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Open AccessJournal ArticleDOI

Force fluctuations within focal adhesions mediate ECM-rigidity sensing to guide directed cell migration.

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TLDR
In this paper, the authors show that a FAK/phosphopaxillin/vinculin pathway is essential for high FA traction and to enable tugging FA traction over a broad range of extracellular matrix rigidities.
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This article is published in Cell.The article was published on 2012-12-21 and is currently open access. It has received 713 citations till now. The article focuses on the topics: Durotaxis & Focal adhesion.

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Mechanotransduction and extracellular matrix homeostasis

TL;DR: Progress towards understanding the molecular, cellular and tissue-level effects that promote mechanical homeostasis has helped to identify key questions for future research.
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Harnessing nanotopography and integrin–matrix interactions to influence stem cell fate

TL;DR: How cell adhesions interact with nanotopography is discussed, and insight is provided as to how materials scientists can exploit these interactions to direct stem cell fate and to understand how the behaviour of stem cells in their niche can be controlled.
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Interplay of matrix stiffness and protein tethering in stem cell differentiation

TL;DR: It is shown that varying substrate porosity did not significantly change protein tethering, substrate deformations, or the osteogenic and adipogenic differentiation of human adipose-derived stromal cells and marrow-derived mesenchymalStem cells.
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Role of the extracellular matrix in regulating stem cell fate

TL;DR: New technologies have offered insights into how stem cells sense signals from the ECM and how they respond to these signals at the molecular level, which ultimately regulate their fate.
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Integrin-mediated mechanotransduction.

TL;DR: Sun, Guo, and Fässler review the function and regulation of integrin-mediated mechanotransduction and discuss how its dysregulation impacts cancer progession.
References
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Matrix elasticity directs stem cell lineage specification.

TL;DR: Naive mesenchymal stem cells are shown here to specify lineage and commit to phenotypes with extreme sensitivity to tissue-level elasticity, consistent with the elasticity-insensitive commitment of differentiated cell types.
Book

Theory of elasticity

TL;DR: The equilibrium of rods and plates Elastic waves Dislocations Thermal conduction and viscosity in solids Mechanics of liquid crystals Index as discussed by the authors The equilibrium of rod and plate elastic waves Elastic waves
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Tensional homeostasis and the malignant phenotype.

TL;DR: It is found that tumors are rigid because they have a stiff stroma and elevated Rho-dependent cytoskeletal tension that drives focal adhesions, disrupts adherens junctions, perturbs tissue polarity, enhances growth, and hinders lumen formation.
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Cell locomotion and focal adhesions are regulated by substrate flexibility

TL;DR: The ability of cells to survey the mechanical properties of their surrounding environment is demonstrated and the possible involvement of both protein tyrosine phosphorylation and myosin-generated cortical forces in this process is suggested.
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Effects of substrate stiffness on cell morphology, cytoskeletal structure, and adhesion

TL;DR: The hypothesis that mechanical factors impact different cell types in fundamentally different ways, and can trigger specific changes similar to those stimulated by soluble ligands, is supported.
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