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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
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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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