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Cellular proliferation is antagonistically regulated by canonical and non-canonical Wnt signals; their dysbalance triggers cancers. It is widely believed that the PI3-K>Akt pathway enhances canonical Wnt signals by affecting transcriptional activity and stability of beta-catenin. Here we demonstrate that the PI3-K>Akt pathway also enhances non-canonical Wnt signals by compartmentalizing beta-catenin. By phosphorylating the phosphoinositide(PI)-binding domain of a multimodular signal transducer,doi:10.1101/149351 fatcat:bmleuzs37zh3tieldwa52cupye