Blocking AMPK β1 myristoylation enhances AMPK activity and protects mice from high-fat diet-induced obesity and hepatic steatosis

AMP-activated protein kinase (AMPK) is a master regulator of cellular energy homeostasis and a therapeutic target for metabolic diseases. Co/post-translational N-myristoylation of glycine-2 (Gly2) of the AMPK β subunit has been suggested to regulate the distribution of the kinase between the cytosol...

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Veröffentlicht in:	Cell reports (Cambridge) 2022-12, Vol.41 (12), p.111862-111862, Article 111862
Hauptverfasser:	Neopane, Katyayanee, Kozlov, Natalie, Negoita, Florentina, Murray-Segal, Lisa, Brink, Robert, Hoque, Ashfaqul, Ovens, Ashley J., Tjin, Gavin, McAloon, Luke M., Yu, Dingyi, Ling, Naomi X.Y., Sanders, Matthew J., Oakhill, Jonathan S., Scott, John W., Steinberg, Gregory R., Loh, Kim, Kemp, Bruce E., Sakamoto, Kei, Galic, Sandra
Format:	Artikel
Sprache:	eng
Schlagworte:	adiposity AMP-Activated Protein Kinases - metabolism AMPK Animals Diet, High-Fat Fatty Liver Mice Mice, Inbred C57BL Myristic Acid - metabolism myristoylation Obesity phosphatase Phosphorylation Protein Phosphatase 2C - metabolism Protein Processing, Post-Translational signal transduction steatosis
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