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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Targeting Wnt/β-catenin signaling and its interplay with TGF-β and Notch signaling pathways for the treatment of chronic wounds

Fig. 1

Canonical Wnt/β-catenin signaling pathway. In the absence of a Wnt ligand (WNT OFF) the “destruction complex” composed of glycogen synthase kinase-3β (GSK-3β), casein kinase 1 alpha (CK1α), Axin and adenomatous polyposis coli (APC), remains bound to β-catenin, where GSK-3β phosphorylates β-catenin which results in its degradation, thus preventing its nuclear translocation for transcription of target genes. In the presence of a Wnt ligand (WNT ON) the disheveled protein inhibits the phosphorylation of β-catenin which leads to its accumulation, stabilization, and nuclear translocation, where it binds to the T cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors for transcription of target genes

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