mTOR and cancer: insights into a complex relationship
By David M. Sabatini. Nature Reviews. Cancer, 2006
1,384 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/435089d5e2fb29be6946a3d35daf5aaedff1d4f0
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- Michael S. Brown
- Shijie Li
- J. Goldstein
- D. Morrison
- David M. Sabatini
- J. Powell
- S. A. Kang
- C. Thoreen
In Molecular Biology
- David M. Sabatini
- M. Laplante
- R. Shaw
- K. Guan
- D. Klionsky
- D. Hardie
- Michael N. Hall
- Timothy R. Peterson
In Oncology
Citations in the corpus
- Potential therapeutic applications of autophagy (2007, background): “, which has triggered an interest in the development of mTOR-catalytic inhibitors for various cancer indication”
- Visualizing stromal cell dynamics in different tumor microenvironments by spinning disk confocal microscopy (2008, neutral): “The macrolide rapamycin operates through the multicomplex protein TOR, and has been shown to be effective in reversing the symptoms observed in PTEN loss of function models (Guertin and Sabatini, 2007; Sabatini, 2006; Yilmaz et al., 2006).”
- AMPK phosphorylation of raptor mediates a metabolic checkpoint. (2008, background): “mTORC1 is composed of four known subunits: mTOR, mLST8/Gbl, PRAS40, and the WD40 repeat-containing subunit raptor (Sabatini, 2006; Sancak et al., 2007; Vander Haar et al., 2007).”
- The 14-3-3 proteins: integrators of diverse signaling cues that impact cell fate and cancer development (2008, background): “Signaling through this pathway converges on the mTOR complex 1 (TORC1) [15,17] and, strikingly, 14-3-3 binds four different regulators of TORC1 signaling.”
- Akt-dependent regulation of NF-{kappa}B is controlled by mTOR and Raptor in association with IKK. (2008, background): “…2004; Hay and Sonenberg 2004). mTOR is associated with two complexes (Bhaskar and Hay 2007): the rapamycin-sensitive TORC1 complex that controls S6K phosphorylation, and TORC2 (Hay and Sonenberg 2004), which is the PDK2 activity that controls ser473 phosphorylation of Akt (Sarbassov et al. 2005).”
- T cell receptor signaling controls Foxp3 expression via PI3K, Akt, and mTOR (2008, neutral): “T cell activation results in the sustained activation of the PI3K/Akt/mTOR network (21), reflected in the phosphorylation of S6 ribosomal protein (pS6), a direct target of the mTOR-regulated p70 S6 kinase S6K1 (27).”
- Metformin, Independent of AMPK, Inhibits mTORC1 In a Rag GTPase-Dependent Manner (2010, background): “mTOR exists in two complexes that consist of distinct sets of protein binding partners (Dann et al., 2007; Sabatini, 2006).”
- Regulation of Immune Responses by mTOR (2011, background): “Rapamycin was found to inhibit the growth of yeast as well as to have immunosuppressive and antitumor properties (6).”
- Autophagy: cellular and molecular mechanisms (2010, background): “Conversely, autophagy is inhibited by increased growth factor signalling through the insulin receptor and its adaptor, IRS1, as well as other growth factor receptors that activate the Class I group of PI3-kinases and Akt, to promote mTOR activity through inhibition of TSC1/TSC2 and increased Rheb GT”
- Cyclin D as a therapeutic target in cancer (2011, background): “In Phase II clinical trials mTOR inhibitors were particularly effective in MCL, which is characterized by almost universal overexpression of cyclin D1, although this may not be accompanied by a reduction in cyclin D1 expression (reviewed in REF”