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. 2020 Dec 30;22(1):331. doi: 10.3390/ijms22010331

Figure 4.

Figure 4

Klf10 deletion activates the proapoptotic PERK-CHOP pathway upon high-sucrose feeding. Eight-week-old WT and Klf10 KO mice were fed either CD or HSD for eight weeks (n = 5–6 mice/group). (A) Western blot analysis of p-PERK, PERK, p-eIF2α, eIF2α, and CHOP in the livers of WT and Klf10 KO mice fed either CD or HSD. (B) Relative expression of genes involved in ER stress (Atf3, Chop, Gadd34, Noxa, and Puma) in the liver was analyzed via qPCR. Target gene expression was normalized to the expression of Rplp0. All data are representative of at least three independent experiments and expressed as mean ± SEM. Charts were produced using GraphPad Prism 5.0. Statistical differences were determined by two-way ANOVA with Mann–Whitney U test using SPSS v17.0. * p < 0.05 vs. genotype-matched, CD-fed group and # p < 0.05 vs. diet-matched, genotype control. WT, wild type; KO, knockout; CD, control chow diet; HSD, high-sucrose diet.