ArticleMolecular and cellular biology2012
RAD51 mutants cause replication defects and chromosomal instability.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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
31 citing papers in PubMed, 52 citations in OpenAlex.
- Modelling DMC1 mediated homologous recombination repair in mouse embryonic stem cells.Frontiers in cell and developmental biology · 2026Article
- RAD51 separation of function mutation disables replication fork maintenance but preserves DSB repair.iScience · 2024Article
- RAD51 restricts DNA over-replication from re-activated origins.The EMBO journal · 2024Article
- Article
- Racial differences in RAD51 expression are regulated by miRNA-214-5P and its inhibition synergizes with olaparib in triple-negative breast cancer.Breast cancer research : BCR · 2023Article
- ZNF212 promotes genomic integrity through direct interaction with TRAIP.Nucleic acids research · 2023Article
- Nucleotide proofreading functions by nematode RAD51 paralogs facilitate optimal RAD51 filament function.Nature communications · 2021Article
- Epigenomic Analysis of RAD51 ChIP-seq Data RevealsCancers · 2021Article
- Trex2 responds to damaged replication forks in diverse ways.Molecular & cellular oncology · 2021Article
- TREX2 Exonuclease Causes Spontaneous Mutations and Stress-Induced Replication Fork Defects in Cells Expressing RAD51Cell reports · 2020Article
- Review
- Prexasertib treatment induces homologous recombination deficiency and synergizes with olaparib in triple-negative breast cancer cells.Breast cancer research : BCR · 2019Article
- Development of hRad51-Cas9 nickase fusions that mediate HDR without double-stranded breaks.Nature communications · 2019Article
- Loss of Cohesin Subunit Rec8 Switches Rad51 Mediator Dependence in Resistance to Formaldehyde Toxicity inGenetics · 2018Article
- Human RAD51 rapidly forms intrinsically dynamic nucleoprotein filaments modulated by nucleotide binding state.Nucleic acids research · 2018Article
- High BCAR1 expression is associated with early PSA recurrence in ERG negative prostate cancer.BMC cancer · 2018Article
- Homologous recombination defects and how they affect replication fork maintenance.AIMS genetics · 2018Review
- A mechanism for 1,4-Benzoquinone-induced genotoxicity.Oncotarget · 2016Article
- Predicting early brain metastases based on clinicopathological factors and gene expression analysis in advanced HER2-positive breast cancer patients.Journal of neuro-oncology · 2015Article
- Potential relationship between inadequate response to DNA damage and development of myelodysplastic syndrome.International journal of molecular sciences · 2015Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
RAD51 is important for restarting stalled replication forks and for repairing DNA double-strand breaks (DSBs) through a pathway called homology-directed repair (HDR). However, analysis of the consequences of specific RAD51 mutants has been difficult since they are toxic. Here we report on the dominant effects of two human RAD51 mutants defective for ATP binding (K133A) or ATP hydrolysis (K133R) expressed in mouse embryonic stem (ES) cells that also expressed normal mouse RAD51 from the other chromosome. These cells were defective for restarting stalled replication forks and repairing breaks. They were also hypersensitive to camptothecin, a genotoxin that generates breaks specifically at the replication fork. In addition, these cells exhibited a wide range of structural chromosomal changes that included multiple breakpoints within the same chromosome. Thus, ATP binding and hydrolysis are essential for chromosomal maintenance. Fusion of RAD51 to a fluorescent tag (enhanced green fluorescent protein [eGFP]) allowed visualization of these proteins at sites of replication and repair. We found very low levels of mutant protein present at these sites compared to normal protein, suggesting that low levels of mutant protein were sufficient for disruption of RAD51 activity and generation of chromosomal rearrangements.
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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.