The mammalian target of rapamycin (mTOR) pathway regulates mitochondrial oxygen consumption and oxidative capacity
What this study shows
In human cultured cells, the amount of mTOR-raptor complex correlated with overall mitochondrial activity. Disrupting the complex with rapamycin lowered mitochondrial membrane potential, oxygen consumption and ATP-synthetic capacity. mTOR and mTOR-raptor complexes were found in purified mitochondrial fractions, and rapamycin markedly changed the mitochondrial phosphoproteome. RNA interference against TSC2, S6K1, raptor or rictor led the authors to conclude that mTOR regulates mitochondrial activity independently of its previously known targets, and they proposed that mTOR activity shifts the balance between mitochondrial and non-mitochondrial ATP production. Boundary: Cultured human cell line with acute pharmacological and RNAi manipulation; the link to lifespan is a hypothesis drawn from lower organisms, not tested here. Drafted from the abstract only.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human Jurkat T cells (per MeSH); rapamycin; RNAi against TSC2, S6K1, raptor and rictor; subcellular fractionation; 2D-DIGE phosphoproteomics) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Human Jurkat T cells (per MeSH); rapamycin; RNAi against TSC2, S6K1, raptor and rictor; subcellular fractionation; 2D-DIGE phosphoproteomics |
| Journal | Journal of Biological Chemistry |
| Year | 2006 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1074/jbc.m603536200 · PMID 16847060 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Rapamycin; RNAi against TSC2, S6K1, raptor, rictor |
| Target | Mitochondrial oxygen consumption, membrane potential, ATP synthesis; mitochondrial phosphoproteome |
| Model | Human cell line |
| Effect | mTOR inhibition with rapamycin lowers mitochondrial respiration and oxidative capacity |
In the Atlas
Related topics
Links in the pathway map
More studies on this topic
- mTOR controls mitochondrial oxidative function through a YY1-PGC-1alpha transcriptional complex (2007)
- L-Arginine Modulates T Cell Metabolism and Enhances Survival and Anti-tumor Activity (2016)
- mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation (2013)
- Sexual Dimorphism in Placental mTORC1 Signaling, Amino Acid Transport, and Mitochondrial Respiration at Term. (2026)
Thank you. Your answer was counted anonymously.