ArticleNature communications2025
CIP2A mediates mitotic recruitment of SLX4/MUS81/XPF to resolve replication stress-induced DNA lesions.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Development of a structurally distinct TopBP1 inhibitor that enhances PARP blockade and reverses osimertinib resistance.Science advances · 2026Article
- CIP2A recruits SLX4-MUS81-XPF in mitosis and protects against replication stress.EMBO reports · 2026Article
- TOPBP1-PLK1 interaction preserves genome integrity during mitosis.Nucleic acids research · 2026Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Perturbed DNA replication can lead to incompletely replicated DNA when cells enter mitosis and can interfere with chromosome segregation. Cells therefore require mechanisms to resolve these lesions during mitosis. The CIP2A-TOPBP1 complex is described to tether fragmented DNA molecules during mitosis. Whether CIP2A also functions in processing of incompletely replicated DNA remained unclear. We show that CIP2A-TOPBP1 form large filamentous structures at sites of incomplete DNA replication during mitosis, and that CIP2A-TOPBP1 facilitate the recruitment of SMX tri-nuclease complex members SLX4, MUS81 and XPF-ERCC1. These structures form in proximity to sites of mitotic DNA synthesis, although CIP2A is not required for mitotic DNA synthesis. In addition to its globular and coiled-coil domain, the unstructured C-terminal domain of CIP2A is essential for CIP2A-TOPBP1 filamentous structure formation and recruitment of the SMX complex. BRCA1
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