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.

In vitro culture of brain endothelial cells leads to a rapid loss of the blood-brain barrier transcriptional and accessible chromatin landscapes that is resistant to the effects of beta-catenin stabilization.

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

Genomic gains in ovarian cancer can promote cisplatin resistance via a FAK, Wnt/beta-catenin and Myc signaling pathway supporting pluripotency genes and tumorspheres that can acquire FAK dependence for survival.

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.

The generation and characterization of true β-catenin null mutant mice conclusively demonstrate that β-catenin is dispensable for T lymphocytes and leukemia stem cells, providing clarifications on a long-standing controversy.

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

Hypersensitivity of cohesin-deficient cells to Wnt signaling is concomitant with beta catenin stabilization and offers promise that Wnt agonists could be therapeutically effective in cohesin mutant cancers.

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.