The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
mTORC1 signaling and the metabolic control of cell growth
Open accessAbstract
mTOR [mechanistic target of rapamycin] is a serine/threonine protein kinase that, as part of mTORC1 (mTOR complex 1), acts as an important molecular connection between nutrient signals and the metabolic processes indispensable for cell growth. While there has been pronounced interest in the upstream mechanisms regulating mTORC1, the full range of downstream molecular targets through which mTORC1 signaling stimulates cell growth is only recently emerging. It is now evident that mTORC1 promotes cell growth primarily through the activation of key anabolic processes. Through a diverse set of downstream targets, mTORC1 promotes the biosynthesis of macromolecules, including proteins, lipids, and nucleotides to build the biomass underlying cell, tissue, and organismal growth. Here, we focus on the metabolic functions of mTORC1 as they relate to the control of cell growth. As dysregulated mTORC1 underlies a variety of human diseases, including cancer, diabetes, autoimmune diseases, and neurological disorders, understanding the metabolic program downstream of mTORC1 provides insights into its role in these pathological states.
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Cites
AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1
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“Lipid synthesis The stimulation of cell growth, as well as the uncontrolled growth of cancer cells, is often accompanied by an increase in de novo lipid synthesis to meet the demand for increased lipids required for organellar and plasma membrane biogenesis [47].”
BackgroundThe Rag GTPases Bind Raptor and Mediate Amino Acid Signaling to mTORC1
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Activation of a metabolic gene regulatory network downstream of mTOR complex 1
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Cited by
AMPK and TOR: The Yin and Yang of Cellular Nutrient Sensing and Growth Control
González, A., Hall, M. N., Lin, S.-C., & Hardie, D. G. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.01.015 · Cited by 797
Metabolic reprogramming in macrophage responses
Liu, Y., Xu, R., Gu, H., Zhang, E., Qu, J., Cao, W., Huang, X., Yan, H., He, J., & Cai, Z. (2021) · Biomarker Research · doi:10.1186/s40364-020-00251-y · Cited by 641
Mechanisms of mTORC1 activation by RHEB and inhibition by PRAS40
Yang, H., Jiang, X., Li, B., Yang, H. J., Miller, M., Yang, A., Dhar, A., & Pavletich, N. P. (2017) · Nature · doi:10.1038/nature25023 · Cited by 548
Developmental origins of metabolic diseases
Hoffman, D. J., Powell, T. L., Barrett, E. S., & Hardy, D. B. (2021) · Physiological Reviews · doi:10.1152/physrev.00002.2020 · Cited by 466
Metabolism of Amino Acids in Cancer
Wei, Z., Liu, X., Cheng, C., Yu, W., & Yi, P. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.603837 · Cited by 429
Metadata
- Authors
- Ben-Sahra, I., & Manning, B. D.
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2017-04
- Volume
- 45
- Pages
- 72-82
- ISSN
- 0955-0674 (ISSN-L)
- OpenAlex
- W2605743056
- Cited by
- 644
- References
- 44
- FWCI
- 4.32
- Type
- journal article
- Language
- en
- Open access
- green
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