Abstract
Several cellular signaling systems exhibit cross talk. Cross talk seems to play an important role in modifying signal effects. In vertebrates, the nuclear factor kappa B (NF-kappaB) signaling pathway plays important roles in immune response, inflammation and apoptosis. Meanwhile, the Wnt/beta-catenin signaling pathway is involved in oncogenesis and development. We show here that RelA, a component of NF-kappaB, specifically suppressed beta-catenin/Tcf-dependent transcription. This suppression did not depend on the trans-acting transcriptional ability of RelA. Furthermore, RelA neither affected the nuclear import of beta-catenin nor the DNA binding ability of the beta-catenin/Tcf complex, suggesting that NF-kappaB modifies this signaling pathway after the binding of the beta-catenin/Tcf complex with target DNA.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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COS Cells
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Cytoskeletal Proteins / antagonists & inhibitors*
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Cytoskeletal Proteins / genetics
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Cytoskeletal Proteins / metabolism
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Electrophoretic Mobility Shift Assay
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Gene Expression Regulation
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Humans
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NF-kappa B / metabolism*
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Proto-Oncogene Proteins / antagonists & inhibitors*
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Proto-Oncogene Proteins / metabolism
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Signal Transduction
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Trans-Activators / antagonists & inhibitors*
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Trans-Activators / genetics
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Trans-Activators / metabolism
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Transcription Factor RelA
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Transcription, Genetic*
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Transfection
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Tumor Cells, Cultured
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Tumor Necrosis Factor-alpha
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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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NF-kappa B
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Proto-Oncogene Proteins
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Trans-Activators
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Transcription Factor RelA
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Tumor Necrosis Factor-alpha
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Wnt Proteins
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Zebrafish Proteins
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beta Catenin