ArticleScientific reports2019
Pharmacological boost of DNA damage response and repair by enhanced biogenesis of DNA damage response RNAs.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- TDP-43 related amyotrophic lateral sclerosis-frontotemporal dementia and links to the DNA damage response: a systematic review and narrative synthesis.Frontiers in molecular neuroscience · 2026Pooled it
- Effect of terahertz irradiation on DNA damage repair in living cells.FEBS open bio · 2026Article
- Disruption of DNA Repair as an Emerging Epigenetic Mechanism Underlying Autism Spectrum Disorder.Current psychiatry reports · 2026Review
- Harnessing machine learning models to repurpose drugs targeting HIV-1 integrase, protease, and reverse transcriptase.Scientific reports · 2026Article
- Non-coding RNA regulation of the radiation-induced DNA damage response and its translational relevance.Discover oncology · 2026Review
- DNA damage response defects induced by the formation of TDP-43 and mutant FUS cytoplasmic inclusions and their pharmacological rescue.Cell death and differentiation · 2025Article
- Weaponizing CRISPR/Cas9 for selective elimination of cells with an aberrant genome.DNA repair · 2025Article
- Traffic light at DSB-transit regulation between gene transcription and DNA repair.FEBS letters · 2025Review
- Multi-protomics analysis identified host cellular pathways perturbed by tick-borne encephalitis virus infection.Nature communications · 2024Article
- Advances in the Synthesis and Biological Applications of Enoxacin-Based Compounds.Biomolecules · 2024Review
- DNA double-strand break-capturing nuclear envelope tubules drive DNA repair.Nature structural & molecular biology · 2024Article
- SARS-CoV-2 N protein-induced Dicer, XPO5, SRSF3, and hnRNPA3 downregulation causes pneumonia.Nature communications · 2024Article
- Trypanosoma cruzi infection induces DNA double-strand breaks and activates DNA damage response pathway in host epithelial cells.Scientific reports · 2024Article
- Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer's disease and aging.Nature communications · 2024Article
- Low androgen signaling rescues genome integrity with innate immune response by reducing fertility in humans.Cell death & disease · 2024Article
- Huntington's Disease Drug Development: A Phase 3 Pipeline Analysis.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Genomic instability in individuals with sex determination defects and germ cell cancer.Cell death discovery · 2023Article
- A microRNA Arising from the Negative Strand of SARS-CoV-2 Genome Targets FOS to Reduce AP-1 Activity.Non-coding RNA · 2023Article
- Tissue fluidification promotes a cGAS-STING cytosolic DNA response in invasive breast cancer.Nature materials · 2023Article
- SARS-CoV-2 infection induces DNA damage, through CHK1 degradation and impaired 53BP1 recruitment, and cellular senescence.Nature cell biology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
A novel class of small non-coding RNAs called DNA damage response RNAs (DDRNAs) generated at DNA double-strand breaks (DSBs) in a DROSHA- and DICER-dependent manner has been shown to regulate the DNA damage response (DDR). Similar molecules were also reported to guide DNA repair. Here, we show that DDR activation and DNA repair can be pharmacologically boosted by acting on such non-coding RNAs. Cells treated with enoxacin, a compound previously demonstrated to augment DICER activity, show stronger DDR signalling and faster DNA repair upon exposure to ionizing radiations compared to vehicle-only treated cells. Enoxacin stimulates DDRNA production at chromosomal DSBs and at dysfunctional telomeres, which in turn promotes 53BP1 accumulation at damaged sites, therefore in a miRNA-independent manner. Increased 53BP1 occupancy at DNA lesions induced by enoxacin ultimately suppresses homologous recombination, channelling DNA repair towards faster and more accurate non-homologous end-joining, including in post-mitotic primary neurons. Notably, augmented DNA repair stimulated by enoxacin increases the survival also of cancer cells treated with chemotherapeutic agents.
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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.