Keeley L. Mui

TL;DR: It is shown that a hyaluronic acid hydrogel system enables, across a physiological range of ECM stiffness, the independent co-presentation of the HAVDI adhesive motif from the EC1 domain of N-Cadherin and the RGD adhesive motiffrom fibronectin.

TL;DR: It is suggested that fibronectin promotes ovarian cancer invasion and metastasis through an α5β1-integrin/c-Met/FAK/Src-dependent signaling pathway, transducing signals through c-Met in an HGF/SF-independent manner.

TL;DR: Two central ideas are discussed: how the dynamic interplay between integrins and cadherins regulates the spatial organization of intracellular signals and the extracellular matrix, and the emerging consensus that intrACEllular force is a central mechanism that dictates cell behavior, guides tissue development and ultimately drives physiology.

TL;DR: It is established that mechanotransduction by a FAK-Cas-Rac-lamellipodin signaling module converts the external information encoded by ECM stiffness into stable intracellular stiffness and mechanosensitive cell cycling, and not only in controlling cellular migration but also for regulating the cell cycle in response to mechanical signals.

TL;DR: It is shown that N-cadherin is induced in smooth muscle cells (SMCs) in response to vascular injury, an in vivo model of tissue stiffening and proliferation and regulates the degree of cell spreading needed for cycling.