Published online 28 November 2005. doi:10.1083/jcb.200510127
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 171, Number 5, 761-763
Terminating Wnt signals
:
a novel nuclear export mechanism targets activated ß-catenin
Meghan E. Thorne3 and
Cara J. Gottardi1,2
1 Department of Medicine, Northwestern University, Chicago, IL 60637
2 Department of Cell and Molecular Biology, Northwestern University, Chicago, IL 60637
3 The Integrated Graduate Program in the Life Sciences, Northwestern University, Chicago, IL 60637
Correspondence to Cara J. Gottardi: c-gottardi{at}northwestern.edu
Abstract
Nuclear targeting of ß-catenin is an obligatory step in Wnt signal transduction, but the factors that control import and export remain to be clarified. In this issue, Hendriksen et al. (p. 785) show that the RanBP3 export factor antagonizes ß-catenin/T cell factor (TCF) transcription by targeting the signaling-competent form of ß-catenin. We speculate that cells may use multiple export mechanisms to inhibit ß-catenin signaling in different ways.
Abbreviations used in this paper: APC, adenomatous polyposis coli; CRM1, exportin chromosome region maintenance 1; GSK3ß, glycogen synthase kinase 3ß; RanBP3, Ran binding protein 3; TCF, T cell factor.

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