Figure 5.

Suggested model for Ryk–CFTR–Dab2-mediated amplification of Wnt 1-, 2-, 3-, and 3a-specific signaling. In the absence of Wnt 1, 2, 3, and 3a, a subset of Dab2 is associated with either homeostatic recycling of CFTR or formation and maintenance of the β-catenin destruction complex. In the presence of these Wnts, Dab2 is recruited to the Ryk–CFTR membrane complex thereby allowing Axin and Dvl3 to be recruited to the LRP5/6-Frizzled membrane complex and facilitating the phosphorylation and degradation of Axin. Freed β-catenin is subsequently able to accumulate and translocate into the nucleus to catalyze gene-specific transcription.