ArticleNature communications2020
FOXL2 directs DNA double-strand break repair pathways by differentially interacting with Ku.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Acetylation-dependent regulation of FOX-Ku interaction by GCN5-SIRT1 axis controls non-homologous end-joining DNA repair.Archives of pharmacal research · 2026Article
- C/EBPγ induces epithelial-mesenchymal transition and facilitates DNA double-strand break repair in lung adenocarcinoma cells.Cell death discovery · 2026Article
- mCell death and differentiation · 2026Article
- Characterization of Forkhead Box Transcription Factor (Animals : an open access journal from MDPI · 2026Article
- Nuclear VPS35 attenuates NHEJ repair by sequestering Ku protein.Molecular medicine (Cambridge, Mass.) · 2025Article
- Homeodomain protein PRRX1 anchors the Ku heterodimers at DNA double-strand breaks to promote nonhomologous end-joining.Nucleic acids research · 2025Article
- BCAT1 Associates with DNA Repair Proteins KU70 and KU80 and Contributes to Regulate DNA Repair in T-Cell Acute Lymphoblastic Leukemia (T-ALL).International journal of molecular sciences · 2024Article
- Synergistic combination of RAD51-SCR7 improves CRISPR-Cas9 genome editing efficiency by preventing R-loop accumulation.Molecular therapy. Nucleic acids · 2024Article
- FOXL2 interaction with different binding partners regulates the dynamics of ovarian development.Science advances · 2024Article
- The forkhead DNA-binding domain binds specific G2-rich RNA sequences.Nucleic acids research · 2023Article
- Functional Diversity of SIRT7 Across Cellular Compartments: Insights and Perspectives.Cell biochemistry and biophysics · 2023Review
- Multifaceted Influence of Histone Deacetylases on DNA Damage Repair: Implications for Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2023Review
- FOXL2 and FOXA1 cooperatively assemble on the TP53 promoter in alternative dimer configurations.Nucleic acids research · 2022Article
- Acquired temozolomide resistance in MGMTCell death & disease · 2022Article
- DCLK1 promotes colorectal cancer stemness and aggressiveness via the XRCC5/COX2 axis.Theranostics · 2022Article
- Advances in Accurate Microbial Genome-Editing CRISPR Technologies.Journal of microbiology and biotechnology · 2021Review
- Guanylate-binding proteins induce apoptosis of leukemia cells by regulating MCL-1 and BAK.Oncogenesis · 2021Article
- An alternative miRISC targets a cancer-associated coding sequence mutation in FOXL2.The EMBO journal · 2020Article
- The Factors and Pathways Regulating the Activation of Mammalian Primordial FolliclesFrontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The balance between major DNA double-strand break (DSB) repair pathways is influenced by binding of the Ku complex, a XRCC5/6 heterodimer, to DSB ends, initiating non-homologous end joining (NHEJ) but preventing additional DSB end resection and homologous recombination (HR). However, the key molecular cue for Ku recruitment to DSB sites is unknown. Here, we report that FOXL2, a forkhead family transcriptional factor, directs DSB repair pathway choice by acetylation-dependent binding to Ku. Upon DSB induction, SIRT1 translocates to the nucleus and deacetylates FOXL2 at lysine 124, leading to liberation of XRCC5 and XRCC6 from FOXL2 and formation of the Ku complex. FOXL2 ablation enhances Ku recruitment to DSB sites, imbalances DSB repair kinetics by accelerating NHEJ and inhibiting HR, and thus leads to catastrophic genomic events. Our study unveils the SIRT1-(de)acetylated FOXL2-Ku axis that governs the balance of DSB repair pathways to maintain genome integrity.
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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.