ArticleMolecular oncology2023
MND1 enables homologous recombination in somatic cells primarily outside the context of replication.
Article in Molecular oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- The dynamics of RAD51 foci formation and elongation in living human cells.Nucleic acids research · 2026Article
- MND1 protein mediates DNA damage repair and is a promising novel therapeutic target in hepatocellular carcinoma.Liver research (Beijing, China) · 2026Article
- MND1 reduces breast cancer chemosensitivity by promoting RAD51-mediated homologous recombination repair.Cell death & disease · 2026Article
- O-GlcNAcylation regulates the DNA damage repair function of MND1 in breast cancer.Breast cancer research : BCR · 2026Article
- High-throughput spheroid-based assay for functional breast cancer precision medicine facilitated by deep learning.Communications medicine · 2026Article
- A Reporter Platform to Study Therapy-Induced Senescence in Live Cancer Cells.Small methods · 2025Article
- Comparative Analysis of Methods for Assessing On-Target Gene Editing Efficiencies.Methods and protocols · 2025Article
- Article
- Chromatin context-dependent effects of epigenetic drugs on CRISPR-Cas9 editing.Nucleic acids research · 2024Article
- Widespread chromatin context-dependencies of DNA double-strand break repair proteins.Nature communications · 2024Article
- Synergistic Antitumor Activity of Talazoparib and Temozolomide in Malignant Rhabdoid Tumors.Cancers · 2024Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Faithful and timely repair of DNA double-strand breaks (DSBs) is fundamental for the maintenance of genomic integrity. Here, we demonstrate that the meiotic recombination co-factor MND1 facilitates the repair of DSBs in somatic cells. We show that MND1 localizes to DSBs, where it stimulates DNA repair through homologous recombination (HR). Importantly, MND1 is not involved in the response to replication-associated DSBs, implying that it is dispensable for HR-mediated repair of one-ended DSBs. Instead, we find that MND1 specifically plays a role in the response to two-ended DSBs that are induced by irradiation (IR) or various chemotherapeutic drugs. Surprisingly, we find that MND1 is specifically active in G2 phase, whereas it only marginally affects repair during S phase. MND1 localization to DSBs is dependent on resection of the DNA ends and seemingly occurs through direct binding of MND1 to RAD51-coated ssDNA. Importantly, the lack of MND1-driven HR repair directly potentiates the toxicity of IR-induced damage, which could open new possibilities for therapeutic intervention, specifically in HR-proficient tumors.
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