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Journal Article

Essential role of BCL9-2 in the switch between β-catenin's adhesive and transcriptional functions

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Bakkers,  Jeroen
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Hammerschmidt,  Matthias
Georges Köhler Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Brembeck, F. H., Schwarz-Romond, T., Bakkers, J., Wilhelm, S., Hammerschmidt, M., & Birchmeier, W. (2004). Essential role of BCL9-2 in the switch between β-catenin's adhesive and transcriptional functions. Genes & Development, 18, 2225-2230.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-9462-7
Abstract
β-Catenin controls both cadherin-mediated cell adhesion and activation of Wnt target genes. We demonstrate here that the β-catenin-binding protein BCL9-2, a homolog of the human proto-oncogene product BCL9, induces epithelial-mesenchymal transitions of nontransformed cells and increases β-catenin-dependent transcription. RNA interference of BCL9-2 in carcinoma cells induces an epithelial phenotype and translocates β-catenin from the nucleus to the cell membrane. The switch between β-catenin's adhesive and transcriptional functions is modulated by phosphorylation of Tyr 142 of β-catenin, which favors BCL9-2 binding and precludes interaction with α-catenin. During zebrafish embryogenesis, BCL9-2 acts in the Wnt8-signaling pathway and regulates mesoderm patterning.