State Key Laboratory of Cellular Stress Biology & State-Province Joint Engineering Laboratory of Targeted Drugs from Natural Products, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Division of Cell Signalling & Immunology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.
Cell Metab. 2020 Feb 4;31(2):217-218. doi: 10.1016/j.cmet.2020.01.005.
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.
即使在充足的氨基酸供应下，葡萄糖的缺乏也会关闭翻译并促进分解代谢过程，以帮助细胞存活。Yoon 等人（2020 年）的最近一份报告表明，葡萄糖是亮氨酰-tRNA 合成酶 LARS1 充分活性所必需的，并且通过 LARS1 维持 mTORC1 功能，从而增强翻译。葡萄糖饥饿通过 AMPK-ULK1 信号通路对 LARS1 的磷酸化作用废除了这两种效应。这项研究支持了葡萄糖饥饿在多个水平上抑制翻译的观点。
