Chan Edmond Y
Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, UK.
Sci Signal. 2009 Aug 18;2(84):pe51. doi: 10.1126/scisignal.284pe51.
High nutrient availability stimulates the mammalian target of rapamycin complex 1 (mTORC1) to coordinately activate anabolic processes, such as protein synthesis, while inhibiting the cellular catabolism of autophagy. Positive regulation of protein synthesis through the mTORC1 substrates p70 ribosomal S6 kinase (p70S6K) and eukaryotic initiation factor 4E binding protein 1 (4E-BP1) has been well characterized. The complementary inhibitory mechanism in which mTORC1 phosphorylates the autophagy regulatory complex containing unc-51-like kinase 1 (ULK1), the mammalian Atg13 protein, and focal adhesion kinase interacting protein of 200 kD (FIP200) has also been elucidated.
高营养可用性刺激雷帕霉素复合物1(mTORC1)的哺乳动物靶点,以协同激活合成代谢过程,如蛋白质合成,同时抑制自噬的细胞分解代谢。通过mTORC1底物p70核糖体S6激酶(p70S6K)和真核起始因子4E结合蛋白1(4E-BP1)对蛋白质合成的正向调节已得到充分表征。mTORC1磷酸化包含unc-51样激酶1(ULK1)、哺乳动物Atg13蛋白和200kD粘着斑激酶相互作用蛋白(FIP200)的自噬调节复合物的互补抑制机制也已阐明。