Effects of the LKB1-proline-rich domain mimicking peptide (11R-WT) on AMPK phosphorylation are inhibited in LKB1-deficient C2C12 myotubes.

<p>(A) C2C12 cells were infected with either shRNA encoding for a non-target or LKB1 sequences and differentiated into myotubes before being transduced with either the 11R-WT or 11R-Sca peptides (40nM). LKB1, total AMPK (tAMPK), phospho- T¹⁷² AMPK, total ACC (tACC), phospho S⁷⁹-ACC and loading control GAPDH protein expression levels were determined using specific antibodies. Images are representative of 3 independent experiments. (B) Signal quantification from 3 experiments. Identical letters indicate values that are not statistically different from each other (P>0.05). (C) 3 months old male C57B6/J mice were euthanized and EDL muscles were rapidly removed and incubated for 30 min in oxygenated (95% O₂, 5% CO₂) DMEM supplemented with 10% fetal bovine serum and 11R-WT (right leg EDL) or 11R-Sca peptides (left leg EDL). AMPK, ACC phosphorylation, total AMPK (t-AMPK) and total ACC (t-ACC) and loading control tubulin alpha expression levels were detected using specific antibodies. Figure displays n = 2 mice and blots are representative of 3 independent experiments (n = 6 mice). (D) Signal quantification of 3 independent experiments. Identical letters indicate values that are not statistically different from each other (P>0.05).