Michelangelo Cordenonsi

TL;DR: YAP/TAZ are identified as sensors and mediators of mechanical cues instructed by the cellular microenvironment and are functionally required for differentiation of mesenchymal stem cells induced by ECM stiffness and for survival of endothelial cells regulated by cell geometry.

TL;DR: In this paper, a number of cancer-associated extrinsic and intrinsic cues conspire to overrule the YAP-inhibiting microenvironment of normal tissues, including changes in mechanotransduction, inflammation, oncogenic signaling, and regulation of the Hippo pathway.

TL;DR: YAP/TAZ appear at the centerpiece of a signaling nexus by which cells take control of their behavior according to their own shape, spatial location and growth factor context, and are appealing therapeutic targets in cancer and regenerative medicine.

TL;DR: It is shown that the activity of TAZ, a transducer of the Hippo pathway, is required to sustain self-renewal and tumor-initiation capacities in breast CSCs and reveals a mechanistic basis of the control of Hippo kinases by cell polarity.

TL;DR: Evidence is provided that YAP and TAZ are integral components of the β-catenin destruction complex that serves as cytoplasmic sink for YAP/TAZ, revealing an unprecedented signaling framework relevant for organ size control, regeneration, and tumor suppression.