Imaging of single cells within a cell population shows the correlation between subcellular accumulation of β-catenin and the transcriptional activation of a target gene.

Wnt/beta-catenin signaling is essential for the specification of dorsal cell fate in amphioxus, suggesting a common evolutionary origin for the formation of the dorsal organizer in chordates.

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.

Hif/Hif-3α has two distinct roles in cells: activating HRE-dependent gene expression and binding to β-catenin to destabilize the nuclear β-catenin complex.

Mechanicals forces and local (Wnt) signaling can synergize to increase β-catenin signaling and produce unique growth phenotypes.

Low expression of Cbfb may be the cause of osteoarthritis, and local admission of Cbfb may rescue and protect against osteoarthritis through decreasing Wnt/β-catenin signaling, and increasing Hippo/Yap signaling and Tgfβ/Smad2/3 signaling in osteoarthritis articular cartilage.

In the developing kidney, secreted molecules of the R-spondin family control progenitor cell proliferation and nephron formation by permitting WNT/β-catenin signalling.

Dkk2, a member of the Dikkopf family of Wnt antagonists, acts as a positive regulator of Wnt signaling during neural crest formation.

Bi-allelic tagging enables the biophysical analysis of oncogenic β-catenin genetic variants in Wnt signaling.

The membrane proteins Reck and Gpr124 are integral components of a novel Wnt7a/Wnt7b-specific signaling complex, and there is a distinctive requirement for Wnt/β-catenin signaling in tip cells during angiogenesis in the central nervous system.