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. 2023 Sep 1;299(10):105209. doi: 10.1016/j.jbc.2023.105209

Figure 4.

Figure 4

PD 102807 induces p-AMPK in a PKC-iota-dependent manner.A and B, cells were stimulated with (A) PD 102807 (100 μM; t = 20 min) or (B) MCh (100 μM; t = 5 min) in the presence or absence of the pan-PKC inhibitor Gö 6983 (1 μM; 15 min preincubation). C and D, cells were stimulated with (C) PD 102807 or (D) MCh in the presence or absence of the selective small molecule PKC-ι inhibitor 1 (10 μM; 15 min preincubation). Phosphorylation status of AMPK was determined using a phospho-specific AMPK antibody. E, cells were transfected with siRNA against PKC-ι and subsequently stimulated with PD 102807. Phosphorylation status of AMPK and ACC was determined using phospho-specific antibodies. F, PKC-ι knockdown was confirmed by immunoblotting. Representative blots are shown. Loading was corrected for β-actin or total AMPK. Data are means ± SD values from 3 to five experiments. ∗p < 0.05, ∗∗∗ p < 0.001, ∗∗∗∗p < 0.0001 versus vehicle stimulation, #p < 0.05, ###p < 0.001 versus respective mock-transfected PD 102807 or MCh; one-way ANOVA followed by Bonferroni multiple comparison test. ACC, ACC, acetyl-CoA carboxylase; AMPK, AMP-activated protein kinase; MCh, methacholine; p-AMPK, phospho-AMPK; PKC-ι, protein kinase C iota.