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Human APC sequesters beta-catenin even in the absence of GSK-3beta in a Drosophila model.

Rao PR, Makhijani K, Shashidhara LS

Centre for Cellular and Molecular Biology, Hyderabad, India. prashanth21676@gmail.com

There have been conflicting reports on the requirement of GSK-3beta-mediated phosphorylation of the tumor suppressor adenomatous polyposis coli (APC) vis-à-vis its ability to bind and degrade beta-catenin. Using a unique combination of loss of function for Shaggy/GSK-3beta and a gain of function for human APC in Drosophila, we show that misexpressed human APC (hAPC) can still sequester Armadillo/beta-catenin. In addition, human APC could suppress gain of Wnt/Wingless phenotypes associated with loss of Shaggy/GSK-3beta activity, suggesting that sequestered Armadillo/beta-catenin is non-functional. Based on these studies, we propose that binding per se of beta-catenin by APC does not require phosphorylation by GSK-3beta.

Published 10 April 2008 in Oncogene, 27(17): 2488-93.
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