The target of rapamycin (TOR) proteins

By B. Raught, A. Gingras, Nahum Sonenberg. Proceedings of the National Academy of Sciences of the United States of America, 2001

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Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake. (2002, background): “Rapamycin treatment in yeast produces a response equivalent to starvation (Schmelzle and Hall, 2000; Raught et al., 2001), and it may be that growth factor withdrawal induces a similar state of pseudostarvation in part by limiting mTOR activity.”
Drosophila's insulin/PI3-kinase pathway coordinates cellular metabolism with nutritional conditions. (2002, background): “…including CNS and imaginal discs also seems plausible, however. protein synthesis, amino acid import, ribosome biogene- Local organ-autonomous dILP signaling might explain sis, and autophagy (Raught et al., 2001; Schmelzle and the relative insensitivity of these tissues to starvation Hall, 2000).”
Cell Wall Integrity Signaling in Saccharomyces cerevisiae (2005, background): “Despite their sequence similarity to lipid kinases (168), they have been shown to possess Ser/Thrspecific protein kinase activity (2, 290).”
The molecular machinery of autophagy: unanswered questions (2005, background): “Inhibition of Tor through starvation or treatment with rapamycin results in partial dephosphorylation of Atg13 and allows autophagic induction (Abeliovich, 2004; Noda and Ohsumi, 1998).”