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. Author manuscript; available in PMC: 2008 Oct 7.

Published in final edited form as: Hepatology. 2008 Oct;48(4):1054–1061. doi: 10.1002/hep.22464

(A) Induction of LC3 lipidation by ER-stress inducers Tg and DTT. Huh7.5 cells without treatment (lane 1), with 300 nM Tg treatment for 16 hours (lane 2), or with 5 mM DTT treatment for 30 minutes (lane 3) were analyzed by Western-blotting for LC3 and actin. (B) Confocal microscopy of autophagic vacuoles. Stable Huh7.5 cells that expressed GFP-LC3 were stained with LysoTracker-red for three hours and further treated with DTT for twenty minutes. (C) Long-lived protein degradation assay. Cells with or without Tg treatment for 16 hours were analyzed for protein degradation as described in the Fig. 3 legend. The overall protein degradation rates in the absence (grey bar) or in the presence (black bar) of BAF are shown in the top panel and the BAF-sensitive protein degradation rates are highlighted in the bottom panel.

(A) Induction of LC3 lipidation by ER-stress inducers Tg and DTT. Huh7.5 cells without treatment (lane 1), with 300 nM Tg treatment for 16 hours (lane 2), or with 5 mM DTT treatment for 30 minutes (lane 3) were analyzed by Western-blotting for LC3 and actin. (B) Confocal microscopy of autophagic vacuoles. Stable Huh7.5 cells that expressed GFP-LC3 were stained with LysoTracker-red for three hours and further treated with DTT for twenty minutes. (C) Long-lived protein degradation assay. Cells with or without Tg treatment for 16 hours were analyzed for protein degradation as described in the Fig. 3 legend. The overall protein degradation rates in the absence (grey bar) or in the presence (black bar) of BAF are shown in the top panel and the BAF-sensitive protein degradation rates are highlighted in the bottom panel.