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. 2009 Sep 25;284(47):32742–32749. doi: 10.1074/jbc.M109.047910

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© 2009 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 1. — A, AlbCre-mediated knockdown of floxed PERK (AlbCre⁺, PERK^fl/fl) in liver (Liv) but not pancreas (Pan), spleen (Spl), or tail of GCN2^+/+ and GCN2^−/− mice (upper panel). GCN2 was deleted in the liver, pancreas, and spleen of GCN2^−/−-AlbCre⁺-PERK^fl/fl mice but not GCN2^+/+-AlbCre⁺-PERK^fl/fl mice (lower panel). WT, wild type; KO, knock-out. B, asparaginase increased phosphorylation of eIF2 in the liver of both wild-type (GCN2^+/+-AlbCre⁻-PERK^fl/fl) and PERK knockdown (GCN2^+/+-AlbCre⁺-PERK^fl/fl) mice. Means not sharing same lowercase letter are different from each other (by one-way ANOVA), p < 0.05. C, phosphorylation of eIF2 is reduced in the liver of GCN2 null mice both with and without AlbCre-mediated PERK knockdown following asparaginase injection. **, main effect of asparaginase to increase p-eIF2 (by two-way ANOVA), p < 0.05. D, hepatic ASNS mRNA expression was not significantly increased following asparaginase treatment in GCN2 null mice with or without AlbCre-mediated deletion of floxed PERK in liver. Abbreviations: S, saline; A, asparaginase.