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. Author manuscript; available in PMC: 2009 Feb 3.
Published in final edited form as: Nat Chem Biol. 2007 May 7;3(6):331–338. doi: 10.1038/nchembio883

Figure 2. SMERs 10, 18 and 28 induce autophagy in mammalian cells.

Figure 2

(a) COS-7 cells transfected with EGFP-LC3 construct for 4 h were treated with DMSO (control), 0.2 μM rapamycin (rap) (positive control), 47 μM SMER10, 43 μM SMER18 or 47 μM SMER28 for 16 h, and analysed by fluorescence microscopy. The effects of treatment on the percentage of EGFP-positive cells with >5 EGFP-LC3 vesicles are shown. Error bars denote S.E.M. p<0.0001 (all SMERs).

(b) HeLa cells stably expressing EGFP-LC3 were treated with DMSO (control), 47 μM SMER10, 43 μM SMER18 or 47 μM SMER28 for 24 h. Confocal sections show cells containing EGFP-positive autophagic vesicles. Nuclei are stained with DAPI. Bar, 20 μM.

(c) HeLa cells stably expressing EGFP-LC3 were treated for 4 h with DMSO (control) or 200 nM bafilomycin A1 (baf), or with 200 nM bafilomycin A1 and 47 μM SMER10, 43 μM SMER18 or 47 μM SMER28. Cells were left untreated or pre-treated with SMERs for 24 h before adding bafilomycin A1. Levels of EGFP-LC3-II were determined by immunoblotting with antibody against EGFP (i) and densitometry analysis relative to actin (ii). Error bars denote S.E.M. p=0.0259 (baf), p<0.0001 (SMER10), p=0.0003 (SMER18 and SMER28) vs control; p=0.0025 (SMER10), p=0.0218 (SMER18), p=0.0195 (SMER28) vs bafilomycin A1.

***, p<0.001; **, p<0.01; *, p<0.05.