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. 2001 Aug;75(16):7749–7755. doi: 10.1128/JVI.75.16.7749-7755.2001

FIG. 3.

FIG. 3

(A) Mutation of the CtBP binding site in EBNA-3C unmasks an activation domain located in the C terminus of EBNA-3C. DG75 cells were transfected with 5 μg of the pUAS-CAT reporter plasmid and with the amounts of pCDNA-3/Gal4DBD-HA (Gal4DBD), pCDNA-3/Gal4DBD-HA-EBNA-3C(580–992). WT, pCDNA-3/Gal4DBD-HA-EBNA-3C(580–992).ΔPLDLS, or pCDNA-3/Gal4DBD-HA-EBNA-3C(580–992).ALDAS effector plasmid DNA as indicated. Cell extracts were prepared 48 h after transfection, and chloramphenicol acetyctransferase (CAT) activity was determined. After normalization to β-galactosidase activity (2 μg of pSV-βgal per transfection was used), the data were expressed as CAT activity relative to the activity from pUAS-CAT with empty control vectors, which was given an arbitrary value of 1. Mean values and standard deviations from three independent experiments are shown. (B) Western -blot analysis of the cell extracts pooled from three independent experiments. The protein extract from transfected cells was resolved by SDS-PAGE (7.5%), blotted, and probed with anti-EBNA-3C A.10.