Figure 1.

Wnt/β-catenin signaling pathway. In resting cells, glycogen synthase kinase 3 (GSK3β) is in a complex with CK1, β-catenin, axin and adenomatous polyposis coli protein. In this state, β-catenin is primed for phosphorylation by GSK3β. The phosphorylated β-catenin is degraded by ubiquitination. In the activated state (upon Wnt binding to Fz), Wnt-Fz and LDL receptor-related protein 5/6 (LRP) coordinate Dvl (disheveled, an adaptor protein) activation, which results in recruitment of axin to the plasma membrane. This leads to dissociation and inactivation of GSK3β, which can no longer phosphorylate β-catenin. Free β-catenin translocates to the nucleus and induces gene expression in a complex with LEF-1/T cell factor (TCF) family transcription factors, down regulating E-cadherin genes and initiating epithelial mesenchymal transition. (Adapted from [8].)