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. 1998 Apr 28;95(9):5281–5286. doi: 10.1073/pnas.95.9.5281

Figure 4.

Figure 4

p300 stimulates HIV transcription. (A) Wild-type 12S E1A but not a 12S E1A p300 binding mutant inhibits activation of the HIV enhancer by Vpr. Jurkat cells were cotransfected with 2 μg of HIV-CAT, 0.5 μg of CMV-Vpr, and 2 μg of wild-type 12S E1A or a 12S E1A p300 binding mutant, as indicated. Relevant control plasmids were used where necessary. Values are represented as -fold activation over the basal level of HIV-CAT. (B) Wild-type 12S E1A but not 12S E1A p300 binding mutant inhibits (ΔκB)HIV-CAT activity. Jurkat cells were cotransfected with 2 μg of (ΔκB)HIV-CAT, 0.5 μg of CMV-Vpr, and either 2 μg of wild-type 12S E1A or a 12S E1A p300 binding mutant, as indicated. Control plasmids were included where necessary. Values are represented as -fold activation over the basal level of HIV-CAT activity. (C) p300 and Vpr function together to activate the HIV enhancer. Jurkat cells were cotransfected with 5 μg of HIV-CAT, 0.2 μg of RSV-RelA where indicated, 1 μg of CMV-Vpr where indicated, and increasing amounts of CMV-p300. Appropriate control vectors were transfected where necessary. Values represent the percent of chloramphenicol conversion in the CAT assay.