Regulation of autophagy

自噬的调节

As mentioned previously, there are a number of stimuli capable of inducing or suppressing

autophagy based on the needs of, or stresses on, the cell. 

如前所述，有许多刺激物能够根据细胞所受的压力和需要来诱导或抑制自噬

The original observation that amino acids inhibited autophagy, was one of the first pieces of evidence that autophagy serves as a nutrient recycling pathway when resources are scarce .

最初的发现是氨基酸会抑制自噬，这是首次证明自噬可在细胞能源短缺时，作为一种养料循环途径

 It has since been demonstrated that amino acid levels regulate the activity of the mammalian target of rapamycin (mTOR)or simply TOR in yeast, controlling the activation state of autophagy (Figure 2).

后来也有研究证明，氨基酸水平调控哺乳动物的雷帕霉素靶标或酵母中的简单TOR受体，以控制自噬的激活

 There are two classes of mTOR signaling complexes, mTORC1 and mTORC2. mTORC1 activates two downstream proteins involved in the initiation of protein translation,  the ribosomal protein S6 kinase (S6K) and eukaryotic translation initiation factor 4E (EIF4E), whereas mTORC2 activates Akt kinase .

已发现两种mTOR的信号复合物，mTORC1和mTORC2. mTORC1活化参与蛋白启示转录的两个下游蛋白质，分别是核糖体S蛋白激酶S6K和真核翻译起始因子4E，而mTORC2激活Akt激酶

Activity of mTORC1 can be inhibited by rapamycin,and amino acid-dependent activation of mTORC1 requires the Rag GTPase, and subsequent translocation of mTORC1 to the lysosomal surface .

mTORC1的活性可以被雷帕霉素抑制，mTORC1的氨基酸依赖性的激活需要Rag GTPase，随后mTORC1会重定位到溶酶体表面

害，翻译不完了，留两句明天翻译~

┭┮﹏┭┮

秃然就有种紧迫感了怎么说

如果真的要读博的话，那不得赶紧搞文章了啊~

真的来不及的，咱就是说

Additional mediators of amino acid signaling of mTOR activation include Vps34, MAP4K3, Rab5 and Rac1 [66].

其它的激活mTOR氨基酸信号激活因子包括Vps34，MAP4K4,Rab5和Rac1

During nutrient deprivation mTORC1 is inhibited, preventing protein translation, and activating phosphorylation of the ULK1/ULK2 complex (Atg1 in yeast).

营养匮乏是，mROTC1是被抑制的，阻止蛋白翻译，激活ULK1/ULK2复合物的磷酸化

This allows for the assembly of the Atg13/ULK1/ULK2/FIP2000 complex and the activation of autophagosome formation [63].

这一过程介导了 Atg13/ULK1/ULK2/FIP2000 复合物的组装，激活了自噬体的形成

好的，昨天剩下的补上了，hhh