AMP-activated protein kinase and autophagy

Autophagy. 2007 May-Jun;3(3):238-40. doi: 10.4161/auto.3710. Epub 2007 May 14.

Abstract

Autophagy is inhibited by TOR-dependent signaling. Interruption of signalling by rapamycin is known to stimulate autophagy, both in mammalian cells and in yeast. However, inactivation of TOR by AMPK has yielded controversial results in the literature with regard to its effect on autophagy: activation of autophagy in yeast but inhibition in hepatocytes. In a recent study, carried out with hepatocytes, HT-29 cells, and HeLa cells, the possible role of AMPK in the control of mammalian autophagy was reexamined. The data suggest that in mammalian cells, as in yeast, AMPK is required for autophagy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases
  • Animals
  • Autophagy*
  • HT29 Cells
  • HeLa Cells
  • Hepatocytes / metabolism
  • Humans
  • Multienzyme Complexes / metabolism*
  • Protein Kinases / metabolism
  • Protein Serine-Threonine Kinases / metabolism*
  • Signal Transduction
  • TOR Serine-Threonine Kinases
  • Yeasts / metabolism

Substances

  • Multienzyme Complexes
  • Protein Kinases
  • MTOR protein, human
  • Protein Serine-Threonine Kinases
  • TOR Serine-Threonine Kinases
  • AMP-Activated Protein Kinases