Skip to main content
. Author manuscript; available in PMC: 2021 May 1.
Published in final edited form as: Biochem Pharmacol. 2020 Mar 10;175:113906. doi: 10.1016/j.bcp.2020.113906

Figure 2. Signaling pathways.

Figure 2.

A. Hedgehog signaling. In absence of Hg ligands PTCH accumulates in the cilia and inhibits the entrance of SMO. SuFu binds to Gli proteins inhibiting its transcription factor function. The partial proteolysis of Gli3 produces a repressor form that inhibit the expression of Hg targets. In presence of Hg ligands (i.e. Shh) occurs the activation of PTCH inducing its degradation. Without PTCH, SMO can accumulate in the cilia preventing the degradation of Gli proteins. The Gli proteins can translocate to the nucleus and activate target gene expression. B. Wnt signaling. In the canonical pathway, β-catenin is degraded by a protein complex that includes Apc and Axin. With the activation of the Frizzled receptor the destruction complex is inhibited by the disheveled protein resulting in the stabilization of β-catenin, its translocation to the nucleus and the activation of the expression of target genes. The non-canonical way is involved on the establishment of cell polarity through small GTPases activation. Inversin has a switch role between the canonical and non-canonical pathway. C. Tyrosine kinases signaling. PDGFRα colocalizes in the cilia. The activation transduces in the activation of MEK1/2, AKT (trough the activation of PI3K) and ERK1/2 resulting in cell cycle entry.