Wnt signal pathways
Canonical Wnt Signal Pathway
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| © KEGG |
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Without the Wnt
From the KEGG pathway map, we can know that a receptor complex is composed by LRP and frizzled. On the downside of the receptor, there is a degradation complex (grey arear on the map which name is scaffold) which mad by Axin, CKI, GSK3B, and the most important two proteins: $\beta$-catenin and APC. CKI and GSK3B both phosphorylate the $\beta$-catenin and then it was degradation by proteosome. On the other side, which is in the nuclear, protein TCF and LEF formed a complex and bind on the DNA which responsible for transcription of the genes. But groucho bind with TCF/LEF to prohibit the release of DNA.
With the present of Wnt
When the receptor complex activated by Wnt, Dishevelled protein (Dvl) and degradation complex are recruited by receptor complex. In this way, the $\beta$-catenin is not ubiquinated and released into the nuclear. Then, $\beta$-catenin releases the groucho and bind with TCF and started to bind the DNA. In this way, wnt signal pathway regulated genes are activated and expressed.
Abnormal in Wnt
Intestine stem cells is a group of fast poliferation cell because the intestine epithelial cells only last for 4 days. Lost of tha APC could cause the fail of $\beta$-catenin phosphorylation and leading the constant of gene transcription (90% of human colon cancer).
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over-expression of wild-type Wts has relatively little effect on wing growth in wild-type flies, but can suppress the over-growth phenotypes associated with mutation of upstream tumor suppressors that activate Yki[1].
Sun, Gongping, and Kenneth D. Irvine. “Regulation of Hippo signaling by Jun kinase signaling during compensatory cell proliferation and regeneration, and in neoplastic tumors.” Developmental biology 350.1 (2011): 139-151. ↩︎
Wnt signal pathways
