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. 2004 Oct;78(19):10738–10746. doi: 10.1128/JVI.78.19.10738-10746.2004

FIG. 5.

FIG. 5.

(A) Repression of the β4-integrin promoter by wild-type HPV8 E2 (left panel) or the HPV8 E2 C terminus (right panel). Normal human keratinocytes were cotransfected with the luciferase reporter plasmid L5.5K under control of the β4-integrin promoter (1.5 μg) and decreasing amounts of pEYFP-HPV8-E2 expression plasmids or with equimolar amounts (eq.) of pEYFP-HPV8-E2C encoding the C-terminal portion of E2. The total amount of DNA was adjusted with empty pEYFP-C1 vector. (B) The E2 BS-II within the β4-integrin promoter contributes to repression by the HPV8 E2 C terminus. A β4-integrin promoter reporter construct (L5.5K-BS-II-mut) (1.5 μg) containing the same mutated BS-II as in Fig. 7A was cotransfected with pEYFP-HPV8-E2 (0.5 or 0.125 μg) or equimolar amounts of pEYFP-HPV8-E2C into HFKs. The total amount of DNA was adjusted with empty pEYFP-C1 vector. All luciferase activities were determined after 48 h and normalized with the protein concentration of the respective luciferase extracts. The value of the control (empty pEYFP-C1 vector only, open bars) was set at 1. Transfections were conducted in triplicates. The indicated values were averaged from three independent experiments. Error bars indicate standard deviations.