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. 2016 Apr 15;27(8):1220–1234. doi: 10.1091/mbc.E15-08-0557

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© 2016 DeRossi, Vacaru, et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 6: — Atorvastatin is synthetically lethal with trappc11 mutation. (A) Transgenic WT and trappc11-mutant embryos expressing a liver-specific marker (Tg(fabp10:dsRed)) were treated with DMSO or the HMG-CoA reductase inhibitor, Atv, between 3 and 5 dpf at the concentrations indicated and analyzed for gross morphology and lethality. (B) Livers were collected from WT (n = 7 clutches), trappc11 (n = 8 clutches), and 5 μM Atv–treated WT embryos between 3 and 5 dpf (n = 7 clutches) and subjected to qPCR to analyze UPR gene expression used to calculate PC1. p values were calculated with Student’s t test. n.s., not significant. (C) Livers from larvae treated with DMSO or 1 μM Atv from 3 to 5 dpf (n = 8 clutches) were collected and analyzed at 5 dpf for the expression of genes involved in N-linked glycosylation. Atorvastatin-induced fold increases are shown relative to DMSO-treated samples.