ArticleNature biomedical engineering2017
Ectopic expression of RAD52 and dn53BP1 improves homology-directed repair during CRISPR-Cas9 genome editing.
Article in Nature biomedical engineering, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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Who cites it
75 citing papers in PubMed, 116 citations in OpenAlex.
- Chromatin Modifications Orchestrate DNA Repair Pathway Choice: Epigenetics Strategies for Enhancing CRISPR-Cas9-Mediated Knock-In Efficiency.Cell proliferation · 2026Review
- Discovery and engineering of retrons for precise genome editing.Nature biotechnology · 2026Article
- Large serine recombinase-mediated gene insertion for high-throughput screens: advantages, design principles, and applications.Nucleic acids research · 2026Review
- Saturating variant analysis of TERC redefines the human telomerase reverse transcription mechanism.bioRxiv : the preprint server for biology · 2026Article
- Parallel Activation and Interference CRISPR (PAIR) with Sequencing Uncovers DNA Repair Networks Guiding Precision Cell Engineering.bioRxiv : the preprint server for biology · 2026Article
- Dispensable players: N-WASP and WASP are not crucial for homology-directed DNA repair.EMBO reports · 2026Article
- Strategies and considerations for the generation of ssDNA-Based HDR templates for CRISPR-based genome editing.BMC genomics · 2026Review
- Efficient high-precision transgene knock-in by Recombinases (Redα/β)-enhanced DNA integration-CRISPR-Cas9 (RED-CRISPR).Nature communications · 2025Article
- CRISPR-Cas9 HDR optimization: RAD52, denatured, and 5'-modified DNA templates in knock-in mice generation.iScience · 2025Article
- Recent advances in therapeutic gene-editing technologies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Metabolic constraint of human telomere length by nucleotide salvage efficiency.Nature communications · 2025Article
- Rescue of the disease-associated phenotype in CRISPR-corrected hiPSCs as a therapeutic approach for inherited retinal dystrophies.Molecular therapy. Nucleic acids · 2025Article
- Promotion or inhibition? This is a question in gene editing.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Development of inducible packaging cell line for rAAV production via CRISPR-Cas9 mediated site-specific integration.Biochemical engineering journal · 2025Article
- Epitranscriptome in action: RNA modifications in the DNA damage response.Molecular cell · 2024Review
- Herbgenomics meets Papaveraceae: a promising -omics perspective on medicinal plant research.Briefings in functional genomics · 2024Review
- Engineering single-cycle MeV vector for CRISPR-Cas9 gene editing.Molecular therapy. Methods & clinical development · 2024Article
- Mutant huntingtin impairs neurodevelopment in human brain organoids through CHCHD2-mediated neurometabolic failure.Nature communications · 2024Article
- Enhancing homology-directed repair efficiency with HDR-boosting modular ssDNA donor.Nature communications · 2024Article
- Precise Gene Knock-In Tools with Minimized Risk of DSBs: A Trend for Gene Manipulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
Abstract
Gene disruption by clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein 9 (Cas9) is highly efficient and relies on the error-prone non-homologous end-joining pathway. Conversely, precise gene editing requires homology-directed repair (HDR), which occurs at a lower frequency than non-homologous end-joining in mammalian cells. Here, by testing whether manipulation of DNA repair factors improves HDR efficacy, we show that transient ectopic co-expression of RAD52 and a dominant-negative form of tumour protein p53-binding protein 1 (dn53BP1) synergize to enable efficient HDR using a single-stranded oligonucleotide DNA donor template at multiple loci in human cells, including patient-derived induced pluripotent stem cells. Co-expression of RAD52 and dn53BP1 improves multiplexed HDR-mediated editing, whereas expression of RAD52 alone enhances HDR with Cas9 nickase. Our data show that the frequency of non-homologous end-joining-mediated double-strand break repair in the presence of these two factors is not suppressed and suggest that dn53BP1 competitively antagonizes 53BP1 to augment HDR in combination with RAD52. Importantly, co-expression of RAD52 and dn53BP1 does not alter Cas9 off-target activity. These findings support the use of RAD52 and dn53BP1 co-expression to overcome bottlenecks that limit HDR in precision genome editing.
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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.