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. 2007 Aug;171(2):513–524. doi: 10.2353/ajpath.2007.070188

Figure 2.

Figure 2

Membrane translocation of GFP-LC3B in response to proteasome inhibition. A: DU145 cells were transfected with GFP-LC3B, treated with vehicle control (a) or MG132 (5 μmol/L, b) for 24 hours and then examined by fluorescence microscopy. B: Quantification of punctated GFP-LC3B-positive HCT 116 (black column), Bax-deficient HCT 116 (white column), and DU145 (gray column) cells following the treatment with MG132 (mean ± SD). C: HCT116-Bax-deficient cells stably expressing GFP-LC3B were treated with vehicle control, lactacystin (5 μmol/L), ALLN (10 μmol/L), or bortezomib (20 nmol/L) for 24 hours. Percentages of cells with punctated GFP-LC3B signals were determined (mean ± SD). D: Bax-positive HCT 116 cells were transfected with GFP-LC3B, treated with MG132 (1 μmol/L) for 24 hours, and then stained with MDC (200 μmol/L), followed by fluorescence microscopy. E: Quantification of punctated MDC-positive cells in Bax-positive HCT 116 (black column), Bax-deficient HCT 116 (white column), and DU145 (gray column) cells treated with MG132. *P < 0.01 by Z-test between the control and the treated groups.