ArticleScientific reports2015
Structurally governed cell mechanotransduction through multiscale modeling.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- A Computational Model of Mechanical Stretching of Cultured Cells on a Flexible Membrane.Research square · 2026Article
- Mathematical modelling of mechanotransduction via RhoA signalling pathways.PLoS computational biology · 2025Article
- Two Complementary Signaling Pathways Depict Eukaryotic Chemotaxis: A Mechanochemical Coupling Model.Frontiers in cell and developmental biology · 2021Article
- Genomics models in radiotherapy: From mechanistic to machine learning.Medical physics · 2020Review
- The Nuclear Option: Evidence Implicating the Cell Nucleus in Mechanotransduction.Journal of biomechanical engineering · 2017Review
- Forcing through Tumor Metastasis: The Interplay between Tissue Rigidity and Epithelial-Mesenchymal Transition.Trends in cell biology · 2016Review
- Multiscale mechanobiology: computational models for integrating molecules to multicellular systems.Integrative biology : quantitative biosciences from nano to macro · 2015Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Mechanotransduction has been divided into mechanotransmission, mechanosensing, and mechanoresponse, although how a cell performs all three functions using the same set of structural components is still highly debated. Here, we bridge the gap between emerging molecular and systems-level understandings of mechanotransduction through a multiscale model linking these three phases. Our model incorporates a discrete network of actin filaments and associated proteins that responds to stretching through geometric relaxation. We assess three potential activating mechanisms at mechanosensitive crosslinks as inputs to a mixture model of molecular release and benchmark each using experimental data of mechanically-induced Rho GTPase FilGAP release from actin-filamin crosslinks. Our results suggest that filamin-FilGAP mechanotransduction response is best explained by a bandpass mechanism favoring release when crosslinking angles fall outside of a specific range. Our model further investigates the difference between ordered versus disordered networks and finds that a more disordered actin network may allow a cell to more finely tune control of molecular release enabling a more robust response.
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Registered trials
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