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

Fig. 5.

Fig. 5

Gluconeogenic regulatory signals were disrupted in the absence of GCN5L1. a Primary hepatocytes were isolated from LKO mice and littermate controls and treated with glucagon (100 nM) at times indicated. Cell lysates were subjected to immunoblotting with the indicated antibodies. b Primary hepatocytes were transfected for 24 h with Ad-CRE luciferase and Ad-β-galactosidase (as infection control) and followed by glucagon incubation for 5 h. Luciferase activity corrected for transfection efficiency was assayed in cell lysates (n = 3 independent experiments). c Glucagon stimulated glucose production was calculated by normalizing glucose production after glucagon stimulation to basal condition of each group from Fig. 4a. d PGC-1α RNA level (n = 5 paired sets of primary hepatocytes) in primary hepatocytes. e Cell lysates from primary hepatocytes were used for immunoblot analysis to assess the levels of FoxO1 (n = 5 paired sets of primary hepatocytes). Values are expressed as mean ± s.e.m.**P < 0.01 versus respective control groups by Student’s t-test