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. Author manuscript; available in PMC: 2017 Nov 16.
Published in final edited form as: Biochem J. 2015 May 1;467(3):461–472. doi: 10.1042/BJ20141142

Figure 2.

Figure 2

PT-1 stimulates AMPK Thr172, but not ACC2 or TBC1D1 phosphorylation, whereas AICAR stimulates all. Western blotting were performed on C57BL/6 soleus and EDL muscles stimulated with PT-1 (100 μM, 1h), AICAR (2 mM, 1h) or combined PT-1+AICAR treatment to assess A) AMPK Thr172, B) ACC2 Ser212, C) TBC1D1 Ser231 in EDL and D) TBC1D1 Thr590 in EDL. E) Glycogen synthase (GS) Ser8 in soleus and EDL. Representative blots are shown in F). To verify the TBC1D1 Ser231 antibody in G), the top band of the doublet recognized by the phospho-Ser231 antibody in AICAR-stimulated mouse EDL was shown to align with total TBC1D1 and H) to be depleted by immunoprecipitation with total TBC1D1 but not TBC1D4. I) Immunoblot of ACC1, ACC2 and ACC1/2 Ser79/Ser212 in mouse muscle and liver as indicated. J) The GS Ser8 phosphorylation was reduced in resting kinase-dead (KD) AMPK overexpressing soleus muscles compared to wild type. */**/***p <0.05/0.01/0.001 T-test or Tukey post hoc difference compared to control, ǂ/ǂǂǂ p<0.05/0.001 Tukey post hoc difference compared to AICAR. n=8 for PT+AICAR experiments, n=6 for wild type vs. kinase-dead (KD) AMPK muscles. Results are mean ± SE.