Figure 5
Figure 5. sHBZ suppresses IFN-γ promoter activity. Luciferase assay of the IFN-γ promoter reporter constructs (−670 to +64) cotransfected with an expression plasmid for sHBZ (A), Tax (B), or both (C) is performed in Jurkat cells, which were stimulated with PMA and ionomycin. Luciferase assays of reporter plasmids containing deletions (D) or point mutations in the NFAT (E) or AP-1 (F) consensus-binding region of IFN-γ promoter are performed. The positions of the deleted or mutated regions are indicated in the left of each graph. Consensus sequences for NFAT and AP-1 binding sites were mutated. Inhibitory index is represented as a ratio of fold activation with empty vector or HBZ expression vector. Representative data (mean ± SD) from 2 independent experiments in triplicate are shown.

sHBZ suppresses IFN-γ promoter activity. Luciferase assay of the IFN-γ promoter reporter constructs (−670 to +64) cotransfected with an expression plasmid for sHBZ (A), Tax (B), or both (C) is performed in Jurkat cells, which were stimulated with PMA and ionomycin. Luciferase assays of reporter plasmids containing deletions (D) or point mutations in the NFAT (E) or AP-1 (F) consensus-binding region of IFN-γ promoter are performed. The positions of the deleted or mutated regions are indicated in the left of each graph. Consensus sequences for NFAT and AP-1 binding sites were mutated. Inhibitory index is represented as a ratio of fold activation with empty vector or HBZ expression vector. Representative data (mean ± SD) from 2 independent experiments in triplicate are shown.

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