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

Onderzoeksoutput: Bijdrage aan tijdschriftArtikelpeer review

682 Citaten (Scopus)

Samenvatting

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 β-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.

Originele taal-2Engels
Pagina's (van-tot)1385-1390
Aantal pagina's6
TijdschriftGenes and Development
Volume18
Nummer van het tijdschrift12
DOI's
StatusGepubliceerd - 15 jun. 2004
Extern gepubliceerdJa

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