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
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Amino Acid Sequence
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Animals
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Cytoskeletal Proteins / genetics*
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Gene Expression Regulation
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Genes, APC
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Humans
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Mutation
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Neoplasms / genetics*
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Oncogenes / genetics
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Proto-Oncogene Proteins
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Trans-Activators*
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Wnt Proteins
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Zebrafish Proteins*
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beta Catenin
Substances
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CTNNB1 protein, human
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Cytoskeletal Proteins
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Proto-Oncogene Proteins
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Trans-Activators
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Wnt Proteins
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Zebrafish Proteins
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beta Catenin