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. 2010 Jan 26;107(7):3146–3151. doi: 10.1073/pnas.0910717107

Fig. 2.

Fig. 2.

Hsp90 inhibitors reduce EBNA1 independent of effects on EBNA1 transcripts or EBNA1 stability. (A) EBV-positive HONE/Akata cells were treated with 17-DMAG (0.17 μM) for 24 h. Expression of the EBNA1 transcript was examined by quantitative RT-PCR. The level of EBNA1 transcript in untreated cells is set as 100. (B) EBV-negative AGS cells were transfected with empty vector (pSG5) or pSG5-EBNA1, followed by a 48-h treatment with no drug or 17-DMAG (0.17 μM) beginning at 4 h after transfection in the presence or absence of the proteasome inhibitor MG-132 (50 μM). (C) HeLa cells were transfected with pSG5-EBNA1 in the presence of Atg5 siRNA or equivalent amounts of a control siRNA, then treated with no drug or 17-DMAG (0.17 μM). (D) LCL1 cells were treated with no drug or 17-DMAG (0.17 μM) in the presence or absence of the autophagy inhibitor 3-MA (10 mM). (E) EBV-positive HONE/Akata cells were treated with no drug or 17-AAG (0.5 μM) for 48 h in the presence or absence of CHX (50 μg/mL) added into medium 12 h before cell harvesting. Whole-cell extracts were prepared and immunoblot analysis was performed to analyze the expression of viral and cellular proteins as indicated (B–E).