Figure 3.

Overview of Wnt/β-catenin signaling Ctenophore pathway. (A) When Wnt signaling is inactive, cytoplasmic β-catenin protein is bound by the 'destruction complex' of axin, glycogen synthase kinase 3 (GSK-3) and adenomatous polyposis coli (APC). While sequestered, GSK-3 phosphorylates β-catenin, which targets β-catenin for ubiquitination and degradation. (B) In the presence of a Wnt ligand, the pathway is activated. Wnt binds to the seven-transmembrane receptor Frizzled and its co-receptor lipoprotein receptor-related protein 5/6 (LRP5/6), which causes Dishevelled (Dsh) to be activated. Dsh inhibits GSK-3, thereby allowing β-catenin to accumulate in the cytoplasm. Eventually, β-catenin gets translocated to the nucleus, where it interacts with the transcription factor T-cell-specific transcription factor/lymphoid enhancer binding factor (TCF/LEF) to activate target genes. The diffusible antagonists (Secreted Frizzled-related (Sfrp), Dickkopf (DKK), Wnt Inhibitory Factor (WIF) and Cerberus (CER)) can modulate Wnt activity by preventing the binding of Wnt to its receptors.