Elevating beta-catenin signaling converts endothelial cells in typically fenestrated central nervous system vasculature to a blood-brain barrier (BBB) phenotype and promotes a BBB gene expression program and chromatin landscape.

Discs large homologue 1 (Dlg1) activates beta-catenin (i.e., canonical Wnt) signaling in CNS endothelial cells to regulate retinal angiogenesis and the development and maintenance of the blood-brain and blood-retina barriers.

A novel ALS-associated variant in UBQLN4 impairs proteasome function and beta-catenin degradation to drive aberrant axon morphogenesis in motor neurons.

The patterning of the nephron is driven by a gradient in the activity of β-catenin and further defined by a network of BMP, PTEN and NOTCH signalling.

A new dynamic mechanistic model explains how the destruction complex negatively regulates Wnt signaling in development and oncogenesis.

The primary molecular mechanosensor involved in a physiological process of mechanically induced cell fate differentiation is revealed here for the first time in vivo, highly sensitive and potentially shared by all metazoan epithelia.

The Chip/LDB-SSDP complex integrates multiple signals to render TCF/LEF enhancers Wnt responsive.

Endothelial tightening by augmenting low level Wnt/β-catenin activity in vessels of the mouse subfornical organ, influences neuronal activation in water-deprived mice, linking endothelial barrier properties to neuro-vascular coupling.

Ascidian mesendoderm is a transient regulatory state upstream of mesoderm and endoderm gene regulatory networks and required for the initiation of both.

NFATc2 maintains the drug-induced TIC phenotypes through trans-activating SOX2/ALDH1A1 expression and scavenging stress from ROS.