The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
mTORC1 Phosphorylates the ULK1-mAtg13-FIP200 Autophagy Regulatory Complex
Abstract
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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In the citing paper
“However, mTORC1 signaling coordinately activates anabolic processes, such as protein synthesis, while inhibiting the cellular catabolism of autophagy (Chan, 2009).”
From Downregulation of MicroRNA-193b-3p Promotes Autophagy and Cell Survival by Targeting TSC1/mTOR Signaling in NSC-34 Cells (2017) · cites this paper as Chan, 2009
In the citing paper
“However, mTORC1 signaling coordinately activates anabolic processes, such as protein synthesis, while inhibiting the cellular catabolism of autophagy (Chan, 2009).”
From Downregulation of MicroRNA-193b-3p Promotes Autophagy and Cell Survival by Targeting TSC1/mTOR Signaling in NSC-34 Cells (2017) · cites this paper as Chan, 2009
In the citing paper
“mTORC1 negatively regulates autophagy through phosphorylating the mediators, unc-51-like kinase 1/2 (ULK-1 and ULK-2), in inhibitory sites”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Chan, 2009
Citations
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Small Molecule Inhibition of the Autophagy Kinase ULK1 and Identification of ULK1 Substrates
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mTORC1 signaling and the metabolic control of cell growth
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Metadata
- Authors
- Chan, E. Y.
- Affiliations
- University of Strathclyde (GB)
- Corresponding author
- Chan, Edmond Y.
- Venue
- Science Signaling
- Published
- 2009-08-18
- Volume
- 2
- Issue
- 84
- Pages
- pe51-pe51
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- OpenAlex
- W2165068125
- Cited by
- 214
- References
- 25
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 5 · 2023: 6 · 2022: 15 · 2021: 8 · 2020: 16 · 2019: 10 · 2018: 14 · 2017: 13 · 2016: 16 · 2015: 21 · 2014: 15 · 2013: 16 · 2012: 16
- FWCI
- 10.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- mTORC1, ULK1, ATG13, FIP200, autophagy regulation, protein phosphorylation, nutrient signaling, p70S6K, 4E-BP1, anabolic-catabolic balance
- MeSH terms
- Autophagy-Related Proteins, Autophagy-Related Protein-1 Homolog, Mechanistic Target of Rapamycin Complex 1, Animals, Autophagy, Humans, Models, Biological, Phosphorylation, Protein-Tyrosine Kinases, Proteins, Transcription Factors, Signal Transduction, Protein Serine-Threonine Kinases, Multiprotein Complexes, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, TOR Serine-Threonine Kinases
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