ArticleMolecular and cellular biology2004
BRCA1 is required for common-fragile-site stability via its G2/M checkpoint function.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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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.
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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
65 citing papers in PubMed, 123 citations in OpenAlex.
- The chromosomal challenge of human embryos: Mechanisms and fundamentals.HGG advances · 2025Review
- Non-canonical role for the BAF complex subunit DPF3 in mitosis and ciliogenesis.Journal of cell science · 2024Article
- Targeting theFrontiers in cell and developmental biology · 2023Review
- Elevated retrotransposon activity and genomic instability in primed pluripotent stem cells.Genome biology · 2021Article
- Mind the replication gap.Royal Society open science · 2021Review
- Fragile site instability: measuring more than breaks.Oncoscience · 2020Article
- Review
- Review
- BRCA1 and S phase DNA repair pathways restrict LINE-1 retrotransposition in human cells.Nature structural & molecular biology · 2020Article
- Visualizing locus-specific sister chromatid exchange reveals differential patterns of replication stress-induced fragile site breakage.Oncogene · 2020Article
- Proteomic characterization of chromosomal common fragile site (CFS)-associated proteins uncovers ATRX as a regulator of CFS stability.Nucleic acids research · 2019Article
- Genome-wide mapping and profiling of γH2AX binding hotspots in response to different replication stress inducers.BMC genomics · 2019Article
- Review
- The concerted roles of FANCM and Rad52 in the protection of common fragile sites.Nature communications · 2018Article
- RAD51 and RTEL1 compensate telomere loss in the absence of telomerase.Nucleic acids research · 2018Article
- 53BP1 can limit sister-chromatid rupture and rearrangements driven by a distinct ultrafine DNA bridging-breakage process.Nature communications · 2018Article
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- Potential biomarkers of DNA replication stress in cancer.Oncotarget · 2017Review
- FANCJ at the FORK.Mutation research · 2016Review
- Chromosomal radiosensitivity of human immunodeficiency virus positive/negative cervical cancer patients in South Africa.Molecular medicine reports · 2016Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Common fragile sites are loci that form chromosome gaps or breaks when DNA synthesis is partially inhibited. Fragile sites are prone to deletions, translocations, and other rearrangements that can cause the inactivation of associated tumor suppressor genes in cancer cells. It was previously shown that ATR is critical to fragile-site stability and that ATR-deficient cells have greatly elevated fragile-site expression (A. M. Casper, P. Nghiem, M. F. Arlt, and T. W. Glover, Cell 111:779-789, 2002). Here we demonstrate that mouse and human cells deficient for BRCA1, due to mutation or knockdown by RNA interference, also have elevated fragile-site expression. We further show that BRCA1 functions in the induction of the G(2)/M checkpoint after aphidicolin-induced replication stalling and that this checkpoint function is involved in fragile-site stability. These data indicate that BRCA1 is important in fragile-site stability and that fragile sites are recognized by the G(2)/M checkpoint pathway, in which BRCA1 plays a key role. Furthermore, they suggest that mutations in BRCA1 or interacting proteins could lead to rearrangements at fragile sites in cancer cells.
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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.