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In the article titled “Hepatic autophagy mediates ER stress–induced degradation of misfolded apolipoprotein B” (HEPATOLOGY 2011; DOI:10.1002/hep.24269), it has come to the author's attention that there is a possible discrepancy with the panel selection for Figure 4. An alternative set of fields from the same set of experiments was selected and replaced the original d, e, and f panels. All text, results, and statistical treatment remain unchanged. DOI 10.1002/hep.24302

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Figure 4. Presence of 3-methyladenine (3-MA) blocks whereas E64d enhances apoB-GFP-LC3 puncta induced by ER stress. (A-C) Confocal microscopy photographs of primary rat hepatocytes treated with tunicamycin (TM, 5 μg/mL) or glucosamine (GLS, 5 mM) in the presence of 3-MA (5 mM) or E64d (5 μg/mL). Colocalization of apoB (b, e, h, red) with GFP-LC3 (a, d, g, green), apoB-GFP-LC3 puncta (c, f, i, yellow). Scale bar = 17 μM. Data analysis from (A-C) is shown in (D), percentage of apoB-GFP-LC3–positive cells, and (E) the numbers of apoB-GFP-LC3 puncta in positive cells; three independent experiments *P < 0.05. The 3-MA blocked conversion of endogenous LC3-II, and E64d reduced LC3 turnover (F) when exposed to TM or GLS treatment, n = 3, *P < 0.05. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

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