ReviewNucleic acids research2010
Overexpression of RAD51 suppresses recombination defects: a possible mechanism to reverse genomic instability.
Review in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 116 citations in OpenAlex.
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- Cancer mutations in RAD51 and its paralogues.PloS one · 2026Article
- RAD51 is chromatin enriched and targetable in BRCA1-deficient cells.Molecular cell · 2025Article
- An artesunate-modified half-sandwich iridium(iii) complex inhibits colon cancer cell proliferation and metastasis through the STAT3 pathway.RSC chemical biology · 2025Article
- Particulate matter-induced epigenetic modifications and lung complications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Differential impact of cytoplasmic vs. nuclear RAD51 expression on breast cancer progression and patient prognosis.International journal of oncology · 2024Article
- RAD51 is a poor prognostic marker and a potential therapeutic target for oral squamous cell carcinoma.Cancer cell international · 2023Article
- SOSSB1 and SOSSB2 mutually regulate protein stability through competitive binding of SOSSA.Cell death discovery · 2023Article
- Retroperitoneal leiomyosarcoma in a female patient with a germline splicing variant RAD51D c.904-2A > T: a case report.Hereditary cancer in clinical practice · 2021Article
- Article
- Epigenomic Analysis of RAD51 ChIP-seq Data RevealsCancers · 2021Article
- Article
- Targeting Rad51 as a strategy for the treatment of melanoma cells resistant to MAPK pathway inhibition.Cell death & disease · 2020Article
- PRMT5 Cooperates with pICln to Function as a Master Epigenetic Activator of DNA Double-Strand Break Repair Genes.iScience · 2020Article
- E2F1 facilitates DNA break repair by localizing to break sites and enhancing the expression of homologous recombination factors.Experimental & molecular medicine · 2019Article
- The F-Box Domain-Dependent Activity of EMI1 Regulates PARPi Sensitivity in Triple-Negative Breast Cancers.Molecular cell · 2019Article
- Gene Ontology and Expression Studies of Strigolactone Analogues on a Hepatocellular Carcinoma Cell Line.Analytical cellular pathology (Amsterdam) · 2019Article
- Dynamin impacts homology-directed repair and breast cancer response to chemotherapy.The Journal of clinical investigation · 2018Article
- β1-Integrin Impacts Rad51 Stability and DNA Double-Strand Break Repair by Homologous Recombination.Molecular and cellular biology · 2018Article
- Inhibition of RAD51 by siRNA and Resveratrol Sensitizes Cancer Stem Cells Derived from HeLa Cell Cultures to Apoptosis.Stem cells international · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
RAD51, a key protein in the homologous recombinational DNA repair (HRR) pathway, is the major strand-transferase required for mitotic recombination. An important early step in HRR is the formation of single-stranded DNA (ss-DNA) coated by RPA (a ss-DNA-binding protein). Displacement of RPA by RAD51 is highly regulated and facilitated by a number of different proteins known as the 'recombination mediators'. To assist these recombination mediators, a second group of proteins also is required and we are defining these proteins here as 'recombination co-mediators'. Defects in either recombination mediators or co-mediators, including BRCA1 and BRCA2, lead to impaired HRR that can genetically be complemented for (i.e. suppressed) by overexpression of RAD51. Defects in HRR have long been known to contribute to genomic instability leading to tumor development. Since genomic instability also slows cell growth, precancerous cells presumably require genomic re-stabilization to gain a growth advantage. RAD51 is overexpressed in many tumors, and therefore, we hypothesize that the complementing ability of elevated levels of RAD51 in tumors with initial HRR defects limits genomic instability during carcinogenic progression. Of particular interest, this model may also help explain the high frequency of TP53 mutations in human cancers, since wild-type p53 represses RAD51 expression.
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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.