Abstract
Control of stability of beta-catenin is central in the wnt signaling pathway. Here, the protein conductin was found to form a complex with both beta-catenin and the tumor suppressor gene product adenomatous polyposis coli (APC). Conductin induced beta-catenin degradation, whereas mutants of conductin that were deficient in complex formation stabilized beta-catenin. Fragments of APC that contained a conductin-binding domain also blocked beta-catenin degradation. Thus, conductin is a component of the multiprotein complex that directs beta-catenin to degradation and is located downstream of APC. In Xenopus embryos, conductin interfered with wnt-induced axis formation.
MeSH terms
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Adenomatous Polyposis Coli Protein
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Amino Acid Sequence
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Animals
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Axin Protein
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Binding Sites
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Body Patterning
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Cytoskeletal Proteins / chemistry
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Cytoskeletal Proteins / genetics
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Cytoskeletal Proteins / metabolism*
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Glycogen Synthase Kinase 3
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Humans
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Mice
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Molecular Sequence Data
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Mutation
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Phosphorylation
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Proteins / chemistry
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Proto-Oncogene Proteins / metabolism
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Repressor Proteins*
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Signal Transduction
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Trans-Activators*
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Tumor Cells, Cultured
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Xenopus / embryology
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Xenopus Proteins
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beta Catenin
Substances
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AXIN2 protein, human
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Adenomatous Polyposis Coli Protein
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Axin Protein
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Axin2 protein, mouse
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CTNNB1 protein, Xenopus
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CTNNB1 protein, human
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CTNNB1 protein, mouse
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Cytoskeletal Proteins
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Proteins
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Proto-Oncogene Proteins
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Repressor Proteins
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Trans-Activators
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Xenopus Proteins
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axin1 protein, Xenopus
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beta Catenin
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Calcium-Calmodulin-Dependent Protein Kinases
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Glycogen Synthase Kinase 3