ReviewDNA repair2008
The consequences of Rad51 overexpression for normal and tumor cells.
Review in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
191 citing papers in PubMed, 367 citations in OpenAlex.
- Trial
- Distinct ways by which Srs2 helicase and Rrp1 translocase shape Rad51-DNA interactions in fission yeast.Nucleic acids research · 2026Article
- Synthetic lethality in cancer: mechanisms, therapeutic exploitation and clinical translation.Signal transduction and targeted therapy · 2026Review
- A Tale of Two Cell Lines: Characterization of Differential Efficacy of Small Molecule Drugs Cediranib and NU-7441 on Primary Versus Metastatic Colorectal Cancer.Pharmacology research & perspectives · 2026Article
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- Cancer mutations in RAD51 and its paralogues.PloS one · 2026Article
- The lactate-lactylation axis in tumor radioresistance: metabolic, epigenetic, and immune mechanisms with emerging links to RNA regulation.Frontiers in immunology · 2026Review
- RAD51AP1 is a versatile RAD51 modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting DNA repair mechanisms in cancer therapy: the role of small molecule DNA repair inhibitors.NAR cancer · 2025Review
- Computationally-designed aptamers targeting RAD51-BRCA2 interaction impair homologous recombination and induce synthetic lethality.Nature communications · 2025Article
- Targeting DNA damage in ageing: towards supercharging DNA repair.Nature reviews. Drug discovery · 2025Review
- Recombinant oncolytic virus NDV-anti-VEGFR2 enhances radiotherapy sensitivity in NSCLC by targeting VEGF signaling and impairing DNA repair.Gene therapy · 2025Article
- Computational prediction of diagnostic biomarker candidates and prognostic gene signature from DNA replication-related genes in breast cancer.Discover oncology · 2025Article
- Exploring Experimental and In Silico Approaches for Antibody-Drug Conjugates in Oncology Therapies.Pharmaceuticals (Basel, Switzerland) · 2025Review
- DNA repair and the contribution to chemotherapy resistance.Genome medicine · 2025Review
- Investigating synthetic lethality and PARP inhibitor resistance in pancreatic cancer through enantiomer differential activity.Cell death discovery · 2025Article
- Molecular basis of FIGNL1 in dissociating RAD51 from DNA and chromatin.Science (New York, N.Y.) · 2025Article
- Integrated Bioinformatics and Experimental Validation of the hsa_circ_0000378/miR-205-5p/RAD51 ceRNA Axis in Breast Cancer.International journal of molecular and cellular medicine · 2025Article
- FIGNL1-FIRRM is essential for meiotic recombination and prevents DNA damage-independent RAD51 and DMC1 loading.Nature communications · 2024Article
- Molecular basis of FIGNL1 in dissociating RAD51 from DNA and chromatin.bioRxiv : the preprint server for biology · 2024Article
131 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
1 author at 1 institution in 1 country.
Funding
Abstract
The Rad51 recombinase is an essential factor for homologous recombination and the repair of DNA double strand breaks, binding transiently to both single stranded and double stranded DNA during the recombination reaction. The use of a homologous recombination mechanism to repair DNA damage is controlled at several levels, including the binding of Rad51 to single stranded DNA to form the Rad51 nucleofilament, which is controlled through the action of DNA helicases that can counteract nucleofilament formation. Overexpression of Rad51 in different organisms and cell types has a wide assortment of consequences, ranging from increased homologous recombination and increased resistance to DNA damaging agents to disruption of the cell cycle and apoptotic cell death. Rad51 expression is increased in p53-negative cells, and since p53 is often mutated in tumor cells, there is a tendency for Rad51 to be overexpressed in tumor cells, leading to increased resistance to DNA damage and drugs used in chemotherapies. As cells with increased Rad51 levels are more resistant to DNA damage, there is a selection for tumor cells to have higher Rad51 levels. While increased Rad51 can provide drug resistance, it also leads to increased genomic instability and may contribute to carcinogenesis.
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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.