Figure 8: Phosphorylation of GCN5 at Ser275 promotes gluconeogenesis. | Nature Communications

Figure 8: Phosphorylation of GCN5 at Ser275 promotes gluconeogenesis.

From: The GCN5-CITED2-PKA signalling module controls hepatic glucose metabolism through a cAMP-induced substrate switch

Figure 8

(a) Effects of forced expression of GCN5(WT) or GCN5(S275A) together with CITED2 on gluconeogenic gene expression in primary hepatocytes exposed (or not) to pCPT-cAMP (6 h). (b,c) Effects of forced expression of GCN5(S275D) on gluconeogenic gene expression (b) and glucose production (c) in primary hepatocytes exposed (or not) to pCPT-cAMP (16 h). (d) qRT-PCR analysis of G6pc and Pck1 expression in primary mouse hepatocytes infected with adenoviruses encoding CITED2 shRNA or GCN5(S275D) and exposed (or not) to pCPT-cAMP for 6 h. (e,f) Effects of GCN5(S275D) expression in the liver of C57BL/6J mice on gluconeogenic gene expression (e) and plasma glycemia (f) under the fasted (24 h) condition. All data are means±s.e.m. (n=3 (a–d) or 7 (e,f)). *P<0.05, **P<0.01 versus control or as indicated (ANOVA with Bonferroni’s post hoc test (a–d) or unpaired Student’s t-test (e,f)). Adenoviral vectors were used for these experiments. RT–PCR, PCR with reverse transcription. ANOVA, analysis of variance.

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