Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration

Owen J. Sansom, Karen R. Reed, Anthony J. Hayes, Heather Ireland, Hannah Brinkmann, Ian P. Newton, Eduard Batlle, Patricia Simon-Assmann, Hans Clevers, Inke S. Nathke, Alan R. Clarke, Douglas J. Winton

    Research output: Contribution to journalArticlepeer-review

    611 Citations (Scopus)

    Abstract

    Although Apc is well characterized as a tumor-suppressor gene in the intestine, the precise mechanism of this suppression remains to be defined. Using a novel inducible Ahcre transgenic line in conjunction with a loxP-flanked Apc allele we, show that loss of Apc acutely activates Wnt signaling through the nuclear accumulation of ß-catenin. Coincidentally, it perturbs differentiation, migration, proliferation, and apoptosis, such that Apc-deficient cells maintain a "crypt progenitor-like" phenotype. Critically, for the first time we confirm a series of Wnt target molecules in an in vivo setting and also identify a series of new candidate targets within the same setting.

    Original languageEnglish
    Pages (from-to)1385-1390
    Number of pages6
    JournalGenes & Development
    Volume18
    Issue number12
    DOIs
    Publication statusPublished - 2004

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