Human macrophage inflammatory protein‐3α/CCL20/LARC/Exodus/SCYA20 is transcriptionally upregulated by tumor necrosis factor‐α via a non‐standard NF‐κB site

FEBS Letters

Harant, Hanna¹  Eldershaw, Suzy A.¹  Lindley, Ivan J.D.¹ 

[1] Department of Inflammatory Diseases, Novartis Research Institute, Brunner Strasse 59, A-1235 Vienna, Austria

关键词: CCL20;    Macrophage inflammatory protein-3α;    Tumor necrosis factor-α;    Chemokine;    Nuclear factor-κB;    Transcriptional;    Promoter;    IL-1;    interleukin-1;    TNF-α;    tumor necrosis factor-α;    PMA;    12-O-tetradecanoylphorbol-13-acetate;    IL-8;    interleukin-8;    EMSA;    electrophoretic mobility shift assay;   

DOI  :  10.1016/S0014-5793(01)03138-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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

【 授权许可】

Unknown