Prof Stephan Huveneers

The endothelium receives and responds to mechanical forces through cell-cell junctions and cell-matrix interactions. Differences in the actomyosin activities between leader and follower cells causes asymmetry at the junctional-interface and results in differential YAP/TAZ activation. I will overview our recent findings of molecular events that take place at VE-cadherin- and integrin-based adhesions that support the guidance between endothelial leader and follower cells during collective migration and angiogenesis.