ArticleGenes & development2003
Stabilization of stalled DNA replication forks by the BRCA2 breast cancer susceptibility protein.
Article in Genes & development, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
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Who cites it
130 citing papers in PubMed, 246 citations in OpenAlex.
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- Insights from three decades of BRCA1/2 modeling in mice.Nature genetics · 2026Review
- Understanding single stranded DNA gaps: from formation to fate.The Biochemical journal · 2026Review
- The RRM domains of PARP14 mediate replication fork degradation in BRCA2-deficient cells.NAR cancer · 2026Article
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- A recurrent pathogenic BRCA2 truncating variant reveals a role for BRCA2-PCAF complex in modulating NF-κB-driven transcription.Nature communications · 2025Article
- Mechanisms and regulation of DNA end resection in the maintenance of genome stability.Nature reviews. Molecular cell biology · 2025Review
- S-phase checkpoint protects from aberrant replication fork processing and degradation.Nucleic acids research · 2025Article
- USP37 counteracts HLTF to protect damaged replication forks and promote survival of BRCA1-deficient cells and PARP inhibitor resistance.Nucleic acids research · 2025Article
- RCC1 knockdown sensitizes drug-resistant colorectal cancer to 5-fluorouracil or doxorubicin by impairing DNA repair.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- The USP1 Inhibitor KSQ-4279 Overcomes PARP Inhibitor Resistance in Homologous Recombination-Deficient Tumors.Cancer research · 2024Article
- Clinical relevance of double heterozygosity revealed by next-generation sequencing of homologous recombination repair pathway genes in South African breast cancer patients.Breast cancer research and treatment · 2024Article
- Molecular mechanism of PARP inhibitor resistance.Oncoscience · 2024Review
- CaMKK2 and CHK1 phosphorylate human STN1 in response to replication stress to protect stalled forks from aberrant resection.Nature communications · 2023Article
- Structural basis for stabilisation of the RAD51 nucleoprotein filament by BRCA2.Nature communications · 2023Article
- A transcriptional response to replication stress selectively expands a subset of Brca2-mutant mammary epithelial cells.Nature communications · 2023Article
- RNAPII-dependent ATM signaling at collisions with replication forks.Nature communications · 2023Article
- Article
- Replication gap suppression depends on the double-strand DNA binding activity of BRCA2.Nature communications · 2023Article
- Review
70 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
How dividing mammalian cells overcome blocks to DNA replication by DNA damage, depleted nucleotide pools, or template-bound proteins is unclear. Here, we show that the response to blocked replication requires BRCA2, a suppressor of human breast cancer. By using two-dimensional gel electrophoresis, we demonstrate that Y-shaped DNA junctions at stalled replication forks disappear during genome-wide replication arrest in BRCA2-deficient cells, accompanied by double-strand DNA breakage. But activation of the replication checkpoint kinase Chk2 is unaffected, defining an unexpected function for BRCA2 in stabilizing DNA structures at stalled forks. We propose that in BRCA2 deficiency and related chromosomal instability diseases, the breakdown of replication forks, which arrest or pause during normal cell growth, triggers spontaneous DNA breakage, leading to mutability and cancer predisposition.
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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.