Figure 1.

Canonical Wnt signaling cascade. Generally, Wnt signaling is “OFF” since without any stimulus, β-catenin is degraded by the proteasome after phosphorylation mediated by the destruction complex (including Axin1 (Axin), Adenomatous polyposis coli (APC), and the glycogen synthase kinase 3β (GSK3β)). Conversely, when Wnt ligands bind to the receptors Frizzled (FZD) and Lipoprotein receptor-related protein 5/6 (LRP), Dishevelled (DvI) is recruited and contributes to the destruction complex inactivation. Consequently, β-catenin is not restricted and can translocate into the nucleus contributing to the activation of the transcription of Wnt-related genes, directly binding the T cell lymphocyte differentiation factors (TCF) and lymphoid enhancer-binding factor 1 (LEF).