mTOR coordinates protein synthesis, mitochondrial activity and proliferation
Open accessAbstract
Protein synthesis is one of the most energy consuming processes in the cell. The mammalian/mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that integrates a multitude of extracellular signals and intracellular cues to drive growth and proliferation. mTOR activity is altered in numerous pathological conditions, including metabolic syndrome and cancer. In addition to its well-established role in regulating mRNA translation, emerging studies indicate that mTOR modulates mitochondrial functions. In mammals, mTOR coordinates energy consumption by the mRNA translation machinery and mitochondrial energy production by stimulating synthesis of nucleus-encoded mitochondria-related proteins including TFAM, mitochondrial ribosomal proteins and components of complexes I and V. In this review, we highlight findings that link mTOR, mRNA translation and mitochondrial functions.
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Morita et al. (2015) review provides evidence that mTORC1 enhances mitochondrial function through increased translation of transcription factors that regulate expression of nuclear-encoded mitochondrial genes.
“Likewise, a review by Morita et al. (2015) provides several lines of evidence to suggest mTORC1 enhances mitochondrial function through the increased translation of transcription factors that regulate the expression of nuclear-encoded mitochondrial genes.”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Morita et al. (2015)
The Background section, “mTOR links protein synthesis, mitochondrial function, and proliferation” (page unavailable), says mTORC1 increases translation of mRNAs encoding mitochondrial regulators and links this to mitochondrial respiration. A separate Background section, “mTOR regulates mitochondrial mass and functions by coordinating multiple levels of gene expression” (page unavailable), describes regulation of nuclear-encoded mitochondrial genes through transcriptional regulators such as YY1 and PGC-1α. The copy does not say that increased translation of those transcriptional regulators is the mechanism linking mTORC1 to mitochondrial function. (LLM, conf=0.86)
Experimental — accuracy not yet measuredA number of studies have demonstrated important roles of both AKT and mTOR in up-regulating glycolysis and respiration in various tissues.
“In turn, a number of studies have demonstrated the important roles of both AKT and mTOR in up-regulating glycolysis and respiration in various tissues [54,55,56,57,58].”
From 20-Hydroxyecdysone Boosts Energy Production and Biosynthetic Processes in Non-Transformed Mouse Cells (2024) · cites this paper as [58]
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Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
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- Authors
- Morita, M., Gravel, S.-P., Hulea, L., Larsson, O., Pollak, M., St-Pierre, J., & Topisirovic, I.
- Affiliations
- McGill University (CA)
- Jewish General Hospital (CA)
- Karolinska University Hospital (SE)
- Segal Cancer Centre; Lady Davis Institute for Medical Research; Sir Mortimer B. Davis-Jewish General Hospital; Montreal, QC Canada
- Department of Biochemistry and Goodman Cancer Research Centre; McGill University; Montreal, QC Canada
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2015-02-16
- Volume
- 14
- Issue
- 4
- Pages
- 473-480
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC4615141
- OpenAlex
- W1992631886
- Cited by
- 552
- References
- 108
- Citations by year
- 2026: 41 · 2025: 49 · 2024: 59 · 2023: 49 · 2022: 75 · 2021: 71 · 2020: 74 · 2019: 38 · 2018: 27 · 2017: 31 · 2016: 29 · 2015: 9
- FWCI
- 3.10
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell Cycle (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (CIHR MOP-115195, 106603_1)
- Topics
- 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
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mTOR, protein synthesis, mRNA translation, mitochondrial function, cell proliferation, TFAM, mitochondrial ribosomal proteins, mitochondrial complex I, mitochondrial complex V, energy metabolism, metabolic syndrome, cancer
- MeSH terms
- Animals, Humans, Mitochondria, Models, Biological, Protein Biosynthesis, Signal Transduction, Cell Proliferation, TOR Serine-Threonine Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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