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Cited by 1,021

The DOI matches its Crossref record.

Regulation of intracellular beta-catenin levels by the adenomatous polyposis coli (APC) tumor-suppressor protein.

Open access
Munemitsu, S, Albert, I, Souza, B, Rubinfeld, B, Polakis, P·1995·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.92.7.3046
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Abstract

The APC tumor-suppressor protein associates with beta-catenin, a cell adhesion protein that is upregulated by the WNT1 oncogene. We examined the effects of exogenous APC expression on the distribution and amount of beta-catenin in a colorectal cancer cell containing only mutant APC. Expression of wild-type APC caused a pronounced reduction in total beta-catenin levels by eliminating an excessive supply of cytoplasmic beta-catenin indigenous to the SW480 colorectal cancer cell line. This reduction was due to an enhanced rate of beta-catenin protein degradation. Truncated mutant APC proteins, characteristic of those associated with cancer, lacked this activity. Mutational analysis revealed that the central region of the APC protein, which is typically deleted or severely truncated in tumors, was responsible for the down-regulation of beta-catenin. These results suggest that the tumor-suppressor activity of mutant APC may be compromised due to a defect in its ability to regulate beta-catenin.

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Metadata

Authors
Munemitsu, S., Albert, I., Souza, B., Rubinfeld, B., & Polakis, P.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
1995-03-28
Volume
92
Issue
7
Pages
3046-3050
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.92.7.3046
OpenAlex
W2039661491
Cited by
1,021
References
0
FWCI
16.70
Type
journal article
Language
en
Open access
green

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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