氨基酸缺乏诱导细胞自噬的哺乳动物雷帕霉素靶蛋白复合体C1信号通路机制研究进展

Advances in Lack of Amino Acid-Mediated Autophagy via Mammalian Target of Rapamycin Complex 1 Signal Pathway

自噬是机体维持自身稳态的一种重要生理活动,当体内氨基酸或葡萄糖等营养缺乏时,细胞会启动自噬。自噬受到多种信号通路的调节,哺乳动物雷帕霉素靶蛋白复合体C1(m TORC1)信号通路是其中重要的一条,它可以使自噬相关基因13(Atg13)磷酸化,抑制自噬起始。本文将围绕近年来报道的氨基酸缺乏诱导细胞自噬的m TORC1信号通路,包括小G蛋白、腺苷酸活化蛋白激酶(AMPK)、微小RNA(miRNA)、氨基酰-tRNA合成酶在其中的作用等研究进展进行综述。

Autophagy is an important physiological activity for keeping organism steady. Cell will active the au- tophagy when the nutrient as amino acid and glucose deficiency. The autophagy is regulated by many signal pathways, and mammalian target of rapamycin complex I （ mTORC1 ） is one of the important pathway, it can make autophagy factor autophagy-related gene 13 （Atg13） phosphorylation to inhibit autophagy starting. In this review, we summarized the results and conclusions from recent works on amino acid-mediated autophagy via the mTORC1 signal pathway including small G protein, adenosine 5 monophosphate-activated protein kinase （AMPK） , microRNA （ miRNA ） and aminoacyl-tRNA synthetase.