β-Catenin-mediated expansion of nephron progenitors is independent of direct β-catenin/chromatin engagement, while progenitor induction proceeds with a β-catenin-driven switch of repressive TCFL1/TCFL2 to activating TCF7/LEF1 factors on transcriptionally poised enhancers.

The developmental transcription factor TBX3 co-operates with β-catenin co-factors to operate tissue-specific transcriptional outputs, during forelimb development and colorectal cancer progression.

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.

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

β-catenin, a key effector of the Wnt signaling pathway, is transported into the nucleus via a direct interaction between its PY-NLS and TNPO1 offering new potential targets for cancer therapeutics.

The inclusion of a new alternatively spliced exon in Tcf7l2 can switch its function to repress transcription of Wnt target genes.

The biogenesis of lipid droplets induced by Wnt3a is controlled by the transcription factor TFAP2, which presumably acts as a 'master' regulator of lipid droplet biogenesis.

A novel population of adipocytes that play essential roles in adaptive thermogenesis via cell autonomous and non-autonomous effects and regulate systemic glucose metabolism in mice.

In chick skeletal muscle, an incoming signal leads to two interdependent outcomes: a cell fate change and an epithelial-mesenchymal transition.