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. Author manuscript; available in PMC: 2019 Jul 17.
Published in final edited form as: Vision Res. 2017 Jun 2;139:47–58. doi: 10.1016/j.visres.2017.02.007

Fig. 1.

Fig. 1.

The canonical Wnt signaling pathway. (A) In the absence of Wnt, β-catenin (β-cat) interacts with the destruction complex formed by a scaffold protein Axin, casein kinase Iα (CKIα) and glycogen synthase kinase 3 beta (GSK-3b) as well as adenomatous polyposis coli (APC), and is constitutively phosphorylated and degraded. (B) In the presence of Wnt, Wnt binds to frizzled receptor (Fzd) and co-receptor low-density lipoprotein receptor-related protein 5 or 6 (LRP5/6). LPR5/6 is phosphorylated, which leads to the recruitment and phosphorylation of Dishevelled (Dvl). Subsequently, Axin is recruited to the receptor complex and the destruction complex is disassembled, blocking the phosphorylation of soluble cytoplasmic β-cat. β-cat is then stabilized and translocates to the nucleus to activate transcription of target genes.