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Once stabilized, -catenin translocates to the nucleus , where it interacts with TCF/LEF transcription factors to activate genes involved in: Cell cycle progression Cell survival Tissue maintenance Metabolic adaptation Core molecular components Wnt ligands extracellular signaling proteins Frizzled receptors & LRP5/6 signal reception at the membrane -catenin central transcriptional effector Destruction complex (APC, AXIN, GSK-3, CK1) regulates -catenin degradation in the absence of Wnt signaling Wnt/-catenin signaling pathway in disease Aberrant activation or suppression of Wnt/-catenin signaling contributes to numerous pathological conditions: Cancer: Hyperactivation promotes uncontrolled proliferation, tumor initiation, progression, and therapeutic resistance (Common in colorectal, breast, pancreatic and liver cancers)