Journal
CELL METABOLISM
Volume 31, Issue 2, Pages 217-218Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2020.01.005
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Funding
- NSFC [31730058]
- MOST of China [2016YFA0502001]
- Wellcome Trust [097726]
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Deficiency of glucose, even under sufficient amino acid supply, turns off translation and promotes catabolic processes to aid cell survival. A recent report by Yoon et al. (2020) shows that glucose is required for the full activity of the leucyl-tRNA synthetase LARS1 and maintains mTORC1 function via LARS1 to enhance translation. Glucose starvation abolishes both effects via phosphorylation of LARS1 by the AMPK-ULK1 signaling pathway. This study supports the idea that glucose starvation inhibits translation at multiple levels.
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