Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
FEBS Lett. 2010 Apr 2;584(7):1287-95. doi: 10.1016/j.febslet.2010.01.017. Epub 2010 Jan 18.
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.
营养饥饿通过抑制 TOR(雷帕霉素靶蛋白)诱导真核细胞自噬,TOR 是一种进化上保守的蛋白激酶。TOR 作为细胞生长的中央调节剂,在协调调节细胞生长和自噬之间平衡的途径界面上发挥关键作用,以响应营养状况、生长因子和应激信号。尽管 TOR 作为自噬的关键调节剂已经有十多年的历史,但它的潜在调节机制尚未被清楚地理解。本综述讨论了近年来对 TOR 调节自噬机制的理解进展,重点介绍了哺乳动物 TOR(mTOR)及其对自噬机制的调节。
FEBS Lett. 2010-1-18
Nat Cell Biol. 2011-1-23
Acta Physiol (Oxf). 2009-2-19
Mol Biol Cell. 2009-4
Proc Natl Acad Sci U S A. 2014-7-7
Autophagy. 2010-3-1
Front Cell Dev Biol. 2025-8-12
Redox Biol. 2025-7-21
Cell Biosci. 2025-7-17
Technol Cancer Res Treat. 2025
Mol Cell Biol. 2009-12-7
Nat Cell Biol. 2009-12
J Proteome Res. 2009-11
Proc Natl Acad Sci U S A. 2009-9-21
Nature. 2009-10-1
Biochem Biophys Res Commun. 2009-11-27
Annu Rev Genet. 2009
Autophagy. 2009-10-18