mTOR inhibits autophagy by controlling ULK1 ubiquitylation, self-association and function through AMBRA1 and TRAF6

By F. Nazio, F. Strappazzon, M. Antonioli, P. Bielli, Valentina Cianfanelli, M. Bordi, C. Gretzmeier, J. Dengjel, M. Piacentini, G. Fimia and 1 more. Nature Cell Biology, 2013

753 citations recorded by the source corpus.

Subfields: Epidemiology, Parasitology, Physiology

View Paper: https://www.semanticscholar.org/paper/e2f8af86a9de328854b970ace8756be9c8f90400

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Citations in the corpus

Autophagy in malignant transformation and cancer progression (2015, positive): “…other effects, this allows for the activation of several proteins that are crucial for the initiation of autophagic responses, such as unc-51-like autophagy-activating kinase 1 (ULK1, the mammalian ortholog of yeast Atg1) and autophagy-related 13 (ATG13) (Hosokawa et al , 2009; Nazio et al , 2013).”
mTOR: a pharmacologic target for autophagy regulation. (2015, positive): “In addition, another layer of ULK1 regulation by mTORC1 has been suggested in which mTORC1 inhibits ULK1 stability by inhibitory phosphorylation of autophagy/beclin 1 regulator 1 (AMBRA1) (71).”
Autophagy-Dependent Ferroptosis: Machinery and Regulation (2020, background): “In addition to phosphorylation, ULK1 undergoes acetylation and ubiquitination (Ub) as an alternative regulatory mechanism (Lin et al., 2012; Nazio et al., 2013).”
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (2012, neutral): “has also been described as relevant to ULK1 regulation and autophagy induction.(488,501) In line with what is described for”