mTOR Controls Cell Cycle Progression through Its Cell Growth Effectors S6K1 and 4E-BP1/Eukaryotic Translation Initiation Factor 4E

By D. Fingar, C. Richardson, Andrew R. Tee, L. Cheatham, Christina Tsou, J. Blenis. Molecular and Cellular Biology, 2004

903 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/fc9f21860ac687343deed04a71780742e6178da4

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In Molecular Biology

1. David M. Sabatini
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Citations in the corpus

• mTOR Is Essential for Growth and Proliferation in Early Mouse Embryos and Embryonic Stem Cells (2004, background): “treatment resulted in impaired G1 progression, which was also rescued by rapamycin-resistant mTOR, rapamycin-resistant p70, or wild-type eIF4E (10).”
• p53 target genes sestrin1 and sestrin2 connect genotoxic stress and mTOR signaling. (2008, positive): “Inhibition of mTOR suppresses cell growth and proliferation (Fingar et al., 2004; Wullschleger et al., 2006).”
• Dysregulation of the TSC-mTOR pathway in human disease (2004, background): “The precise mechanism by which mTOR activates these translational regulators, and other important mTOR functions, such as transcriptional regulation and cell cycle regulation, have been described and discussed extensivel”
• Multifaceted role of mTOR (mammalian target of rapamycin) signaling pathway in human health and disease (2023, background): “Preclinical and early clinical studies revealed that TOR-KI inhibitors can stop the cell cycle in the G1 phase and suppress the transcription of cyclin D1, which is mTORC1 dependent and activated by AKT.(9,293) These inhibitors also inhibit the activity of Akt and SGK1, which phosphorylate p27, lead”
• Upstream and downstream of mTOR. (2004, background): “In addition, eIF4E mediates mTOR-dependent cell cycle progression (Fingar et al. 2004), and activated 4E-BP1 attenuates the progression through the G1 phase of the cell cycle and blocks transformation by c-Myc (Lynch et al.”
• mTOR, translation initiation and cancer (2006, background): “Enhancement of the eIF4E/4E-BP interaction, through the expression of a constitutively active 4E-BP mutant (all phosphorylation sites mutated to Ala), leads to a decrease in cell size and inhibition of cell cycle progression in a manner that mimics rapamycin treatment (Fingar et al., 2002, 2004).”