The enhancer in the long control region of human papillomavirus type 16 is up-regulated by PEF-1 and down-regulated by Oct-1.
The minimal enhancer in the long control region of human papillomavirus type 16 regulates cell type and constitutive expression from the promoter P97. This region contains at least four DNase I footprints (fp4e, fp5e, fp6e, and fp7e). We have shown that fp5e is crucial to enhancer function and have described an apparently novel factor (PEF-1) binding fp5e (S. Cuthill, G. J. Sibbet, and M. S. Campo, Mol. Carcinog. 8:9-104, 1993). Further analyses reveal that Oct-1 or an Oct-related factor binds fp5e at a site overlapping that of PEF-1. The binding of Oct-1 to fp5e has been demonstrated by electrophoretic mobility shift assays, by oligonucleotide competition studies, and by using an Oct-1-specific anti-POU serum. The location of the Oct-1 site has been confirmed by a panel of mutants across fp5e. Mutations that block PEF-1 binding to fp5e also block enhancer/promoter activity of the long control region, whereas mutations that block Oct-1 binding significantly increase enhancer/promoter activity. Thus, although both PEF-1 and Oct-1 interact with fp5e, they appear to regulate human papillomavirus expression in opposite ways.[1]References
- The enhancer in the long control region of human papillomavirus type 16 is up-regulated by PEF-1 and down-regulated by Oct-1. Sibbet, G.J., Cuthill, S., Campo, M.S. J. Virol. (1995) [Pubmed]
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