Let-7 coordinately suppresses components of the amino acid sensing pathway to repress mTORC1 and induce autophagy
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Summary
Let-7 induced autophagy in the brain to eliminate protein aggregates, establishing its physiological relevance for in vivo autophagy modulation and peripheral delivery of let-7 anti-miR repressed autophagy in muscle and white fat, suggesting that let-7 autophagy regulation extends beyond CNS.
- Type
- dissertation
- Published
- 2014-10-07
- Cited by
- 85
- References
- 44
- Access
- Open access
- OpenAlex
- https://openalex.org/W25295787
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:11887061
Keywords
CMOS, Amplifier, RF power amplifier, Electrical engineering, Electronic engineering
References
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- An expanded Ragulator is a GEF for the Rag GTPases that signal amino acid levels to mTORC1
- Modulation of glutamine metabolism by the PI(3)K–PKB–FOXO network regulates autophagy
- Synaptic Vesicle Protein NTT4/XT1 (SLC6A17) Catalyzes Na+-coupled Neutral Amino Acid Transport*
- Regulation of TORC1 by Rag GTPases in nutrient response
- The let-7 family of microRNAs.
- Amino acid sensing and regulation of mTORC1.
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- Intranuclear inclusions of expanded polyglutamine protein in spinocerebellar ataxia type 3.
- Autophagy in Health and Disease: A Double-Edged Sword
- The Rag GTPases Bind Raptor and Mediate Amino Acid Signaling to mTORC1
- Ragulator-Rag complex targets mTORC1 to the lysosomal surface and is necessary for its activation by amino acids
- Amino acid signalling upstream of mTOR
- A genome-wide siRNA screen reveals multiple mTORC1 independent signaling pathways regulating autophagy under normal nutritional conditions
Cited by
- miR-Let7A Modulates Autophagy Induction in LPS-Activated Microglia
- Let-7 Represses Carcinogenesis and a Stem Cell Phenotype in the Intestine via Regulation of Hmga2
- mTOR and its tight regulation for iNKT cell development and effector function
- Autophagy in Polyglutamine Disease: Imposing Order on Disorder or Contributing to the Chaos?
- Lin28 and let-7 in cell metabolism and cancer.
- A cardiac myocyte-restricted Lin28/let7 regulatory axis promotes hypoxia-mediated apoptosis by inducing the AKT signaling suppressor PIK3IP1
- Lin28 and let-7 in the Metabolic Physiology of Aging.
- LIN28/let-7 Axis as a Regulator of Myocardial Ischemic Injury
- Therapeutic targeting of autophagy in myocardial infarction and heart failure
- MicroRNA let-7g regulates mouse granulosa cell autophagy by targeting insulin-like growth factor 1 receptor.
- Knockdown of MicroRNA Let-7a Improves the Functionality of Bone Marrow-Derived Mesenchymal Stem Cells in Immunotherapy.
- MicroRNAs and the Metabolic Hallmarks of Aging
- Molecular links among non‐biodegradable nanoparticles, reactive oxygen species, and autophagy
- Oncogenic mechanisms of Lin28 in breast cancer: new functions and therapeutic opportunities
- Emerging Role of MicroRNAs in mTOR Signaling
- MicroRNA-125b-5p mediates post-transcriptional regulation of hepatitis B virus replication via the LIN28B/let-7 axis
- let‐7 regulates radial migration of new‐born neurons through positive regulation of autophagy
- MicroRNAs and Autophagy: Fine Players in the Control of Chondrocyte Homeostatic Activities in Osteoarthritis
- Overexpression of let-7a increases neurotoxicity in a PC12 cell model of Alzheimer's disease via regulating autophagy.
- The Regulatory Role of microRNAs in the Mouse and Human Brain
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