The Molecular Basis of Wnt/β-Catenin Signaling Pathways in Neurodegenerative Diseases

Figure 1

Wnt/β-catenin signaling. (a) When Wnt is present (Wnt-ON), it binds to Frizzled (fz) and its coreceptor lipoprotein receptor-related protein (LRP), thereby activating Dishevelled (Dsh). The destruction complex comprising axis inhibition protein (AXIN), adenomatous polyposis coli (APC), and glycogen synthase kinase-3β (GSK-3β) is disassembled. Hence, β-catenin is stabilized, translocates to the nucleus, binds to T cell factor/lymphoid enhancer-binding factor (TCF/LEF), and regulates gene expression. (b) When Wnt is absent, β-catenin is phosphorylated by the destruction complex and ubiquitinated by the E3 ligase β-transducin repeat-containing protein (β-TrCP), directing it towards proteasomal degradation. Hence, there is no transcription of downstream genes.

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