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Table 2 Canonical Wnt pathway from [1]

From: A pedagogical walkthrough of computational modeling and simulation of Wnt signaling pathway using static causal models in MATLAB

Canonical Wnt signaling pathway. The canonical Wnt signaling pathway is a transduction mechanism that contributes to embryo development and controls homeostatic self-renewal in several tissues [8]. Somatic mutations in the pathway are known to be associated with cancer in different parts of the human body. Prominent among them is the colorectal cancer case [23]. In a succinct overview, the Wnt signaling pathway works when the Wnt ligand gets attached to the frizzled(fzd)/LRP coreceptor complex. Fzd may interact with the disheveled (Dvl) causing phosphorylation. It is also thought that Wnts cause phosphorylation of the LRP via casein kinase 1 (C K1) and kinase G S K3. These developments further lead to attraction of axin which causes inhibition of the formation of the degradation complex. The degradation complex constitutes of axin, the β-catenin transportation complex APC, C K1, and G S K3. When the pathway is active, the dissolution of the degradation complex leads to stabilization in the concentration of β-catenin in the cytoplasm. As β-catenin enters into the nucleus, it displaces the Groucho and binds with transcription cell factor TCF, thus instigating transcription of Wnt target genes. Groucho acts as lock on TCF and prevents the transcription of target genes which may induce cancer. In cases when the Wnt ligands are not captured by the coreceptor at the cell membrane, axin helps in the formation of the degradation complex. The degradation complex phosphorylates β-catenin which is then recognized by F b o x/WD repeat protein βT r C P. βT r C P is a component of ubiquitin ligase complex that helps in ubiquitination of β-catenin, thus marking it for degradation via the proteasome. Cartoons depicting the phenomena of Wnt activation are shown in Fig. 1 a, b, respectively.