Target of rapamycin (TOR): an integrator of nutrient and growth factor signals and coordinator of cell growth and cell cycle progression

By D. Fingar, J. Blenis. Oncogene, 2004

1,302 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/d47d4f4bc4b7a30b1d572cf34be84bda33435dfa

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. David M. Sabatini
2. K. Guan
3. Michael N. Hall
4. M. Laplante
5. B. Manning
6. J. Blenis
7. M. Karin
8. A. Budanov

In Physiology

1. David M. Sabatini
2. Michael N. Hall
3. K. Guan
4. B. Manning
5. Jingxiang Huang
6. J. Blenis
7. M. Karin
8. A. Budanov

Citations in the corpus

• mTOR and S6K1 mediate assembly of the translation preinitiation complex through dynamic protein interchange and ordered phosphorylation events. (2005, positive): “Full and sustained S6K activation requires additional inputs by PI3K-dependent and -independent mechanisms and requires multiple growth-factor-induced phosphorylation events (Fingar and Blenis, 2004; Inoki et al., 2005; Martin and Blenis, 2002).”
• Rapamycin differentially inhibits S6Ks and 4E-BP1 to mediate cell-type-specific repression of mRNA translation (2008, background): “In addition, temsirolimus, as well as other rapamycin analogues, is currently in clinical trials against other cancers because of its antiangiogenic and cytostatic properties (11).”
• Akt-dependent regulation of NF-{kappa}B is controlled by mTOR and Raptor in association with IKK. (2008, background): “Additionally, a primary effector of Akt action is mTOR (mammalian target of rapamycin), itself a ser/thr kinase that phosphorylates S6K and 4EBP1 to regulate translation (Fingar and Blenis 2004; Hay and Sonenberg 2004).”
• Regulation of Dendritic Morphogenesis by Ras–PI3K–Akt–mTOR and Ras–MAPK Signaling Pathways (2005, background): “As in a variety of other cell types, the soma size in neurons is also controlled by mTOR signaling (Fingar and Blenis, 2004).”
• Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster (2010, background): “This effect on translation is mediated by the downstream targets of TORC1: S6K and 4E-BP (Fingar and Blenis, 2004; Wullschleger et al., 2006).”
• A complex interplay between Akt, TSC2, and the two mTOR complexes (2009, background): “mTORC1-mediated phosphorylation of S6K1/2 and 4EBP1/2 stimulates mRNA translation and, ultimately, cell growth and proliferation [6,7].”
• Targets of curcumin (2011, background): “The main function of mTORC1 is to regulate cell growth, proliferation and survival by sensing mitogen, energy and nutrient signals [126].”
• Hypoxia regulates TSC1/2-mTOR signaling and tumor suppression through REDD1-mediated 14-3-3 shuttling. (2008, background): “Two of the most wellstudied targets of mTORC1 phosphorylation that mediate these effects are ribosomal S6 kinase 1 (S6K1) and the eukaryotic initiation factor 4E (eIF4E)-binding protein 4E-BP1 (Fingar and Blenis 2004).”
• Rheb binds and regulates the mTOR kinase. (2005, background): “mTOR also directly phosphorylates and, in collaboration with PDK1, activates the p70 S6 kinase [10]; the latter regulates cell size [11] through incompletely defined mechanisms.”
• The TSC1-TSC2 complex: a molecular switchboard controlling cell growth. (2008, background): “an increase in cell size), but they have also been found to regulate aspects of cell proliferation, survival and metabolism in specific settings (for focused reviews on the function of TOR proteins, see [27–30]).”