ArticleGenes & development2005
Homologous recombination and nonhomologous end-joining repair pathways regulate fragile site stability.
Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 126 citations in OpenAlex.
- Mechanisms of Hydroxyurea-Mediated DNA Damage Potentiation in Fanconi Anemia Cells.International journal of molecular sciences · 2026Article
- Local Genomic Instability of theGenes · 2024Article
- Beta human papillomavirus 8 E6 allows colocalization of non-homologous end joining and homologous recombination repair factors.PLoS pathogens · 2022Article
- Novel and emerging biotechnological crop protection approaches.Plant biotechnology journal · 2021Review
- Moving beyond PARP Inhibition: Current State and Future Perspectives in Breast Cancer.International journal of molecular sciences · 2021Review
- Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review.Frontiers in molecular biosciences · 2021Review
- Beta Human Papillomavirus 8E6 Attenuates Non-Homologous End Joining by Hindering DNA-PKcs Activity.Cancers · 2020Article
- Article
- Visualizing locus-specific sister chromatid exchange reveals differential patterns of replication stress-induced fragile site breakage.Oncogene · 2020Article
- Article
- Proteomic characterization of chromosomal common fragile site (CFS)-associated proteins uncovers ATRX as a regulator of CFS stability.Nucleic acids research · 2019Article
- Inhibiting Wee1 and ATR kinases produces tumor-selective synthetic lethality and suppresses metastasis.The Journal of clinical investigation · 2019Article
- Pathways for maintenance of telomeres and common fragile sites during DNA replication stress.Open biology · 2018Review
- 53BP1 can limit sister-chromatid rupture and rearrangements driven by a distinct ultrafine DNA bridging-breakage process.Nature communications · 2018Article
- Article
- Looping-out mechanism for resolution of replicative stress at telomeres.EMBO reports · 2017Article
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- Potential biomarkers of DNA replication stress in cancer.Oncotarget · 2017Review
- Identification of Fhit as a post-transcriptional effector of Thymidine Kinase 1 expression.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017Article
- Article
13 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
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Common fragile sites are specific loci that form gaps and constrictions on metaphase chromosomes exposed to replication stress, which slows DNA replication. These sites have a role in chromosomal rearrangements in tumors; however, the molecular mechanism of their expression is unclear. Here we show that replication stress leads to focus formation of Rad51 and phosphorylated DNA-PKcs, key components of the homologous recombination (HR) and nonhomologous end-joining (NHEJ), double-strand break (DSB) repair pathways, respectively. Down-regulation of Rad51, DNA-PKcs, or Ligase IV, an additional component of the NHEJ repair pathway, leads to a significant increase in fragile site expression under replication stress. Replication stress also results in focus formation of the DSB markers, MDC1 and gammaH2AX. These foci colocalized with those of Rad51 and phospho-DNA-PKcs. Furthermore, gammaH2AX and phospho-DNA-PKcs foci were localized at expressed fragile sites on metaphase chromosomes. These findings suggest that DSBs are formed at common fragile sites as a result of replication perturbation. The repair of these breaks by both HR and NHEJ pathways is essential for chromosomal stability at these sites.
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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.