ArticleProceedings of the National Academy of Sciences of the United States of America2017
CTCF prevents genomic instability by promoting homologous recombination-directed DNA double-strand break repair.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 83 citations in OpenAlex.
- Dual roles for a chromatin insulator-H2Av axis in the DNA damage response and hematopoietic development in Drosophila.G3 (Bethesda, Md.) · 2026Article
- Deacetylase-independent HDAC1 condensation defines temozolomide response in glioblastoma.Nature chemical biology · 2026Article
- Using the DNA language model, GROVER, to parse effects of sequence, chromatin and regulatory features on genome stability.Bioinformatics (Oxford, England) · 2026Article
- CTCF primes repressive chromatin for rapid BRCA1/BARD1 recruitment to drive homologous recombination repair of DNA double-strand breaks.Nucleic acids research · 2026Article
- CTCF regulates wild-type and recombinant AAV gene expression by shaping viral chromatin.bioRxiv : the preprint server for biology · 2026Article
- The interaction between virus-bound KLF4 and host-bound PARP1 directs the localization of wild-type adeno-associated virus type 2 (wtAAV2) to cellular sites of DNA damage.Journal of virology · 2026Article
- Molecular Mimics: How Viral Genomes Dupe Their Host by Usurping CTCF to Establish Infection.Viruses · 2026Review
- The Chromaverse Is Colored by Triplexes Formed Through the Interactions of Noncoding RNAs with HNPRNPU, TP53, AGO, REL Proteins, Intrinsically-Disordered Regions, and Flipons.International journal of molecular sciences · 2026Article
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- PARP inhibitor resistance in IDH1-mutant cancers due to loss of end protection factors, 53BP1 and REV7.NAR cancer · 2025Article
- An essential role of the E3 ubiquitin ligase RNF126 in ensuring meiosis I completion during spermatogenesis.Journal of advanced research · 2025Article
- CTCF binding landscape is shaped by the epigenetic state of the N-terminal nucleosome in relation to CTCF motif orientation.Nucleic acids research · 2025Article
- Review
- D-2-hydroxyglutarate impairs DNA repair through epigenetic reprogramming.Nature communications · 2025Article
- Roles for the 3D genome in the cell cycle, DNA replication, and double strand break repair.Frontiers in cell and developmental biology · 2025Review
- Nucleotide excision repair of aflatoxin-induced DNA damage within the 3D human genome organization.Nucleic acids research · 2024Article
- Multifaceted role of CTCF in X-chromosome inactivation.Chromosoma · 2024Review
- ARID1A regulates DNA repair through chromatin organization and its deficiency triggers DNA damage-mediated anti-tumor immune response.Nucleic acids research · 2024Article
- DNA fragility at topologically associated domain boundaries is promoted by alternative DNA secondary structure and topoisomerase II activity.Nucleic acids research · 2024Article
- For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.Annual review of virology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CTCF is an essential epigenetic regulator mediating chromatin insulation, long-range regulatory interactions, and the organization of large topological domains in the nucleus. Phenotypes of CTCF haploinsufficient mutations in humans, knockout in mice, and depletion in cells are often consistent with impaired genome stability, but a role of CTCF in genome maintenance has not been fully investigated. Here, we report that CTCF maintains genome stability, is recruited to sites of DNA damage, and promotes homologous recombination repair of DNA double-strand breaks (DSBs). CTCF depletion increased chromosomal instability, marked by chromosome breakage and end fusions, elevated genotoxic stress-induced genomic DNA fragmentation, and activated the ataxia telangiectasia mutated (ATM) kinase. We show that CTCF could be recruited to drug-induced 53BP1 foci and known fragile sites, as well as to I-SceI endonuclease-induced DSBs. Laser irradiation analysis revealed that this recruitment depends on ATM, Nijmegen breakage syndrome (NBS), and the zinc finger DNA-binding domain of CTCF. We demonstrate that CTCF knockdown impaired homologous recombination (HR) repair of DSBs. Consistent with this, CTCF knockdown reduced the formation of γ-radiation-induced Rad51 foci, as well as the recruitment of Rad51 to laser-irradiated sites of DNA lesions and to I-SceI-induced DSBs. We further show that CTCF is associated with DNA HR repair factors MDC1 and AGO2, and directly interacts with Rad51 via its C terminus. These analyses establish a direct, functional role of CTCF in DNA repair and provide a potential link between genome organization and genome stability.
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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.