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Bcr interferes with β‐catenin–Tcf1 interaction
Author(s) -
Ress Angelika,
Moelling Karin
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.01.034
Subject(s) - breakpoint cluster region , wnt signaling pathway , catenin , transcription factor , microbiology and biotechnology , effector , tcf4 , cancer research , chemistry , beta catenin , tyrosine kinase , biology , signal transduction , gene , genetics , enhancer
The β‐catenin/Tcf complex is a downstream effector of the Wnt signalling pathway. It is a transcription complex, which activates gene expression and contributes to proliferation and tumor progression. Tcf1 in complex with β‐catenin is able to activate β‐catenin‐dependent gene expression. We demonstrate that expressed Bcr is able to bind the transcription factor Tcf1 to disrupt the Tcf1/β‐catenin complex. Phosphorylation of Bcr by the tyrosine kinase pp60 src can lead to dissociation of the transcriptionally inactive Bcr/Tcf1 complex. Thus two independent mechanisms may regulate Tcf/β‐catenin‐mediated transcription via Bcr: binding to β‐catenin as we have previously shown and to Tcf1 as shown here.