You want Wnt to be named after butterfly stripes? Last sentence below gives away wnt and lack of it leading to colon polyps/cancer. It does a million other things though. Might as well call it signaling molecule 145626.
The activation of the pathway occurs at the cellular membrane, where Wnt ligands bind to the seven transmembrane-domain protein receptors Frizzled (Fzd) and/or to the low-density lipoprotein receptor-related protein (LRP) 5/6. This interaction leads to the inhibition of the axin degradasome destruction complex, which is a multiprotein complex that controls the cytoplasmic amount of β-catenin via phosphorylation, and, thereby, triggers β-catenin degradation by the proteasome in the absence of Wnt [10]. The destruction complex comprises the tumor suppressor adenomatous polyposis coli (APC), the axin scaffold protein, and two Ser/Thr kinases: glycogen synthase kinase 3 (GSK3) β and casein kinase 1 (CK1). In the absence of Wnt ligands, CK1 phosphorylates β-catenin at Ser45 residue and GSK3β at Ser33/Ser37/Thr41 residues. Then, the β-transducin repeats-containing protein (β-TrCP), an E3-ubiquitin ligase, ubiquitinates phosphorylated β-catenin, which becomes a target for proteasomal degradation [10].
When Wnt binds to Fzd and/or LRP5/6 receptors, the Wnt/β-catenin pathway is activated and the axin degradasome is inhibited [9]. As a consequence, Dishevelled (Dvl) is activated and recruits the degradasome complex to the plasma membrane, and, thereby, promotes the interaction between LRP5/6 and axin [11,12]. Consequently, LRP5/6 is phosphorylated at specific amino acidic residues (Ser1490, Thr1530, Thr1572, Ser1590, Ser1607) [13], acting as a direct competitive inhibitor of GSK3β [14].
Moreover, inactivation of GSK3β through Akt-dependent Ser9 phosphorylation prevents the phosphorylation of β-catenin, which allows its stabilization and accumulation in the cytoplasm. Stabilized β-catenin translocates to the nucleus where it binds to transcription factors, notably T-cell factor (TCF) and lymphoid enhancing factor (LEF), TCF/LEF. This interaction displaces the co-TCF/LEF repressor Groucho, whose function under basal conditions is to compact chromatin [15]. Groucho and TCF/LEF form a multiprotein complex, which is also termed Wnt enhanceosome, that recruits transcriptional co-activators and histone modifiers such as the ATP-dependent helicase Brahma-related gene 1 (BRG1, also known as SMARCA4), cyclic adenosine mono phosphate response element (CREB)-binding protein (CBP), p300, B-cell lymphoma 9 (BCL9), and pygo [15,16]. The Wnt enhanceosome regulates chromatin remodeling and activates the transcription of β-catenin-dependent genes involved in cell growth and survival, including C-MYC, CCND1, BIRC5, and CDKN1a [9]. C-myc is a proto-oncogene that activates cyclin D1 and simultaneously inhibits p21 and p27, which leads to uncontrolled cell proliferation