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Fig. 3 | BMC Cancer

Fig. 3

From: HBV-related hepatocarcinogenesis: the role of signalling pathways and innovative ex vivo research models

Fig. 3

Targeted phosphorylation’s are required for ubiquitylation and degradation of β-catenin. Axin acts as scaffold that brings CK1, GSK3 and β-catenin in close proximity. CK1 initiates the process by phosphorylating Ser45 at the N-terminus of β-catenin, followed by sequential phosphorylation at Thr41, Ser37 and Ser33 by GSK3. β-Trcp recognizes the phosphorylated residues Ser33 and Ser37, targeting β-catenin for ubiquitylation and proteasomal degradation. These regulatory phosphorylation sites are commonly mutated in liver cancer. [Casein Kinase 1 (CK1); Glycogen Synthase Kinase 3 (GSK3); β-transducin-repeat-containing protein (β-Trcp)]

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