Review Advance Articles

Vitamin D deficiency as a potential risk factor for accelerated aging, impaired hippocampal neurogenesis and cognitive decline: a role for Wnt/β-catenin signaling

Figure 2. Activation of the Wnt canonical pathway induces β-catenin-regulated gene expression. Left panel: binding of Wnt to a Frizzled receptor (Fzd) allows its association to Dishevelled proteins (DVL) sequestering Axin and avoiding the formation of the complex composed of Axin, the adenomatous polyposis coli (APC), the kinases casein kinase 1 (CK1) and glycogen synthase kinase 3 beta (GSK3β), which phosphorylates β-catenin, resulting in β-catenin being ubiquitinated by the β-Trcp ubiquitin ligase, followed by proteasomal degradation. Right panel: in the absence of Wnt β-catenin is degraded, whereas Wnt-mediated activation of Fzd induces expression of genes regulated by β-catenin [92].