Journal
CELL CYCLE
Volume 8, Issue 2, Pages 210-213Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.8.2.7394
Keywords
chibby; 14-3-3; -catenin; Wnt; Akt; signaling; nuclear export; protein trafficking
Categories
Funding
- American Diabetes Association [107JF42]
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [DK073191]
Ask authors/readers for more resources
Chibby (Cby) is an evolutionarily conserved antagonist of beta-catenin, a central player of the canonical Wnt signaling pathway, which acts as a transcriptional coactivator. Cby physically interacts with the C-terminal activation domain of beta-catenin and blocks its transcriptional activation potential through competition with DNA-binding Tcf/Lef transcription factors. Our recent study revealed a second mechanism for Cby-mediated beta-catenin inhibition in which Cby cooperates with 14-3-3 adaptor proteins to facilitate nuclear export of beta-catenin, following phosphorylation of Cby by Akt kinase. Therefore, our findings unravel a novel molecular mechanism regulating the dynamic nucleo-cytoplasmic trafficking of beta-catenin and provide new insights into the crosstalk between the Wnt and Akt signaling pathways. Here, we review recent literature concerning Cby function and discuss our current understanding of the relationship between Wnt and Akt signaling.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available