mTOR Signaling in Growth, Metabolism, and Disease
By R. A. Saxton, David M. Sabatini. Cell, 2017
4,160 citations recorded by the source corpus.
The mechanistic Target of Rapamycin (mTOR) coordinates eukaryotic cell growth and metabolism with environmental inputs including nutrients and growth factors. Extensive research over the past two decades has established a central role for mTOR in regulating many fundamental cell processes, from protein synthesis to autophagy, and deregulated mTOR signaling is implicated in the progression of cancer and diabetes, as well as the aging process. Here, we review recent advances in our understanding of mTOR function, regulation, and importance in mammalian physiology. We also highlight how the mTOR-signaling network contributes to human disease, and discuss the current and future prospects for therapeutically targeting mTOR in the clinic.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/df716f957ed9a424cfadba7578aea688d7c161ec
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In Molecular Biology
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Citations in the corpus
- The role of ubiquitination in tumorigenesis and targeted drug discovery (2020, background): “The mTORC1 and mTORC2 signaling pathways are not independent.(127) The activation of mTORC1 is inseparable from AKT activated by mTORC2, and the feedback inhibition of mTORC2 activation requires mTORC1-mediated Sin1 phosphorylation.”
- Reprogramming of fatty acid metabolism in cancer (2019, background): “Both are multiprotein complexes, and are distinguished mainly through their associations of either Raptor (regulatory protein associated with mTOR) in mTORC1, or Rictor (rapamycin-insensitive companion of mTOR) in mTORC2.(90) AKT is a potent activator of mTORC1 by phosphorylating and inactivating it”
- Multifaceted role of mTOR (mammalian target of rapamycin) signaling pathway in human health and disease (2023, background): “mTORC2 is activated by growth factors which in turn activates AKT and AGC family leading to increased cellular proliferation and survival.(1,38) Growth factors are known to regulate several signaling cascades that intersect on TSC, including receptor tyrosine kinases (RTK), IGF-1, Wnt, TNFα, inflamm”
- Oncogenic activation of PI3K-AKT-mTOR signaling suppresses ferroptosis via SREBP-mediated lipogenesis (2020, background): “mTOR signaling is mediated by two branches, mTORC1 and mTORC2 (28).”