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J Biol Chem. 1996 Sep 20;271(38):23445-51.

Interferon regulatory factor-2 directs transcription from the gp91phox promoter.

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1
Herman B. Wells Center for Pediatric Research, Section of Pediatric Hematology/Oncology, Indiana University School of Medicine, Indianapolis, Indiana 46202-5225, USA.

Abstract

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.

PMID:
8798551
[Indexed for MEDLINE]
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