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Direct control of mitochondrial function by mTOR
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Journal Article
Direct control of mitochondrial function by mTOR
2009
Overview
mTOR is a central regulator of cellular growth and metabolism. Using metabolic profiling and numerous small-molecule probes, we investigated whether mTOR affects immediate control over cellular metabolism by posttranslational mechanisms. Inhibiting the FKBP12/rapamycin-sensitive subset of mTOR functions in leukemic cells enhanced aerobic glycolysis and decreased uncoupled mitochondrial respiration within 25 min. mTOR is in a complex with the mitochondrial outer-membrane protein Bcl-xl and VDAC1. Bcl-xl, but not VDAC1, is a kinase substrate for mTOR in vitro, and mTOR regulates the association of Bcl-xl with mTOR. Inhibition of mTOR not only enhances aerobic glycolysis, but also induces a state of increased dependence on aerobic glycolysis in leukemic cells, as shown by the synergy between the glycolytic inhibitor 2-deoxyglucose and rapamycin in decreasing cell viability.
Publisher
National Academy of Sciences,National Acad Sciences
Subject
/ Aniline Compounds - pharmacology
/ Glucose
/ Humans
/ Intracellular Signaling Peptides and Proteins - antagonists & inhibitors
/ Intracellular Signaling Peptides and Proteins - metabolism
/ Oxygen Consumption - drug effects
/ Protein-Serine-Threonine Kinases - antagonists & inhibitors
/ Protein-Serine-Threonine Kinases - metabolism
/ Proteins
