- Elucidation of the molecular mechanism of the breakage-fusion-bridge (BFB) cycle using a CRISPR-dCas9 cellular model.Nucleic acids research · 2024Article
- Developmental signals control chromosome segregation fidelity during pluripotency and neurogenesis by modulating replicative stress.Nature communications · 2024Article
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- Article
- The nuclear isoforms of the Fragile X mental retardation RNA-binding protein associate with genomic DNA bridges.Molecular biology of the cell · 2023Article
- Connections between sister and non-sister telomeres of segregating chromatids maintain euploidy.Current biology : CB · 2023Article
- A pan-cancer analysis of the oncogenic role of ERCC6L.BMC cancer · 2022Article
- Asymmetric Histone Inheritance: Establishment, Recognition, and Execution.Annual review of genetics · 2022Review
- Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy.Nature communications · 2022Article
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
Accurate duplication and transmission of identical genetic information into offspring cells lies at the heart of a cell division cycle. During the last stage of cellular division, namely mitosis, the fully replicated DNA molecules are condensed into X-shaped chromosomes, followed by a chromosome separation process called sister chromatid disjunction. This process allows for the equal partition of genetic material into two newly born daughter cells. However, emerging evidence has shown that faithful chromosome segregation is challenged by the presence of persistent DNA intertwining structures generated during DNA replication and repair, which manifest as so-called ultra-fine DNA bridges (UFBs) during anaphase. Undoubtedly, failure to disentangle DNA linkages poses a severe threat to mitosis and genome integrity. This review will summarize the possible causes of DNA bridges, particularly sister DNA inter-linkage structures, in an attempt to explain how they may be processed and how they influence faithful chromosome segregation and the maintenance of genome stability.
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.