The oncogenic activation of beta-catenin.

Current opinion in genetics & development ·Vol. 9 ·No. 1 ·1999-02-00 ·Pages 15-21

Polakis P

Abstract

The activation of beta-catenin to an oncogenic state can result from the inactivation of the tumor suppressor adenomatous polyposis coli (APC), by direct mutation in the beta-catenin gene, or by the activation of wnt receptors. Once activated, beta-catenin most likely promotes tumor progression through its persistent interaction with one or more of its numerous downstream targets.

MeSH Terms

Amino Acid Sequence Animals Cytoskeletal Proteins/genetics Gene Expression Regulation Genes, APC Humans Mutation Neoplasms/genetics Oncogenes/genetics Proto-Oncogene Proteins Trans-Activators Wnt Proteins Zebrafish Proteins beta Catenin

Chemicals

CTNNB1 protein, human Cytoskeletal Proteins Proto-Oncogene Proteins Trans-Activators Wnt Proteins Zebrafish Proteins beta Catenin

Authors & Affiliations

1 authors, click to expand affiliations / ORCID

Polakis P

Onyx Pharmaceuticals, 3031 Research Drive, Richmond, California 94806, USA. ppolakis@onyx-pharm.com

Article Info

Journal

Current opinion in genetics & development

Abbr.

Curr Opin Genet Dev

ISSN

0959-437X

DOI

10.1016/s0959-437x(99)80003-3

ppolakis@onyx-pharm.com

Published

1999-02-00

Pages

15-21

Language

English

Region

England

NLM ID

9111375

Subset

External Links

PubMed source DOI: 10.1016/s0959-437x(99)80003-3 View journal details

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The oncogenic activation of beta-catenin.

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