ArticleiScience2025
Mechanical control of the alternative splicing factor PTBP1 regulates extracellular matrix stiffness induced proliferation and cell spreading.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Ptbp1 Condensates With Phase Separation-Like Features in Cardiomyocyte Nuclei Regulate Splicing of Proliferative Genes in Neonatal Cardiomyocytes.Development, growth & differentiation · 2026Article
- PTBP1 at the host-virus interface: mechanistic roles in viral RNA translation, replication, and immune modulation.Molecular biology reports · 2026Review
- Nitric oxide drives proteomic diversity through alternative splicing.Molecular cell · 2026Article
- Integrative multiomic analysis reveals co-ordinated alternative splicing in human bone marrow stromal stem cells.Scientific reports · 2026Article
- Forces that shape the transcriptome: Linking cellular mechanosensing to mRNA splicing.The Journal of biological chemistry · 2026Review
- Endothelial PTBP1 Deletion in Transplanted Cardiac Tissue Limits Cardiac Allograft Vasculopathy.bioRxiv : the preprint server for biology · 2026Article
- The bidirectional interplay between RNA processing and mechanotransduction.Cell reports · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells sense mechanical cues and convert them into biochemical responses to regulate biological processes such as embryonic development, aging, cellular homeostasis, and disease progression. In this study, we introduce a large-scale, systematic approach to identify proteins with mechanosensitive nuclear localization, highlighting their potential roles in mechanotransduction. Among the proteins identified, we focus here on the splicing factor PTBP1. We demonstrate that its nuclear abundance is regulated by mechanical cues such as cell density, size, and extracellular matrix (ECM) stiffness and that PTBP1 medicates the mechanosensitive alternative splicing of the endocytic adapter protein Numb. Furthermore, we show that PTBP1 and Numb alternative splicing is critical for ECM stiffness-induced epithelial cell spreading and proliferation as well as for mesenchymal stem cell differentiation into osteoblasts on a stiff matrix. Our results underscore the emerging role of alternative splicing in mechanotransduction and provide novel mechanistic insights into how matrix stiffness modulates cellular mechanoresponses.
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Registered trials
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