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⁺.

In triple-layered rotavirus particles, strong interaction between the external and middle layers provides high mechanical strength for protection tasks, while weaker interaction between the middle and inner layers favors transcription.

Robust wrinkling pattern of the frilled dragon’s spectacular erectile ruff emerges from an elastic instability during homogeneous growth of the embryonic neck fold frustrated by its attachment to adjacent tissues.

The principle underlying the appearance of the growth plate, an organ responsible for longitudinal growth, has implications for various cartilage pathologies including growth abnormalities in children, trauma and osteoarthritis.

The mechanical response of adherent cells in structured environments is shown to be shaped by the intricate interplay between the three different isoforms of an essential molecular motor.

Nanoscale changes to individual collagen fibrils drive lung fibrosis.

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

Elastic forces generated by the giant protein titin define both passive and active tension of skeletal muscle fibers and protect the sarcomeric myosin filaments from severe disruption during contraction.

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.

Meniscal Gli1+ cells are mesenchymal progenitors that contribute to the development and injury repair of meniscus.