Abstract
beta-catenin functions in both cell adhesion and transcription. Properly choosing between these functions is crucial for normal development, and the wrong choice can lead to cancer. Recent studies have revealed molecular switches that help dictate whether beta-catenin interacts with adhesive or transcriptional complexes. Cara Gottardi and Barry Gumbiner identify Wnt-induced beta-catenin conformational changes that favor assembly into transcription complexes, whereas alpha-catenin-associated beta-catenin appears to favor adhesion. Furthermore, Felix Brembeck and colleagues reveal that phosphorylation dissociates beta-catenin from adhesion complexes while enhancing BCL9-2 binding to promote transcription.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Cell Adhesion / physiology*
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Cytoskeletal Proteins / chemistry
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Cytoskeletal Proteins / genetics*
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Cytoskeletal Proteins / physiology*
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Humans
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Models, Biological
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Multiprotein Complexes
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Neoplasm Proteins / physiology
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Phosphorylation
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Trans-Activators / chemistry
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Trans-Activators / genetics*
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Trans-Activators / physiology*
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Transcription Factors
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Transcription, Genetic*
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Tyrosine / chemistry
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alpha Catenin
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beta Catenin
Substances
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BCL9 protein, human
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CTNNA1 protein, human
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CTNNB1 protein, human
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Cytoskeletal Proteins
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Multiprotein Complexes
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Neoplasm Proteins
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Trans-Activators
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Transcription Factors
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alpha Catenin
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beta Catenin
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Tyrosine