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. 2015 Dec 29;113(2):E117–E126. doi: 10.1073/pnas.1514076113

Fig. 4.

Fig. 4.

NFR-mediated ATF4 transcriptional signature is controlled by eIF2α phosphorylation. (A) EIF2αWT and eIF2α S51A MEFs treated for 6 h with the indicated concentration of NFR or TM (10 μg/mL) and analyzed by WB with the indicated antibodies. In the absence of eIF2α phosphorylation, ATF4 and CHOP induction are completely abolished. Tubulin (Tbl) is used as the loading control. (B) Heat map comparing gene up-regulation in eIF2αWT and eIF2α S51A MEFs treated for 6 h with 20 μM NFR. Genes that were up-regulated >twofold in eIF2αWT were included and listed in order of fold induction. Each row corresponds to a single gene. Right panel shows the 30 highly induced genes in eIF2αWT compared with eIF2α S51A MEFs. (C) Pie chart of the 646 genes induced by NFR >2-fold in eIF2αWT MEFs (identified in B), of which 544 (84%) showed a reduced or no induction in eIF2α S51A MEFs. (D) eIF2αWT and eIF2α S51A MEFs treated for 6 h with the indicated concentration of NFR or TM were analyzed for expression of indicated genes by real-time PCR relative to β-actin (data are presented as fold change compared with untreated cells, and mean and SEM of technical triplicates of one representative experiment are shown).