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Fig. 7 | Retrovirology

Fig. 7

From: HIV latency reversing agents act through Tat post translational modifications

Fig. 7

JQ1 consistently rescued HIV D4A7 splicing. HEK293T cells were transfected with the pLTR.gp140/EGFP.Rev∆38/DsRed splicing reporter without (a) or with 100 ng of pTat101 (AD8)-Flag that was either wild-type (shown in Fig. 2) or had the specific mutations: b K28A, c K50A, d K50/51A, e K71A or f R53A. Transfected cells were then treated with a panel of LRAs for 48 h, harvested and DsRed expression was quantified using flow cytometry. The fold change in the proportion of spliced product [DsRed/(DsRed + EGFP) × 100] in the no Tat or Tat mutants relative to WT Tat+ DMSO is represented. Comparisons of each condition to DMSO were made using the 2-way ANOVA test. Only statistically significant comparisons are shown *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. The black lines represent the mean ± SEM. DMSO (1:5000), VOR = vorinostat (0.5 μM), PAN = panobinostat (30 nM), JQ1 (+) (1 μM), CTN = chaetocin (30 nM), DIS = disulfiram (500 nM), or PMA/PHA = phorbol myristate acetate/phytohaemagglutinin (10 nM PMA, 10 μg/mL PHA)

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