Activation of β-catenin-Tcf signaling in colon cancer by mutations in β-catenin or APC

Patrice J. Morin, Andrew B. Sparks, Vladimir Korinek, Nick Barker, Hans Clevers, Bert Vogelstein, Kenneth W. Kinzler

Onderzoeksoutput: Bijdrage aan tijdschriftArtikelpeer review

3591 Citaten (Scopus)

Samenvatting

Inactivation of the adenomatous polyposis coli (APC) tumor suppressor gene initiates colorectal neoplasia. One of the biochemical activities associated with the APC protein is down-regulation of transcriptional activation mediated by β-catenin and T cell transcription factor 4 (Tcf-4). The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity. Furthermore, colorectal tumors with intact APC genes were found to contain activating mutations of β-catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of β-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or β-catenin.

Originele taal-2Engels
Pagina's (van-tot)1787-1790
Aantal pagina's4
TijdschriftScience
Volume275
Nummer van het tijdschrift5307
DOI's
StatusGepubliceerd - 21 mrt. 1997
Extern gepubliceerdJa

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