Growing roles for the mTOR pathway.

By Dos D. Sarbassov, Siraj M. Ali, David M. Sabatini. Current Opinion in Cell Biology, 2005

1,640 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/1bd08caa1696834732c9cc4b650d92a9a36f2bc8

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

Citations in the corpus

DEPTOR is an mTOR Inhibitor Whose Frequent Overexpression in Multiple Myeloma Cells Promotes their Survival (2009, background): “Mammalian TOR (mTOR) is an evolutionarily conserved serine/ threonine kinase that integrates signals from growth factors, nutrients, and stresses to regulate multiple processes, including mRNA translation, cell-cycle progression, autophagy, and cell survival (reviewed in Sarbassov et al., 2005).”
Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “The most important targets regulated by IGF-1-signaling pathway are the transcription factors FoxO [177] and TOR protein kinase [178].”
Inhibition of mTOR by Rapamycin Abolishes Cognitive Deficits and Reduces Amyloid-β Levels in a Mouse Model of Alzheimer's Disease (2010, background): “The target of rapamycin (TOR) pathway is a major signaling hub that integrates nutrient/growth factor availability with cell metabolism[12] through two distinct complexes, mTORC1 and mTORC2[13].”
Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “In response to PI3K activation, PDK1 and the mammalian target of rapamycin (mTOR, acting in the rapamycin-insensitive TORC2 complex) activate Akt via phosphorylation of two key residues, T308 and S473, respectively (Mora et al. 2004; Sarbassov et al. 2005).”
Prolonged rapamycin treatment inhibits mTORC2 assembly and Akt/PKB. (2006, methodology): “The mTOR complex 2 (mTORC2) contains mTOR, rictor, and mLST8, and recent work shows that it regulates the prosurvival kinase Akt/PKB by phosphorylating it on S473 (Hresko and Mueckler, 2005; Sarbassov et al., 2005b).”
SREBP Activity Is Regulated by mTORC1 and Contributes to Akt-Dependent Cell Growth (2008, background): “Role of SREBP in Akt-Dependent Cell Growth silencing results in reduction of Akt phosphorylation on threonine 450 (Figure S8), which has been shown to be a substrate for mTORC2 (Facchinetti et al., 2008; Ikenoue et al., 2008).”
Resistance exercise increases AMPK activity and reduces 4E‐BP1 phosphorylation and protein synthesis in human skeletal muscle (2006, background): “The precise mechanism by which AMPK may be reducing 4E-BP1 Thr36/47 phosphorylation remains to be determined; however, it is well documented that mTOR signalling can be influenced by phosphorylation–dephosphorylation at various sites (Sarbassov et al. 2005).”
Immunoregulatory Functions of mTOR Inhibition (2009, background): “Details of mTORC1 signalling can be found in recent comprehensive review”
Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “However there are p70S6K mutants lacking the carboxyl terminal domain that can be phosphorylated on thr 389 in a rapamycin insensitive manner (5, 211).”
Nutritional Control of Growth and Development in Yeast (2012, background): “…pathways for energy charge and growth factors impinge on TORC1 through the heterodimeric Tsc1/2 tubular sclerosis complex, which stimulates the GTPase activity of the Rheb small G protein, whose binding to TORC1 in its GTP-bound state is necessary for TORC1 kinase activity (Sarbassov et al. 2005).”