A. S. Yap

This study shows that c-Src activation in endothelial cells causes vascular expansion through focal adhesion signaling and localized matrix degradation, which can be inhibited to prevent abnormal vascular growth.

This study shows that pre-existing mechanical tension at adherens junctions impairs apoptotic extrusion in epithelia, and this effect can be reversed by reducing tension.

This study shows BECLIN1 is critical for intestinal homeostasis, as its deletion in adult mice causes fatal enteritis with compromised gut barrier integrity and morphological abnormalities.

The paper shows that caveola disassembly under mechanical stress reinforces the actin cortex at adherens junctions, enhancing epithelial resistance to tensile stress.

The paper identifies a mechanism where desmosome-anchored intermediate filaments enable RhoA signaling at adherens junctions to maintain epithelial homeostasis under tension.

The paper shows that apical extrusion prevents apoptosis from triggering inflammation in epithelia by eliminating apoptotic cells before they activate an IL-8-driven inflammatory response.

This study uses zebrafish to show that focal adhesions regulate endothelial cell elongation and junction linearization during vascular development.

The paper explains how E-cadherin-actin interactions mediate mechanical signals from cortical flows to inhibit epithelial cell migration based on contact orientation.

The paper shows collagen polarization drives epithelial elongation by inducing localized cell proliferation through β1-integrin and ERK signaling.

The paper identifies a feedback loop between RhoA and E-cadherin that drives asymmetric vertex motion in epithelial tissues through tension and frictional drag.

The paper investigates how epithelial cell monolayers switch from extensile to contractile behavior as intercellular contacts weaken, revealing mechanotransductive responses and implications for cell sorting and tissue dynamics.

This study shows cavin3 interacts with BRCA1 to regulate DNA repair and cellular stress response, with implications for cancer.

The paper shows caveolae regulate epithelial tension through lipid signaling, enabling the elimination of oncogene-transformed cells by apical extrusion.

This study shows Snail induces cell extrusion through RhoA contractile signaling and reduced basal adhesion, independent of EMT.

This study identifies a mechanosensitive RhoA pathway mediated by G12 and Myosin VI that protects epithelia from acute tensile stress by increasing junctional actomyosin.