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The promoter of the cholecystokinin (CCK) gene possesses evolutionary conserved juxtaposed E-box and cAMP/TPA responsive elements (CRE/TRE). We have examined the functional interaction of these two sites. As previously noted, c-Jun/c-Fos heterodimers greatly increase promoter activity through association with the CRE/TRE. Mutation of the E-box enhanced the activation by c-Jun/c-Fos, as well as stimulation by forskolin and bFGF, that acts through the CRE/TRE site. Moreover, c-Jun/c-Fos stimulation was inhibited by co-expression of c-Myc and Max. The results indicate that factors associating with the E-box exhibit a negative cooperative effect on the activation via the CRE/TRE element. We propose that this mechanism plays a significant role in CCK gene transcription and other genes with juxtaposed E-box and CRE/TRE.

Original publication




Journal article



Publication Date





15 - 18


Animals, Base Sequence, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Basic-Leucine Zipper Transcription Factors, Cholecystokinin, Cyclic AMP, Cyclic AMP Response Element-Binding Protein, DNA-Binding Proteins, Gene Expression Regulation, Helix-Loop-Helix Motifs, Humans, Leucine Zippers, Mice, Molecular Sequence Data, Mutagenesis, Promoter Regions, Genetic, Proto-Oncogene Proteins c-fos, Proto-Oncogene Proteins c-jun, Proto-Oncogene Proteins c-myc, Response Elements, Tetradecanoylphorbol Acetate, Transcription Factors, Tumor Cells, Cultured