ArticleDNA repair2020
CRISPR/CAS9-based DNA damage response screens reveal gene-drug interactions.
Article in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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.
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Who cites it
27 citing papers in PubMed.
- Dysregulation of the DNA repair‑immune axis: Targeted therapeutic strategies for autoimmune diseases (Review).International journal of molecular medicine · 2026Review
- Parallel Activation and Interference CRISPR (PAIR) with Sequencing Uncovers DNA Repair Networks Guiding Precision Cell Engineering.bioRxiv : the preprint server for biology · 2026Article
- Bloom syndrome helicase is required for efficient HIV-1 reverse transcription in macrophages.bioRxiv : the preprint server for biology · 2026Article
- Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes.NAR cancer · 2026Article
- The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.Nucleic acids research · 2026Article
- Integrative proteomics reveals MSH6 to modulate PARP inhibitor sensitivity in BRCA1/2-proficient ovarian cancer.PloS one · 2026Article
- The DNA replication checkpoint prevents PCNA/RFC depletion to protect forks from HLTF-induced collapse in human cells.Molecular cell · 2025Article
- 'Where is my gap': mechanisms underpinning PARP inhibitor sensitivity in cancer.Biochemical Society transactions · 2025Review
- Article
- Metabolic Rewiring in the Face of Genomic Assault: Integrating DNA Damage Response and Cellular Metabolism.Biomolecules · 2025Review
- TDP1 splice-site mutation causes HAP1 cell hypersensitivity to topoisomerase I inhibition.Nucleic acids research · 2025Article
- Genome-aware annotation of CRISPR guides validates targets in variant cell lines and enhances discovery in screens.Genome medicine · 2024Article
- The Fanconi anemia pathway induces chromothripsis and ecDNA-driven cancer drug resistance.Cell · 2024Article
- The PRC2.1 Subcomplex Opposes G1 Progression through Regulation of CCND1 and CCND2.bioRxiv : the preprint server for biology · 2024Article
- The loss of DNA polymerase epsilon accessory subunits POLE3-POLE4 leads to BRCA1-independent PARP inhibitor sensitivity.Nucleic acids research · 2024Article
- Article
- Requirement of WDR70 for POLE3-mediated DNA double-strand breaks repair.Science advances · 2023Article
- Revolutionizing DNA repair research and cancer therapy with CRISPR-Cas screens.Nature reviews. Molecular cell biology · 2023Review
- SMG8/SMG9 Heterodimer Loss Modulates SMG1 Kinase to Drive ATR Inhibitor Resistance.Cancer research · 2022Article
- Drug-gene Interaction Screens Coupled to Tumor Data Analyses Identify the Most Clinically Relevant Cancer Vulnerabilities Driving Sensitivity to PARP Inhibition.Cancer research communications · 2022Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
DNA damage response (DDR) is critically important for cell survival, genome maintenance, and its defect has been exploited therapeutically in cancer treatment. Many DDR-targeting agents have been generated and have entered the clinic and/or clinical trials. In order to provide a global and unbiased view of DDR network, we designed a focused CRISPR library targeting 365 DDR genes and performed CRISPR screens on the responses to several DDR inhibitors and DNA-damaging agents in 293A cells. With these screens, we determined responsive pathways enriched under treatment with different types of small-molecule agents. Additionally, we showed that POLE3/4-deficient cells displayed enhanced sensitivity to an ATR inhibitor, a PARP inhibitor, and camptothecin. Moreover, by performing DDR screens in isogenic TP53 wild-type and TP53 knock-out cell lines, our results suggest that the performance of our CRISPR DDR dropout screens is independent of TP53 status. Collectively, our findings indicate that CRISPR DDR screens can be used to identify potential targets of small-molecule drugs and reveal that TP53 status does not affect the outcome of these screens.
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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.