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. 2019 Nov 8;10:769. doi: 10.3389/fendo.2019.00769

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Copyright © 2019 Kari, Vasko, Priya and Kirschner.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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LKB1 is responsible for PKA-mediated stimulation of AMPK. (A) FTC-133 cells were treated with PKA activator (PKA) and/ or inhibitor (PKI) for the times shown, and immunoblotted for total and phospho- isoforms of LKB1, AMPK, and mTOR. Note that pLKB1 and pAMPK increase after PKA activator and this is blocked by PKI. (B) FTC-133 were treated as above and probed for total or phospho-TAK1 and for pCAMKII. IL-1 treatment is used as a positive control for pTAK1 induction, although induction is very modest in these cells. Note that neither protein is activated in response to PKA. GAPDH is shown as a loading control.