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mTOR regulation of autophagy
Authors:Chang Hwa Jung
Affiliation:Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, 6-155 Jackson Hall, 321 Church Street SE, Minneapolis, MN 55455, USA
Abstract: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.
Keywords:mTOR, mammalian target of rapamycin   mTORC1, mTOR complex 1   mTORC2, mTOR complex 2   raptor, regulatory associated protein of mTOR   rictor, rapamycin insensitive companion of mTOR   Atg, Autophagy-related gene   TSC, tuberous sclerosis complex   Rheb, ras homolog enriched in brain   PKB, protein kinase B   GAP1, general amino acid permease 1   AMPK, 5&prime  -AMP-activated protein kinase   hVps34, human ortholog of yeast vacuolar protein sorting 34   ULK1, UNC-51-like kinase 1   ULK2, UNC-51-like kinase 2   FIP200, focal adhesion kinase (FAK) family interacting protein of 200   kDa   GATE-16, Golgi-associated ATPase enhancer of 16   kDa   GABARAP, γ-aminobutyric acid (GABA) receptor associated protein   TGN, trans-Golgi network
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