Involvement of two NF-kappaB binding sites in PMA-induced expression of the human leukotactin-1/CCL15 gene in U937 monocytoid cells.
Leukotactin-1 (Lkn-1)/CCL15, is a recently cloned chemotactic chemokine that appears to play important roles in the inflammatory process by recruiting immune cells to inflammatory sites. Expression of the Lkn-1/CCL15 gene is inducible in monocytes but its transcriptional regulation has not been studied. To identify Lkn-1/CCL15 regulatory sequences in monocytic cells, U937 cells were transiently transfected with the luciferase reporter gene linked to various deletions of the Lkn-1/CCL15 promoter region. The region -269 to -43 bp from the transcription start site proved to be important for induction by PMA. This region contained two potential NF-kappaB sites: one between -191 and -182 bp, and the other between -60 and -51 bp. Mutation of either element reduced PMA-induced expression and electrophoretic mobility shift assays revealed that NF-kappaB recognized both potential NF-kappaB sites. In addition, PMA-induction of Lkn-1/CCL15 in transiently transfected U937 cells was blocked by proteasome inhibitor 1. These observations demonstrate that the two NF-kappaB binding sites are essential for PMA-induced Lkn-1/CCL15 expression in human monocytes.[1]References
- Involvement of two NF-kappaB binding sites in PMA-induced expression of the human leukotactin-1/CCL15 gene in U937 monocytoid cells. Shin, Y.H., Shim, J.J., Hur, M.W., Kang, C.J., Kim, J. Mol. Cells (2004) [Pubmed]
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