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. Author manuscript; available in PMC: 2018 Mar 15.
Published in final edited form as: Crit Rev Oncol Hematol. 2015 Dec 24;99:141–149. doi: 10.1016/j.critrevonc.2015.12.005

Figure 1.

Figure 1

A: “Wnt Off”. In the absence of Wnt ligands, a destruction complex composed of Axin-1 and its tumor suppressor partners Adenomtous Polyposis Coli (APC), Glycogen synthase kinase 3 beta (GSK3B) and Casein kinase 1 (CK1α) is formed. The destruction complex phosphorylates ß-catenin and targets it for proteasomal degradation regulating the cytoplasmic level of ß-catenin.

B: “Wnt On”. Wnt ligands bind to the Frizzled/ Lrp5/6 (Low density lipoprotein receptor-related proteins 5 or 6) receptors leading to the phosphorylation of a negative regulator of the destruction complex, Dishevelled (Dvl). Dvl recruits Axin, inhibiting its interaction with other components of the destruction complex. ß-catenin is then free to accumulate in the cytoplasm and translocates to the nucleus, where it activates the trancscription of Wnt target genes after association with transcription factors of the TCF/Lef family and co-activators such as CBP (cyclic AMP response element-binding protein) and p300. Arrows indicate activation/induction, blunt ended lines indicate inhibition/blockade.