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. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: Cell Death Differ. 2008 Oct 10;16(1):175–183. doi: 10.1038/cdd.2008.143

Figure 3.

Figure 3

Panel A, western analysis of LC3 processing in the presence or absence of lysosomal protease inhibitors pepstatin A and E64D. DT-EGF causes increased LC3-II, which was further stimulated by treatment with pepstatin and E64D in the glioblastoma cells but not in the HN12 epithelial cells. The histogram shows quantitation of the ratio of LC3-II compared to actin for U87MG cells. Panel B, processing of the autophagy cargo protein betaine homocysteine methyltransferase (BHMT). The arrow indicates the processed form of the protein that is produced in autophagolysosomes. U87MG and U373MG glioblastoma cells display DT-EGF-induced BHMT processing, HN12 epithelial cells do not. GFP-Myc indicates the loading control, which was expressed from the GST-BHMT by an IRES sequence (26).