谷氨酰胺分解
mTORC1型
谷氨酰胺
安普克
生物
自噬
谷氨酰胺酶
柠檬酸循环
PI3K/AKT/mTOR通路
生物化学
代谢途径
激酶
细胞生物学
新陈代谢
蛋白激酶A
信号转导
氨基酸
细胞凋亡
作者
Clément Bodineau,Mercedes Tomé,Piedad del Socorro Murdoch,Raúl V. Durán
出处
期刊:Autophagy
[Informa]
日期:2022-04-26
卷期号:18 (11): 2749-2750
被引量:18
标识
DOI:10.1080/15548627.2022.2062875
摘要
Cancer cells metabolize glutamine mostly through glutaminolysis, a metabolic pathway that activates MTORC1. The AMPK-MTORC1 signaling axis is a key regulator of cell growth and proliferation. Our recent investigation identified that the connection between glutamine and AMPK is not restricted to glutaminolysis. Rather, we demonstrated the crucial role of ASNS (asparagine synthetase (glutamine-hydrolyzing)) and the GABA shunt for the metabolic control of the AMPK-MTORC1 axis during glutamine sufficiency. Our results elucidated a metabolic network by which glutamine metabolism regulates the MTORC1-macroautophagy/autophagy pathway through two independent branches involving glutaminolysis and ASNS-GABA shunt.Abbreviations: αKG: alpha-ketoglutarate; AMPK: AMP-activated protein kinase; ASNS: asparagine synthetase (glutamine-hydrolyzing); GLUD/GDH: glutamate dehydrogenase; GLS: glutaminase; GOT1: glutamic-oxaloacetic transaminase 1; MTORC1: mechanistic target of rapamycin kinase complex 1; TCA: tricarboxylic acid.
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