Role of AMPK in regulation of LC3 lipidation as a marker of autophagy in skeletal muscle

During induction of the autophagosomal degradation process, LC3-I is lipidated to LC3-II and associates to the cargo isolation membrane allowing for autophagosome formation. Lipidation of LC3 results in an increased LC3-II/LC3-I ratio, and this ratio is an often used marker for autophagy in various...

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Veröffentlicht in:Cellular signalling 2016-06, Vol.28 (6), p.663-674
Hauptverfasser: Fritzen, Andreas Mæchel, Frøsig, Christian, Jeppesen, Jacob, Jensen, Thomas Elbenhardt, Lundsgaard, Anne-Marie, Serup, Annette Karen, Schjerling, Peter, Proud, Chris G., Richter, Erik A., Kiens, Bente
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Sprache:eng
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Zusammenfassung:During induction of the autophagosomal degradation process, LC3-I is lipidated to LC3-II and associates to the cargo isolation membrane allowing for autophagosome formation. Lipidation of LC3 results in an increased LC3-II/LC3-I ratio, and this ratio is an often used marker for autophagy in various tissues, including skeletal muscle. From cell studies AMPK has been proposed to be necessary and sufficient for LC3 lipidation. The aim of the present study was to investigate the role of AMPK in regulation of LC3 lipidation as a marker of autophagy in skeletal muscle. We observed an increase in the LC3-II/LC3-I ratio in skeletal muscle of AMPKα2 kinase-dead (KD) (p
ISSN:0898-6568
1873-3913
DOI:10.1016/j.cellsig.2016.03.005