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. 2018 Mar 1;16(3):77. doi: 10.3390/md16030077

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Comparison of ATG5^+/+ and ATG5^−/− cell viability in response to known modulators of autophagy. Concentration-dependent changes in the viability of wild-type and ATG5-null mouse embryonic fibroblasts (MEFs) after exposure to (A) thapsigargin, (B) tunicamycin, (C) oligomycin A, and (D) rapamycin A. ATG5^+/+ and ATG5^−/− cells were exposed, in parallel, to increasing concentrations of each compound (0.3 nM to 1 µM) for 48 h. Cell viability was determined by a WST-8 proliferation/cytotoxicity assay, with the viability of vehicle-treated cells defined as 100%. Data points show mean viability ± SE (n = 3 wells per treatment) from a representative comparison that was repeated in three independent experiments.

Comparison of ATG5^+/+ and ATG5^−/− cell viability in response to known modulators of autophagy. Concentration-dependent changes in the viability of wild-type and ATG5-null mouse embryonic fibroblasts (MEFs) after exposure to (A) thapsigargin, (B) tunicamycin, (C) oligomycin A, and (D) rapamycin A. ATG5^+/+ and ATG5^−/− cells were exposed, in parallel, to increasing concentrations of each compound (0.3 nM to 1 µM) for 48 h. Cell viability was determined by a WST-8 proliferation/cytotoxicity assay, with the viability of vehicle-treated cells defined as 100%. Data points show mean viability ± SE (n = 3 wells per treatment) from a representative comparison that was repeated in three independent experiments.