Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 403, Issue 1, Pages 79-84Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.10.118
Keywords
beta-catenin; TCF; NF-kappa B; Cyclin D1
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Funding
- Ministry for Health, Welfare and Family Affairs, Republic of Korea [A080947]
- Korea Health Promotion Institute [A080947] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Signaling crosstalk between the beta-catenin and NF-kappa B 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. beta-catenin activated transcription from the cyclin D1 promoter, while co-expression of NF-kappa B p65 reduced beta-catenin-induced transcription. Chromatin immunoprecipitation revealed lithium chloride-induced binding of beta-catenin on one of the T-cell activating factor binding sites. More interestingly, beta-catenin binding was greatly reduced by NF-kappa B p65, possibly by the protein-protein interaction between the two proteins. Such a dynamic and complex binding of beta-catenin and NF-kappa B on promoters might contribute to the regulated expression of their target genes. (C) 2010 Elsevier Inc. All rights reserved.
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