NF-κB p65 represses β-catenin-activated transcription of cyclin D1.
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.
National Research Lab for RNA Cell Biology, BK21 Graduate Program for RNA Biology, Institute of Nanosensor and Biotechnology and Department of Molecular Biology, Dankook University, Gyeonggi-do 448-701, Republic of Korea.
Injoo
I
Hwang
Yong Seok
YS
Choi
Mi-Ya
MY
Jeon
Sunjoo
S
Jeong
D002460:Cell Line; D019938:Cyclin D1 / Q000235:genetics*; D005786:Gene Expression Regulation; D006801:Humans; D047468:Immunoprecipitation; D011401:Promoter Regions, Genetic; D051996:Transcription Factor RelA / Q000378:metabolism*; D014158:Transcription, Genetic; D015533:Transcriptional Activation; D051176:beta Catenin / Q000378:metabolism*
D051996:Transcription Factor RelA; D051176:beta Catenin; D019938:Cyclin D1