自噬
PI3K/AKT/mTOR通路
mTORC1型
雷帕霉素的作用靶点
细胞生物学
调节器
激酶
生物
蛋白激酶B
营养感应
交易激励
细胞生长
RPTOR公司
ATG5型
信号转导
mTORC2型
TFEB
细胞内
生物化学
基因
基因表达
细胞凋亡
作者
Nerea Deleyto-Seldas,Alejo Efeyan
标识
DOI:10.3389/fcell.2021.655731
摘要
The mechanistic target of rapamycin (mTOR), master regulator of cellular metabolism, exists in two distinct complexes: mTOR complex 1 and mTOR complex 2 (mTORC1 and 2). MTORC1 is a master switch for most energetically onerous processes in the cell, driving cell growth and building cellular biomass in instances of nutrient sufficiency, and conversely, allowing autophagic recycling of cellular components upon nutrient limitation. The means by which the mTOR kinase blocks autophagy include direct inhibition of the early steps of the process, and the control of the lysosomal degradative capacity of the cell by inhibiting the transactivation of genes encoding structural, regulatory, and catalytic factors. Upon inhibition of mTOR, autophagic recycling of cellular components results in the reactivation of mTORC1; thus, autophagy lies both downstream and upstream of mTOR. The functional relationship between the mTOR pathway and autophagy involves complex regulatory loops that are significantly deciphered at the cellular level, but incompletely understood at the physiological level. Nevertheless, genetic evidence stemming from the use of engineered strains of mice has provided significant insight into the overlapping and complementary metabolic effects that physiological autophagy and the control of mTOR activity exert during fasting and nutrient overload.
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