ArticleNucleic acids research2024
Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed.
- Phosphoproteomics identifies the DYRK1B protein kinase as a regulator of processing bodies.Journal of cell science · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Small-molecule inhibitors of the protein kinase DYRK as potential therapeutic candidates in cancer.Cell chemical biology · 2026Article
- PHF20 stabilizes the GAS7-F-actin axis to drive DNA damage repair and chemoresistance in cutaneous squamous cell carcinoma.Cell death & disease · 2026Article
- Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Nuclear actin-based movements support DNA double-strand break (DSB) repair. However, molecular determinants that promote filamentous actin (F-actin) formation on the damaged chromatin remain undefined. Here we describe the DYRK1A kinase as a nuclear activity that promotes local F-actin assembly to support DSB mobility and repair, accomplished in part by its targeting of actin nucleator spire homolog 1 (Spir1). Indeed, perturbing DYRK1A-dependent phosphorylation of S482 mis-regulated Spir1 accumulation at damaged-modified chromatin, and led to compromised DSB-associated actin polymerization and attenuated DNA repair. Our findings uncover a role of the DYRK1A-Spir1 axis in nuclear actin dynamics during early DSB responses, and highlight the intricate details of nuclear cytoskeletal network in DSB repair and genome stability maintenance.
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Registered trials
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