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      Human macrophage inflammatory protein-3alpha/CCL20/LARC/Exodus/SCYA20 is transcriptionally upregulated by tumor necrosis factor-alpha via a non-standard NF-kappaB site.

      Febs Letters
      5' Flanking Region, genetics, Base Sequence, Cell Line, Chemokine CCL20, Chemokines, CC, Cloning, Molecular, Electrophoretic Mobility Shift Assay, Humans, Luciferases, metabolism, Macrophage Inflammatory Proteins, Molecular Sequence Data, NF-kappa B, Promoter Regions, Genetic, Protein Binding, Receptors, CCR6, Receptors, Chemokine, Response Elements, Transcription Factor RelA, Transcription, Genetic, drug effects, Transcriptional Activation, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, pharmacology

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          Abstract

          The 5'-flanking sequences of the human macrophage inflammatory protein-3alpha/CCL20 gene were cloned and transfected into G-361 human melanoma cells in a luciferase reporter construct. Tumor necrosis factor-alpha (TNF-alpha) treatment stimulated luciferase expression, and promoter truncations demonstrated that TNF-alpha inducibility is conferred by a region between nt -111 and -77, which contains a non-standard nuclear factor-kappaB (NF-kappaB) binding site. The requirement for NF-kappaB was demonstrated as follows: (i) mutations in this NF-kappaB site abrogated TNF-alpha responsiveness; (ii) TNF-alpha activated a construct containing two copies of the CCL20 NF-kappaB binding site; (iii) overexpression of NF-kappaB p65 activated the CCL20 promoter; (iv) NF-kappaB from nuclear extracts of TNF-alpha-stimulated cells bound specifically to this NF-kappaB site.

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