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

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 beta-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.

journal_name

Genes Dev

journal_title

Genes & development

authors

Sansom OJ,Reed KR,Hayes AJ,Ireland H,Brinkmann H,Newton IP,Batlle E,Simon-Assmann P,Clevers H,Nathke IS,Clarke AR,Winton DJ

doi

10.1101/gad.287404

subject

Has Abstract

pub_date

2004-06-15 00:00:00

pages

1385-90

issue

12

eissn

0890-9369

issn

1549-5477

pii

18/12/1385

journal_volume

18

pub_type

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