Figure 1: Hepatic expression of GCN5 is upregulated in obese diabetic mice via cAMP-PKA signalling. | Nature Communications

Figure 1: Hepatic expression of GCN5 is upregulated in obese diabetic mice via cAMP-PKA signalling.

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

Figure 1

(a,b) qRT-PCR analysis of Gcn5 mRNA and immunoblot (IB) analysis of nuclear GCN5 in the liver of C57BL/6J mice maintained on normal chow (NC) or a HFD (a) or of db/db or db/m (control) mice (b) after deprivation of food for 16 h. RT–PCR data are means±s.e.m. (n=7 (a) or 6 (b)). Histone H1 was examined as a loading control for immunoblot analysis. (c) Immunoblot analysis of GCN5, PCAF, CBP and p300 in the liver of db/db or db/m mice deprived of food for 16 h. Quantitative data are means±s.e.m. (n=3). (d) Primary mouse hepatocytes were incubated in the absence or presence of 100 μM pCPT-cAMP or the PKA inhibitor H89 (20 μM) for the indicated times. Cell lysates were then subjected to immunoblot analysis of PCAF or to IP followed by immunoblot analysis with antibodies to GCN5. Data are representative of at least three independent experiments. Statistical analysis was performed with the unpaired Student’s t-test (a–c). *P<0.05 versus NC (a) or db/m mice (b,c). RT–PCR, PCR with reverse transcription.

Back to article page