Elongation of C. elegans embryos requires stiffness and force to be specifically oriented in a coordinated manner in different cells.

During embryonic development, tissue stiffness, which provides an important signal to motile cells, changes locally within tens of minutes in a well-controlled manner.

Collectively migrating cells control their stiffness by Fascin-dependent control of Myosin activity, and this migratory cell stiffness regulates Myosin activity and stiffness within the cellular substrate to ultimately promote migration.

Multiple functions of human T lymphocytes are shown to be potentiated within a wide range of physiological cell and tissue rigidities.

The combination of molecular imaging, genetic and pharmacological approaches revealed that BCR signaling and PKCβ-dependent activation of focal adhesion kinase (FAK) is required for B cell mechanosensing.

Genetically altering the size of the molecular spring element in the giant protein titin established that titin determines the stiffness of skeletal muscle and the number of sarcomeres in series.

Upon activation of T cell receptors at the contact site, T cells were substantially stiffened at the cell body as well as at the lamellipodia, which is mediated by Ca²⁺.

The spatial organization of pathogenic bacteria into microcolonies can be shaped by the stiffness of the substrate that they colonize, via modifications of the bacterial motility.

Elucidating the contribution of augmented artificial skin-stretch stimulation to the fingertips to the immediate illusion of a higher stiffness and to an increased predictive grip force control.

Neurodegeneration driven by pathogenic aggregating proteins reorganizes the actin cytoskeleton, causing cellular stiffening and abolishing force generation required for endocytic events.