Differential Nuclear Translocation and Transactivation Potential of β-Catenin and Plakoglobin

摘要: β-Catenin and plakoglobin are homologous proteins that function in cell adhesion by linking cadherins to the cytoskeleton signaling transactivation together with lymphoid-enhancing binding/T (LEF/TCF) transcription factors. Here we compared nuclear translocation abilities of β-catenin mammalian cells. Overexpression each two MDCK cells resulted formation aggregates. The β-catenin-containing structures also contained LEF-1 vinculin, while was inefficient recruiting these molecules, suggesting its interaction vinculin is significantly weaker. Moreover, transfection translocated endogenous β-catenin, but not nucleus. Chimeras consisting Gal4 DNA-binding domain domains either or were equally potent transactivating a Gal4-responsive reporter, whereas activation LEF-1– responsive higher β-catenin. wild-type mutant lacking induced accumulation nucleus LEF-1–responsive transactivation. It further shown constitutive β-catenin–dependent SW480 colon carcinoma localization can be inhibited overexpressing N-cadherin α-catenin. results indicate (a) differ their complexing vinculin; (b) LEF-1–dependent preferentially driven β-catenin; (c) cytoplasmic partners cadherin α-catenin, sequester it cytoplasm inhibit transcriptional activity.