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      Monocyte expression of the human prointerleukin 1 beta gene (IL1B) is dependent on promoter sequences which bind the hematopoietic transcription factor Spi-1/PU.1.

      Molecular and Cellular Biology
      Animals, Base Sequence, Binding Sites, CCAAT-Enhancer-Binding Proteins, Consensus Sequence, DNA Mutational Analysis, DNA-Binding Proteins, metabolism, Gene Expression Regulation, HeLa Cells, Humans, In Vitro Techniques, Interleukin-1, genetics, Mice, Molecular Sequence Data, Monocytes, physiology, Nuclear Proteins, Promoter Regions, Genetic, RNA, Messenger, Retroviridae Proteins, Oncogenic, Sequence Alignment, Sequence Deletion, Sequence Homology, Nucleic Acid, Transcription, Genetic, Transcriptional Activation

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          Abstract

          Interleukin-1 beta (IL-1 beta) is produced primarily by stimulated monocytes, suggesting that the IL1B gene, which codes for this protein, depends upon at least one cell-type-specific factor. Our previous characterization of the IL1B promoter indicated that the region between -131 and +12 is sufficient to direct cell-type-specific expression of a reporter gene (F. Shirakawa, K. Saito, C.A. Bonagura, D.L. Galson, M.J. Fenton, A.C. Webb, and P. E. Auron, Mol. Cell. Biol. 13:1332-1344, 1993). We now show that a sequence located between positions -50 and -39 of the IL1B promoter binds the tissue-restricted Ets domain transcription factor Spi-1/PU.1 (Spi-1). Mutation of this site abrogates binding of this factor and reduces the ability of the IL1B promoter to function in macrophages. A second Spi-1 binding site located between positions -115 and -97 also is required for maximal IL1B promoter activity in the presence of the proximal Spi-1 binding site. In addition, an activation domain-deficient Spi-1 expression vector acts as a dominant-negative inhibitor of reporter gene expression in a monocyte cell line. Finally, the IL1B promoter, which is inactive in Spi-1-deficient HeLa cells, is activated in these cells by cotransfection with a Spi-1 expression vector. Thus, the cell-type-specific expression of the IL1B promoter appears to be dependent on the binding of Spi-1.

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