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.

During cardiogenesis, the major role of glucose is not the catabolic extraction of energy but the anabolic biosynthesis of nucleotides.