Fig. 1

a Representation of Canonical Wnt/β-catenin pathway. OFF- State: β-catenin is regulated by the destruction complex in the absence of Wnt ligands. GSK-3β and CK1 facilitates the phosphorylation of β-catenin at specific serine and threonine sites rendering it a target for proteosomal degradation by β-TRCP. As a result of this degradation, β-catenin is prevented from translocating into the nucleus prompting Groucho (co-repressor) to be bound to TCF thereby repressing gene transcription. ON- State: Once binding of Wnt ligand to Fzd and LRP5/6 co-receptors occurs, Dvl-fzd complex is formed resulting to the phosphorylation of LRP5/6 by GSK-3β and triggering the recruitment of Axin2 from the destruction complex. The disassembly of the complex promotes stabilization and accumulation of cytoplasmic β-catenin which eventually translocate to the nucleus where Groucho is dislodged and TCF is converted into a transcription factor ensuring the transcription of many genes including c-Myc, Ascl2, cyclin D1 which are essential stem cell regulators as well as mediators of proliferation and differentiation. b Schematic of Non-Canonical Wnt pathway. In the PCP pathway, Fz activates Dvl through G-proteins in the absence of LRP receptors. Subsequent activation of the Rho GTPases, Rho and Rac results to the induction of cytoskeletal changes. In the Wnt/Calcium pathway, Dvl activates protein kinase C (PKC) and the release of intracellular calcium and calcium/calmodulin-dependent protein kinase II (CaMKII) which in turn activates the release of NFAT and NFkB. NFAT and NFkB subsequently translocate into the nucleus to transcribe regulatory genes that govern cell migration. It is still unclear whether G-proteins are involved in this particular pathway. Adapted from [209]