ArticleNucleic acids research2015
Nuclear domain 'knock-in' screen for the evaluation and identification of small molecule enhancers of CRISPR-based genome editing.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers.
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Who cites it
182 citing papers in PubMed, 283 citations in OpenAlex.
- Germline RBBP8 variants associated with early-onset breast cancer compromise replication fork stability.The Journal of clinical investigation · 2020Trial
- Activation of Pol theta-mediated end joining begins during mitotic commitment.bioRxiv : the preprint server for biology · 2026Article
- A bulk cell heterozygous knock-in strategy for targeted protein degradation.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
- Multimodal analysis of a rare BARD1 missense variant suggests its pathogenicity is conditional.NPJ breast cancer · 2026Article
- CRISPR-MiX: A pooled single-stranded donor strategy to enhance HDR efficiency in human iPSCs.Molecular therapy. Nucleic acids · 2026Article
- HUH-tagged Cas9 as a platform for efficient ssODN-mediated knock-in via embryo and adult injection in insects.Communications biology · 2026Article
- Membrane curvature elastic stress triggers recruitment of PML-II onto the inner nuclear membrane.Molecular biology of the cell · 2026Article
- Harnessing DNA barcoding to enhance and sustain polyclonality in gene-edited hematopoietic stem cells.Molecular therapy. Methods & clinical development · 2025Article
- Repurposing clinically safe drugs for DNA repair pathway choice in CRISPR genome editing and synthetic lethality.Nature communications · 2025Article
- C8orf33 dictates DNA double-strand break repair choice by modulating KAT8-mediated H4K16 acetylation.Cell death & disease · 2025Article
- Coiled-coil interactions drive the ectopic condensation of overexpressed MAD1 to promote mitotic slippage in cancer cells.iScience · 2025Article
- Telomeric SUMO level influences the choices of APB formation pathways and ALT efficiency.The Journal of cell biology · 2025Article
- PALB2 and 53BP1 govern post-resection homologous recombination DNA repair.Molecular cell · 2025Article
- Refined DNA repair manipulation enables a universal knock-in strategy in mouse embryos.Nature communications · 2025Article
- Recent advances in therapeutic gene-editing technologies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Distinct roles of the two BRCA2 DNA-binding domains in DNA damage repair and replication fork preservation.Cell reports · 2025Article
- Inherited deficiency of DIAPH1 identifies a DNA double strand break repair pathway regulated by γ-actin.Nature communications · 2025Article
- SETD1A-dependent EME1 transcription drives PARPi sensitivity in HR deficient tumour cells.British journal of cancer · 2025Article
122 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
CRISPR is a genome-editing platform that makes use of the bacterially-derived endonuclease Cas9 to introduce DNA double-strand breaks at precise locations in the genome using complementary guide RNAs. We developed a nuclear domain knock-in screen, whereby the insertion of a gene encoding the green fluorescent protein variant Clover is inserted by Cas9-mediated homology directed repair (HDR) within the first exon of genes that are required for the structural integrity of subnuclear domains such as the nuclear lamina and promyelocytic leukemia nuclear bodies (PML NBs). Using this approach, we compared strategies for enhancing CRISPR-mediated HDR, focusing on known genes and small molecules that impact non-homologous end joining (NHEJ) and homologous recombination (HR). Ultimately, we identified the small molecule RS-1 as a potent enhancer of CRISPR-based genome editing, enhancing HDR 3- to 6-fold depending on the locus and transfection method. We also characterized U2OS human osteosarcoma cells expressing Clover-tagged PML and demonstrate that this strategy generates cell lines with PML NBs that are structurally and functionally similar to bodies in the parental cell line. Thus, the nuclear domain knock-in screen that we describe provides a simple means of rapidly evaluating methods and small molecules that have the potential to enhance Cas9-mediated HDR.
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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.