Fibronectin can shift from a globular to fibrillated form when adsorbing to implant surfaces, and this shift makes it accessible to attachment by Staphylococcus epidermidis, which is the leading cause of implant-associated infections.

Data-driven mathematical modeling suggests that leading neural crest cells in a moving stream can robustly communicate with trailing cells by remodeling their extracellular matrix, thereby enabling long-distance collective migration.

A fibronectin matrix constantly remodels to the area of highest mechanical stress, and the resulting fibronectin-mediated inter-tissue adhesion impedes neural tube convergence.

Investigation of defined extracellular matrix proteins in differentiation of human pluripotent stem cells to cardiomyocytes reveals fibronectin, in addition to soluble factors, is required for cardiogenesis.

The fibronectin synergy site is only required in vivo when forces exceed or αvβ3 integrin levels fall below certain thresholds.

Kindlin-2 co-operates with talin to activate fibronectin-binding integrins on fibroblasts and subsequently induces cell spreading by recruiting paxillin to small, peripheral nascent adhesions.

A signalling cascade involving PI3K/Akt1 remodels the extra-cellular matrix to achieve atypical cellular responses and control cell fate specification within the embryonic endoderm.

Matrix metalloprotease (MMP)-14 cleaves Tie2 at three distinct sites within the fibronectin type-III (FN3) domain and its pharmacological blockade inhibits Tie2 pathological shedding to exert barrier protective effects.

The membrane type I-matrix metalloproteinase is essential for the release of collagen fibrils from plasma membrane fibripositors, which is required for the transition from embryonic to postnatal tendon development.

Analysis of a double mutant in the Hippo pathway transcription factors Yap1 and Wwtr1 reveals novel roles for these factors in posterior body formation and epidermal morphogenesis in the vertebrate embryo.