Signaling crosstalk between the β-catenin and NF-κB pathways represents a functional network. To test whether the crosstalk also occurs on their common target genes, the cyclin D1 promoter was used as a model because it contains binding sites for both proteins. β-catenin activated transcription from the cyclin D1 promoter, while co-expression of NF-κB p65 reduced β-catenin-induced transcription. Chromatin immunoprecipitation revealed lithium chloride-induced binding of β-catenin on one of the T-cell activating factor binding sites. More interestingly, β-catenin binding was greatly reduced by NF-κB p65, possibly by the protein-protein interaction between the two proteins. Such a dynamic and complex binding of β-catenin and NF-κB on promoters might contribute to the regulated expression of their target genes.
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