Fig. 1. Simplified scheme of canonical Wnt signalling pathway in an inactive and active state. (a) When inactive, cytoplasmic concentration of the protein β-catenin is regulated by the destruction complex, a multi-unit structure that targets it for proteasome degradation.^1–3 At this stage, regulated genes’ translation is blocked by Groucho/TLE repressor action on TCF/LEF transcription factors.^4,5 (b) Activation of Wnt signalling occurs upon binding of Wnt ligands (shown here as PDB 6AHY) on Fz receptors, followed by oligomerization with LRP 5/6, promoting sequestering of the destruction complex (as one of varied mechanisms for its inactivation) and impeding β-catenin degradation.^6–9 Consequently, cytoplasmic β-catenin levels increase and it translocates into the nucleus, binding TCF/LEF and calling other transcription-promoters to allow gene expression.^12,13 The mechanism is further regulated by binding of R-spondin agonists on leucine-rich repeat-containing G-protein-coupled receptor (LGR) 5, inhibiting ubiquitin ligase activity on Fz receptors to increase their membrane population.^14,15.