Fig. 7: Schematic drawing representing the mechanism of Wnt/β-catenin pathway activation by FBXW11F517S and β-cateninI35T (CTNNB1I35T). | Nature Communications

Fig. 7: Schematic drawing representing the mechanism of Wnt/β-catenin pathway activation by FBXW11F517S and β-cateninI35T (CTNNB1I35T).

From: Wnt/β-catenin activation by mutually exclusive FBXW11 and CTNNB1 hotspot mutations drives salivary basal cell adenoma

Fig. 7

FBXW11 is part of the Skp1-cullin 1-F-box (SCF) complex that regulates β-catenin levels by promoting its ubiquitination and subsequent proteasomal degradation (left). FBXW11 functions as substrate adaptor and is required for binding of phosphorylated β-catenin to the SCF complex. β-catenin phosphorylation is mediated by the destruction complex, which includes APC, AXIN, GSK3 and CK1. The reduced binding of FBXW11F517S to β-cateninWT (middle) and FBXW11WT to β-cateninI35T (right) inhibits the activity of the SCF complex, leading to accumulation of β-catenin in the cytoplasm and its subsequent translocation to the nucleus.

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