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. 2019 Feb 1;33(3-4):150–165. doi: 10.1101/gad.320481.118

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© 2019 Bhatt et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 2. — Autophagy deficiency impairs oncogenic signaling. (A,B) Representative IHC of pACC^S79 in KP and KL tumors at 18 wk after Lenti-Cre infection at high magnification (A) and low magnification (B). (C–E) Representative IHC of pS6, pERK, and Ki67 at the indicated times. (F) Quantification of pS6, pERK, and Ki67 from C–E. (G) Representative IHC of active caspase-3 at the indicated times. (H) Quantification of active caspase-3 from G. (I) Representative images of positive β-galactosidase staining at 18 wk after Lenti-Cre infection. (J) Comparison of metabolites between Atg7^+/+ and Atg7^−/− KL tumors obtained by liquid chromatography/mass spectrometry (LC-MS). (K) Levels of metabolites that show a significant difference between Atg7^+/+ and Atg7^−/− KL tumors. For all of the graphs, the error bar indicates ±SEM. (*) P < 0.05; (**) P < 0.01; (***) P < 0.001. See also Supplemental Figure S3.