Abstract
Expression of CCL23 is induced by external stimuli including PMA in monocytes, but its transcriptional regulation has not been studied to date. Serial deletion analysis of its 5' flanking region revealed that the region -293 to +31 was important for induction by PMA. Cis-acting elements at the -269/-264 (NFAT site), -167/-159 (NF-kappaB site), and -51/-43 (AP-1 site) positions were identified as the critical sites for the CCL23 expression in U937 cells. We demonstrated the binding of the transcription factors to the consensus sites. Specific inhibitors for signal pathways reduced PMA-induced expression of CCL23, confirming involvement of these transcription factors.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Base Sequence
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Binding Sites
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Carcinogens / pharmacology
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Cells, Cultured / drug effects
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Cells, Cultured / metabolism
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Chemokines, CC / genetics*
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Chemokines, CC / metabolism
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Gene Expression Regulation*
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Humans
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Molecular Sequence Data
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Monocytes / cytology
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Monocytes / drug effects
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Monocytes / physiology*
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NF-kappa B / genetics
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NF-kappa B / metabolism
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NFATC Transcription Factors / metabolism
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Promoter Regions, Genetic / genetics*
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Protein Binding
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Regulatory Sequences, Nucleic Acid
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Tetradecanoylphorbol Acetate / pharmacology
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Transcription Factor AP-1 / metabolism
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Transcription, Genetic
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U937 Cells
Substances
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CCL23 protein, human
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Carcinogens
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Chemokines, CC
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NF-kappa B
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NFATC Transcription Factors
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Transcription Factor AP-1
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Tetradecanoylphorbol Acetate