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PMID:15198980
| Citation |
Sansom, OJ, Reed, KR, Hayes, AJ, Ireland, H, Brinkmann, H, Newton, IP, Batlle, E, Simon-Assmann, P, Clevers, H, Nathke, IS, Clarke, AR and Winton, DJ (2004) Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration. Genes Dev. 18:1385-90 |
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| 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. |
| Links |
PubMed PMC423189 Online version:10.1101/gad.287404 |
| Keywords |
Adenomatous Polyposis Coli Protein/deficiency; Animals; Cell Differentiation; Cell Movement; Cytoskeletal Proteins/metabolism; Immunohistochemistry; Intestinal Mucosa/cytology; Mice; Mice, Knockout; Mice, Transgenic; Phenotype; Proto-Oncogene Proteins/physiology; RNA, Messenger/analysis; RNA, Messenger/isolation & purification; Signal Transduction; Trans-Activators/metabolism; Tumor Suppressor Proteins/deficiency; Wnt Proteins; beta Catenin |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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