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. 2019 Nov 7;20(22):5543. doi: 10.3390/ijms20225543

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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AMPK induction precedes ULK1 activation upon rapamycin treatment. HEK293T cells were denoted in time after 100 nM rapamycin treatment. (A) The markers of autophagy (LC3, p62), AMPK, ULK1 (ULK1-Ser555-P), and mTOR (p70S6K-P, 4E-BP1-P) were followed by immunoblotting. GAPDH was used as the loading control. (B) Densitometry data represent the intensity of p62 and LC3 II normalized for GAPDH, ULK1-Ser555-P normalized for the total level of ULK1, p70S6K-P normalized for the total level of p70S6K, 4E-BP1-P normalized for the total level of 4E-BP1, and AMPK-Thr172-P normalized for the total level of AMPK. For each of the experiments, three independent measurements were carried out. Error bars represent standard deviation, asterisks indicate statistically significant difference from the control: ns—nonsignificant; * p < 0.05; ** p < 0.01. (C) Computer simulation of rapamycin treatment. The relative activity of AMPK-Thr172-P, mTOR, ULK1-Ser555-P and autophagy (ATG) are plotted in time.