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Nutrient regulation of mTORC1 at a glance
被引:225
|作者:
Condon, Kendall J.
[1
,2
,3
,4
]
Sabatini, David M.
[1
,2
,3
,4
]
机构:
[1] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA
[2] MIT, Howard Hughes Med Inst, Dept Biol, Cambridge, MA 02139 USA
[3] Broad Inst, Cambridge, MA 02142 USA
[4] MIT, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA
基金:
美国国家科学基金会;
美国国家卫生研究院;
关键词:
Cell growth;
Lysosome;
mTORC1;
Autophagy;
Signaling;
Nutrients;
Amino acids;
Glucose;
TUMOR-SUPPRESSOR COMPLEX;
AMINO-ACID LEVELS;
RAG GTPASES;
TRANSPORTER SLC38A9;
CRYSTAL-STRUCTURE;
BINDING PARTNER;
GAP ACTIVITY;
LIFE-SPAN;
AUTOPHAGY;
RAPAMYCIN;
D O I:
10.1242/jcs.222570
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
The mechanistic target of rapamycin (mTOR) signaling pathway coordinates environmental and intracellular cues to control eukaryotic cell growth. As a pivot point between anabolic and catabolic processes, mTOR complex 1 (mTORC1) signaling has established roles in regulating metabolism, translation and autophagy. Hyperactivity of the mTOR pathway is associated with numerous human diseases, including diabetes, cancer and epilepsy. Pharmacological inhibition of the mTOR pathway can extend lifespan in a variety of model organisms. Given its broad control of essential cellular processes and clear relevance to human health, there is extensive interest in elucidating how upstream inputs regulate mTORC1 activation. In this Cell Science at a Glance article and accompanying poster, we summarize our understanding of how extracellular and intracellular signals feed into the mTOR pathway, how the lysosome acts as an mTOR signaling hub, and how downstream signaling controls autophagy and lysosome biogenesis.
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