The DOI matches its Crossref record; 155 of the 155 references it cites were found in a registry or an index.
Regulation of mTORC1 by PI3K signaling
Open accessAbstract
The class I phosphoinositide 3-kinase (PI3K) - mechanistic target of rapamycin complex 1 (mTORC1) signaling network directs cellular metabolism and growth. Activation of mTORC1, which is composed of mTOR, Raptor, mLST8, PRAS40, and DEPTOR, depends on the Rag and Rheb GTPases, and requires signals from amino acids, glucose, oxygen, energy (ATP), and growth factors (including cytokines and hormones such as insulin). Here we discuss the signal transduction mechanisms through which growth factor-responsive PI3K signaling activates mTORC1. We focus on how PI3K-dependent activation of Akt and spatial regulation of the TSC complex (composed of TSC1, TSC2, and TBC1D7) switches on Rheb at the lysosome, where mTORC1 is activated. Integration of PI3K- and amino acid-dependent signals upstream of mTORC1 at the lysosome is detailed in a working model. A coherent understanding of the PI3K-mTORC1 network is imperative as its dysregulation has been implicated in diverse pathologies including cancer, diabetes, autism, and aging.
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1 retracted
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Cited by
The PI3K Pathway in Human Disease
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Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways
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Vyas, S., Zaganjor, E., & Haigis, M. C. (2016) · Cell · doi:10.1016/j.cell.2016.07.002 · Cited by 1,735
Sperm tsRNAs contribute to intergenerational inheritance of an acquired metabolic disorder
Chen, Q., Yan, M., Cao, Z., Li, X., Zhang, Y., Shi, J., Feng, G.-H., Peng, H., Zhang, X., Zhang, Y., et al. (2016) · Science · doi:10.1126/science.aad7977 · Cited by 1,470
Metadata
- Authors
- Dibble, C. C., & Cantley, L. C.
- Venue
- Trends in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2015-09
- Volume
- 25
- Issue
- 9
- Pages
- 545-555
- ISSN
- 0962-8924 (ISSN-L)
- OpenAlex
- W1804602290
- Cited by
- 836
- References
- 155
- FWCI
- 5.32
- Type
- journal article
- Language
- en
- Open access
- green
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