Abstract
CCL15 exerts biological effects on a variety of cells, including monocytes. NF-kappaB has been reported to be involved in the transcription of the CCL15 gene. In this study, we have identified an AP-1 element located at -76/-65, which appears to regulate the transcription of the CCL15 gene. We also confirmed that the AP-1 factor binds to the element. Specific inhibitors for MAPK pathways and expression of dominant negative MKK4 or JNK1 reduced PMA-induced transcriptional activation of CCL15. Our findings indicate that transcription of the CCL15 gene is regulated by AP-1 and NF-kappaB through MEK and JNK MAPK pathways in monocytoid cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Chemokines, CC / genetics*
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Gene Expression Regulation / drug effects*
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Humans
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Macrophage Inflammatory Proteins
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Monocytes / drug effects
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Monocytes / metabolism*
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Monokines / genetics*
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NF-kappa B / metabolism*
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Point Mutation / genetics
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Promoter Regions, Genetic / drug effects
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Protein Binding
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Response Elements / genetics*
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Signal Transduction / drug effects
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Tetradecanoylphorbol Acetate / pharmacology
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Transcription Factor AP-1 / metabolism*
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Transcription, Genetic / drug effects*
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U937 Cells
Substances
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CCL15 protein, human
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Chemokines, CC
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Macrophage Inflammatory Proteins
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Monokines
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NF-kappa B
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Transcription Factor AP-1
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Tetradecanoylphorbol Acetate