I. Noordstra

Endothelial c-Src mediates neovascular tuft formation in Oxygen-Induced Retinopathy

This study shows that c-Src is essential for neovascular tuft formation in Oxygen-Induced Retinopathy, as its depletion reduces tuft formation without affecting cell death, proliferation, or adhesion.

A truncation mutant of adenomatous polyposis coli (APC) impairs apical cell extrusion through elevated epithelial tissue tension

This study shows that an APC truncation mutant increases epithelial tissue tension via RhoA/ROCK, impairing apical cell extrusion and potentially contributing to disease.

c-Src induced vascular malformations require localised matrix degradation at focal adhesions

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.

Desmosome-anchored intermediate filaments facilitate tension-sensitive RhoA signaling for epithelial homeostasis

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

Organization and dynamics of the cortical complexes controlling insulin secretion in β-cells.

The paper investigates cortical complexes in β-cells that regulate insulin secretion, identifying non-neuronal proteins and showing their role in organizing secretory machinery at integrin-based adhesions.

An E-cadherin-actin clutch translates the mechanical force of cortical flow for cell-cell contact to inhibit epithelial cell locomotion

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

Enhanced RhoA signaling stabilizes E-cadherin in migrating epithelial monolayers.

The paper shows that RhoA signaling at adherens junctions stabilizes E-cadherin during epithelial migration by increasing junctional contractility and mechanical tension.

Endothelial junctional membrane protrusions serve as hotspots for neutrophil transmigration

The paper identifies endothelial junctional membrane protrusions as preferred sites for neutrophil transmigration during inflammation and shows they depend on Rac1 activity.

Caveolae set levels of epithelial monolayer tension to eliminate tumor cells

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