TOR signaling in growth and metabolism.

By S. Wullschleger, R. Loewith, Michael N. Hall. Cell, 2006

6,014 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/4da2f2f01afe662323534fe803371fa3e3e19c43

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Citations in the corpus

GSK3 signaling in neural development (2010, background): “TSC1 and TSC2 form a heterodimer that negatively regulates mammalian target of rapamycin (mTOR) signallin”
AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1 (2011, neutral): “mTORC1 activity reflects cellular nutritional statu”
Translational regulation of gene expression during conditions of cell stress. (2010, background): “The TOR pathway is the major nutrient-sensing pathway in mammalian cells, the central component of which is the TOR kinase (Wullschleger et al., 2006) that is found in two different multiprotein complexes, termed TORC1 and TORC2 (Wullschleger et al., 2006).”
Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, positive): “The mammalian target of rapomycin (mTOR) is a serine/threonine kinase that controls anabolic cellular processes in response to a variety of environmental stimuli including amino acids, glucose and oxidative stress [445, 446].”
Kisspeptins and reproduction: physiological roles and regulatory mechanisms. (2012, background): “Several systems have been identified during the last years as key elements for sensing the cellular energy status, thus allowing the coupling of energy availability of any cell and its functional activity (45, 84, 263, 295, 394, 478, 502).”
Exploring autophagy with Gene Ontology (2016, background): “Starvation, and particularly nitrogen starvation, induces autophagy, via the TOR signaling pathway [35], and GO terms describing the cellular response to nitrogen starvation, ‘cellular response to nitrogen compound’ and ‘cellular response to nitrogen levels’, are present among the top significant ge”
Dynamics and diversity in autophagy mechanisms: lessons from yeast (2009, background): “Although the Tor protein forms two distinct complexes, Tor complex 1 (TORC1) and TORC2 (Ref”
ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS (2010, background): “TSC2, an important repressor of mTORC1 activity (7), also participated in regulation of mTORC1 signaling by ROS, as repression ofmTORC1occurred inTsc2but notTsc2MEFs in response to H2O2, (Fig.”
SREBP Activity Is Regulated by mTORC1 and Contributes to Akt-Dependent Cell Growth (2008, background): “mTORC1 is regulated by both nutrients and growth factors and plays a conserved role in cell growth control (Wullschleger et al., 2006).”
Role of AMPK-mTOR-Ulk1/2 in the Regulation of Autophagy: Cross Talk, Shortcuts, and Feedbacks (2011, background): “, by phosphorylation of S6K1 and 4E-BP, while simultaneously inhibiting self-consuming processes such as autophagy (94, 110).”
Glutaminolysis activates Rag-mTORC1 signaling. (2012, background): “In mammalian cells, mTOR integrates several stimuli to regulate cell growth, metabolism, and aging (Wullschleger et al., 2006; Zoncu et al., 2011b).”
A Role for Autophagy in the Extension of Lifespan by Dietary Restriction in C. elegans (2008, background): “How might dietary restriction induce autophagy? As described above, dietary restriction appears to extend lifespan, at least in part, by down-regulating the TOR pathway, and inhibition of TOR is known to trigger autophagy in yeast and mammals [12].”
Essential function of TORC2 in PKC and Akt turn motif phosphorylation, maturation and signalling (2008, background): “Mammalian target of rapamycin (mTOR) is a central cell growth controller (Hay and Sonenberg, 2004; Wullschleger et al, 2006). mTOR exists in two different complexes, mTORC1 and mTORC2 (Loewith et al, 2002; Sabatini, 2006).”
Metformin, Independent of AMPK, Inhibits mTORC1 In a Rag GTPase-Dependent Manner (2010, background): “Increased mammalian target of rapamycin (mTOR) signaling has been implicated in a number of specific human pathologies, including obesity, type 2 diabetes, and cancer (Dann et al., 2007; Marshall, 2006; Um et al., 2006; Wullschleger et al., 2006).”
Targeting metabolic transformation for cancer therapy (2010, background): “Akt also activates mTOR, another master regulator of metabolism, which itself contributes to the anabolic growth of cancer cell”