ArticleMolecular medicine (Cambridge, Mass.)2025
Nuclear VPS35 attenuates NHEJ repair by sequestering Ku protein.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Retromer-targeted therapy for neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- A Spatiotemporal Atlas of the Androgen Receptor Proximal Interactome.bioRxiv : the preprint server for biology · 2026Article
- MCM2-7 proteins promote NF-κB transcriptional activity through cooperative promoter recruitment.Bioscience reports · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
Vacuolar protein sorting-associated protein 35 (VPS35), a pivotal constituent of the retromer complex, mediates the retrograde trafficking of endosomal cargoes in the cytoplasm. Intriguingly, VPS35 displays a dual localization pattern, residing both in the cytoplasm and the nucleus, but its nuclear role remains elusive. In this study, we unravel a nuclear function of VPS35, demonstrating it impedes DNA repair by inhibiting non-homologous end joining (NHEJ). Mechanistically, VPS35 interacts with the Ku protein, sequestering it away from DNA damage sites. Consequently, nuclear VPS35 halts the activation of DNA-PKcs, hindering the recruitment of XLF and DNA-Ligase 4, ultimately suppressing NHEJ efficiency. Furthermore, in response to DNA damage, VPS35 dissociates from Ku protein and orchestrates a strategic relocation from the nucleus to the cytoplasm. Thus, our findings suggest VPS35 attenuates NHEJ repair by restricting Ku protein availability at DNA damage sites, offering a potential avenue for fine-tuning DNA repair efficiency.
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