Figure 4.

WNT Pathways. The extracellular signaling molecule WNT activates three pathways: (1) Early cell fate decisions are controlled via the canonical pathway (middle): it comprises the regulation of gene expression by inducing β-catenin-mediated transcriptional activation. Interaction of WNT with the transmembrane receptor frizzled (FZ) activates dishevelled (DVL), which induces the disassembly of a complex consisting of axin, adenomatosis polysis coli (APC), glycogen synthase kinase 3β (GSK3β) and β-catenin. In non-stimulated cells, GSK3β phosphorylates β-catenin, thereby triggering its degradation. Activitation of the pathway effectively increases the levels of β-catenin in the cyctoplasm, which is then translocated to the nucleus. Here it it forms the β-catenin-T-cell specific transcription factor complex that activates the transcription of target genes. (2) In the planar cell polarity pathway (left), FZ functions through G-proteins to activate DVL, which thereupon signals to Rho GTPases (Rho or Rac or both). Activated Ras signals through the c-Jun amino (N)-terminal kinase (JNK). Activation of Rho-GTPases induces changes in the cytoskeleton. In neurons, this pathway is involved in dendritic arborization. (3) In the WNT/calcium pathway (right), activation of DVL activates protein kinase C (PKC) and induces the release of intracellular calcium, which activates a calcium/calmodulin-dependent protein kinase II (CaMKII).

Klipp and Liebermeister BMC Neuroscience 2006 7(Suppl 1):S10   doi:10.1186/1471-2202-7-S1-S10