mTORC1 Phosphorylates the ULK1-mAtg13-FIP200 Autophagy Regulatory Complex

被引:177
作者
Chan, Edmond Y. [1 ]
机构
[1] Univ Strathclyde, Strathclyde Inst Pharm & Biomed Sci, Glasgow G4 0NR, Lanark, Scotland
关键词
C-ELEGANS; SACCHAROMYCES-CEREVISIAE; AXON OUTGROWTH; PROTEIN; ULK1; DISEASE; UNC-51; ATG13;
D O I
10.1126/scisignal.284pe51
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
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页数:3
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