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. 2016 Mar 14;113(13):3609–3614. doi: 10.1073/pnas.1523686113

Fig. 1.

Fig. 1.

Identification of SPR as a drug that inhibits EBV SM function. (A) HEK293 cells were stably transfected with a KSHV ORF59-GFP reporter plasmid and transduced with a lentivirus expressing inducible EBV SM protein. Fluorescence microscopy was performed on reporter cells in the presence or absence of SPR. Cells expressed GFP protein only when SM was expressed (+SM) but were GFP-negative when treated with 10 μM SPR (S). (B) SPR inhibits SM-dependent ORF59-GFP RNA accumulation. The expression of ORF59-GFP fusion RNA was measured by qRT-PCR 24 h after 10 μM SPR treatment. (C) SPR inhibits ORF59-GFP protein accumulation. Immunoblotting with anti-GFP or actin antibody was performed on lysates from cells treated as shown. (D) The reporter cell line was induced to express SM and treated with either vehicle (–S) or treated with SPR (+S). Cells were fixed 30 h after induction and stained with either DAPI (blue) or anti-SM antibodies (red). (E) 293 cells were transfected with CMV UL44-GFP and empty vector (–) or SM (+) and treated with either vehicle or 10 μM SPR as shown.