Axin–Glycogen synthase kinase 3 beta protein-protein interaction (Null)

The Axin–Glycogen synthase kinase 3 beta (GSK3β) protein-protein interaction is a critical regulatory event in the canonical Wnt pathway. Axin acts as a scaffold, directly binding GSK3β and positioning it to phosphorylate β-catenin within a multiprotein “destruction complex,” marking β-catenin for degradation[1][4]. This interaction is essential for maintaining controlled β-catenin signaling, regulating cell proliferation, differentiation, and fate. Dysregulation or mutation in components of the destruction complex (such as Axin, GSK3β, or their interface) is implicated in several cancers, developing considerable therapeutic interest in modulating this interface as a drug target[1][2][4]. However, the target is structurally an interaction surface, not a traditional single protein or receptor, which poses specific challenges for drug development. If you need standardized database entries, consider mapping this to the individual proteins ("Axin" and "Glycogen synthase kinase 3 beta (GSK3β)") or to "Wnt/β-catenin destruction complex," instead of to the interface itself.

Other names

Axin–GSK3β interactionWnt destruction complex Axin–GSK3β interfaceAxin scaffold–GSK3β binding

Inhibitors would block Axin–GSK3β binding, thereby altering the phosphorylation and destruction of β-catenin, leading to increased or decreased β-catenin signaling in cells