Phosphatidylinositol 3-kinase (PI3K) signaling does not activate the Wnt cascade

S.S. Ng, T. Mahmoudi, E.M. Danenberg, I. Bejaoui, W.B.M. de Lau, H.C. Korswagen, M. Schutte, H. Clevers

Research output: Contribution to journal/periodicalArticleScientificpeer-review

Abstract

Mutational activation of the phosphatidylinositol 3-kinase (PI3K) pathway occurs in a wide variety of tumors, whereas activating Wnt pathway mutants are predominantly found in colon cancer. Because GSK3 is a key component of both pathways, it is widely assumed that active PI3K signaling feeds positively into the Wnt pathway by protein kinase B (PKB)-mediatefd inhibition of GSK3. In addition, PKB has been proposed to modulate the canonical Wnt signaling through direct stabilization and nuclear localization of beta-catenin. Here, we show that compartmentalization by Axin of GSK3 prohibits cross-talk between the PI3K and Wnt pathways and that Wnt-mediated transcriptional activity is not modulated by activation of the PI3K/PKB pathway.
Original languageEnglish
Pages (from-to)35308-35313
JournalJournal of Biological Chemistry
Volume284
Issue number51
DOIs
Publication statusPublished - 2009

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