Journal
FEBS LETTERS
Volume 584, Issue 7, Pages 1287-1295Publisher
WILEY
DOI: 10.1016/j.febslet.2010.01.017
Keywords
Mammalian target of rapamycin; Autophagy-related gene 1; UNC-51-like kinase 1; UNC-51-like kinase 2; Autophagy-related gene 13
Funding
- American Diabetes Association [7-07-CD-08]
- National Institutes of Health [DK072004]
- Minnesota Obesity Center [P30DK50456]
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Nutrient starvation induces autophagy in eukaryotic cells through inhibition of TOR (target of rapamycin), an evolutionarily-conserved protein kinase. TOR, as a central regulator of cell growth, plays a key role at the interface of the pathways that coordinately regulate the balance between cell growth and autophagy in response to nutritional status, growth factor and stress signals. Although TOR has been known as a key regulator of autophagy for more than a decade, the underlying regulatory mechanisms have not been clearly understood. This review discusses the recent advances in understanding of the mechanism by which TOR regulates autophagy with focus on mammalian TOR (mTOR) and its regulation of the autophagy machinery. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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