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

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Official URL:https://doi.org/10.1101/gad.317604
PubMed:View item in PubMed
Creators Name:Brembeck, F.H. and Schwarz-Romond, T. and Bakkers, J. and Wilhelm, S. and Hammerschmidt, M. and Birchmeier, W.
Journal Title:Genes & Development
Journal Abbreviation:Genes Dev
Volume:18
Number:18
Page Range:2225-2230
Date:15 September 2004
Keywords:{Alpha}-Catenin, BCL9, Epithelial-Mesenchymal Transition, Mesoderm Patterning, Tyrosine Phosphorylationp, Wnt8, Animals, Mice, Zebrafish
Abstract:{Beta}-Catenin controls both cadherin-mediated cell adhesion and activation of Wnt target genes. We demonstrate here that the {beta}-catenin-binding protein BCL9-2, a homolog of the human proto-oncogene product BCL9, induces epithelial-mesenchymal transitions of nontransformed cells and increases {beta}-catenin-dependent transcription. RNA interference of BCL9-2 in carcinoma cells induces an epithelial phenotype and translocates {beta}-catenin from the nucleus to the cell membrane. The switch between {beta}-catenin's adhesive and transcriptional functions is modulated by phosphorylation of Tyr 142 of {beta}-catenin, which favors BCL9-2 binding and precludes interaction with {alpha}-catenin. During zebrafish embryogenesis, BCL9-2 acts in the Wnt8-signaling pathway and regulates mesoderm patterning.
ISSN:0890-9369
Publisher:Cold Spring Harbor Laboratory Press (U.S.A.)
Item Type:Article

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