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Figure 2


Fig. 2. Wnt signaling pathways. (A) Canonical Wnt signaling (red) is mediated by secreted Wnt ligands (green) binding to a co-receptor complex that consists of Fzd and Lrp5/6 receptors. This activates the intracellular effector protein dishevelled (Dvl), which results in the stabilization and nuclear accumulation of β-catenin, leading to the activation of LEF/TCF-dependent transcription. (B) Non-canonical Wnt signaling involves at least two pathways: the Ca2+/protein kinase C (PKC) and RhoA/JNK pathways. In Ca2+/PKC signaling (purple), Wnt binding activates Fzd receptors causing G protein (G{alpha}, Gβ, G{gamma})-dependent Ca2+ release. This activates PKC and calmodulin-dependent protein kinase II (CaMKII). In RhoA/JNK signaling (yellow), Wnt proteins activate Rho signaling, including Rho/Rac, and JNK through Dvl, leading to ATF/CREB activation. Non-canonical Wnt signaling often antagonizes β-catenin-dependent canonical signaling through mechanisms that remain poorly understood. PM, plasma membrane.





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