Mechanism and medical implications of mammalian autophagy
Abstract
Autophagy is a highly conserved catabolic process induced under various conditions of cellular stress, which prevents cell damage and promotes survival in the event of energy or nutrient shortage and responds to various cytotoxic insults. Thus, autophagy has primarily cytoprotective functions and needs to be tightly regulated to respond correctly to the different stimuli that cells experience, thereby conferring adaptation to the ever-changing environment. It is now apparent that autophagy is deregulated in the context of various human pathologies, including cancer and neurodegeneration, and its modulation has considerable potential as a therapeutic approach.
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ULK1 activation is accurately regulated by mTORC1 and AMPK activity.
“Its activation is accurately regulated by mTORC1 and AMPK activity [3].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [3]
ULK1 is the master regulator of autophagy induction, triggering a cascade of signals through direct phosphorylation of ATG proteins that culminate in autophagosome formation.
“ULK1 is considered as the master regulator of autophagy induction, triggering a cascade of signals, through direct phosphorylation of ATG proteins, that culminate in autophagosome formation [3, 43].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [3]
ATG14 is a component of the class III PI3K complex 1 (PI3KC3-C1), formed by VPS34, Beclin 1 and p115.
“ATG14 is a component of the class III PI3K complex 1(PI3KC3-C1), formed by the catalytic subunit vacuolar protein sorting 34 (VPS34), Beclin 1 and general vesicular transport factor p115.”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [3]
The class III PI3K complex 1 activates phosphatidylinositol-3-phosphate production on the origin site of omegasome.
“This complex activates the phosphatidylinositol-3-phosphate (PI3P) production on the origin site of omegasome [3].”
From A gene toolbox for monitoring autophagy transcription (2021) · cites this paper as [3]
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- Authors
- Dikic, I., & Elazar, Z.
- Affiliations
- Weizmann Institute of Science (IL)
- Corresponding author
- Elazar, Zvulun
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2018-04-04
- Volume
- 19
- Issue
- 6
- Pages
- 349-364
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- OpenAlex
- W2795845448
- Cited by
- 2,771
- References
- 25
- Citations by year
- 2026: 176 · 2025: 305 · 2024: 349 · 2023: 425 · 2022: 455 · 2021: 432 · 2020: 357 · 2019: 220 · 2018: 50 · 2012: 1
- FWCI
- 37.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Publikationsdatenbank der Fraunhofer-Gesellschaft (Fraunhofer-Gesellschaft) (submittedVersion)
- Fraunhofer-Publica (Fraunhofer-Gesellschaft) (submittedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagy, cellular stress response, cytoprotection, autophagy regulation, cancer, neurodegeneration, inflammation
- MeSH terms
- Animals, Autophagy, Humans, Mammals, Neoplasms, Neurodegenerative Diseases
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