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Volume 271, Number 38, Issue of September 20, 1996 pp. 23445-23451
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Interferon Regulatory Factor-2 Directs Transcription from the gp91^phox Promoter

(Received for publication, March 29, 1996, and in revised form, July 8, 1996)

From the Herman B. Wells Center for Pediatric Research, Section of Pediatric Hematology/Oncology, and Departments of Pediatrics and Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202-5225

Repressor elements in the gp91^phox promoter are necessary to restrict tissue-specific transcription to mature phagocytes. Deletion of these elements leads to significant promoter activity in cell lines such as HEL and K562 that do not normally express gp91^phox. The 100 to +12 base pair gp91^phox promoter region is sufficient to direct maximal de-repressed transcription in these cells. However, promoter activity is dramatically decreased following a 16-base pair truncation that deletes an interferon-stimulated response element. This element interacts with IRF-1 and IRF-2, members of the interferon regulatory factor family of transcription factors. In addition, this promoter region is bound by a factor with properties similar to BID, a DNA-binding protein that also interacts with three upstream sites within the gp91^phox promoter. Transient transfection studies using mutated promoters indicate that both the IRF and BID binding sites are required for maximal gp91^phox promoter activity. Overexpression of IRF-1 or IRF-2 in K562 cells leads to transactivation of gp91^phox promoter constructs, which is dependent on the presence of an intact IRF binding site. IRF-2 predominates in macrophages that express the gp91^phox gene as well as in HEL and K562 cells. We conclude that IRF-2 and BID activate gp91^phox promoter activity in the absence of transcriptional repression.

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