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. 2017 Sep 12;8:523. doi: 10.1038/s41467-017-00521-8

Fig. 7.

Fig. 7

Mitochondrial GCN5L1 controls FoxO1 stability via controlling ERK activation. ac Primary hepatocytes were isolated and incubated with U0126 (U) or SB203580 (SB) for 8 h. Cell lysates were analyzed by immunoblotting. (n = 3 independent experiments). a Quantification of FoxO1 was normalized to β-Actin, relative to vehicle treated control. b RNA levels of G6Pase and PEPCK were analyzed by real-time PCR (n = 3 independent experiments). c Glucose production was assayed by secretion into the media from these cells (n = 3 independent experiments). d Immunoblot analysis to assay the activation of ERK in primary hepatocytes. Quantification of p-ERK was normalized to total-ERK, relative to control group (n = 5 paired sets of primary hepatocytes). e Primary hepatocytes were isolated and infected with adenovirus expressing GCN5L1(G), Mt-GCN5L1(MTG) or ER-GCN5L1(ERG) for 24 h. Cell lysates were analyzed by immunoblotting of p-ERK. Values are expressed as mean ± s.e.m. *P < 0.05; **P < 0.01 by Student’s t-test