p(HGNC:ULK1)
AMPK is central to several mechanisms that trigger autophagy — most importantly, activating phosphoryla- tion of ULK1 (Ser317 and Ser777) and inhibitory phos- phorylation of mTORC1 (REFS21,31) . PubMed:30116051
Conversely, mTORC1 inhibits ULK1 by Ser757 phosphorylation 3,4,31 . PubMed:30116051
AMPK is central to several mechanisms that trigger autophagy — most importantly, activating phosphoryla- tion of ULK1 (Ser317 and Ser777) and inhibitory phos- phorylation of mTORC1 (REFS21,31) . PubMed:30116051
Unc-51-like kinase 1 (ULK1) is primarily an autophagy-initiating protein 3,10,19 , as is the mTORC1- suppressed transcrip- tion factor EB (TFEB), which orchestrates the synthesis of lysosomal and other proteins critical for maintaining ALN flux 20–23 . PubMed:30116051
Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051
Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051
Activation of ULK1 triggers autophagosome nucleation through activating phospho- rylation of AMBRA and beclin 1 within the autophagy- specific PIK3C3 complex 10 (FIG. 3) . PubMed:30116051
The mammalian target of rapamycin (mTOR) kinase negatively modulates autophagy by phosphorylating Atg1, an autophagy initiating factor, while adenosine monophosphate-activated protein kinase (AMPK), a major sensor for the cellular energy status, activates autophagy through inhibiting mTOR signaling as well as by direct phosphorylation of Atg1 (Egan et al., 2011; Kim et al., 2011). Increased mTOR activity results in autophagy downregulation and tau accumulation. PubMed:23528736
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.