Article
Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy.
The Journal of cell biology - 14 Dec 2009
Risson Valérie, Mazelin Laetitia, Roceri Mila, Sanchez Hervé, Moncollin Vincent, Corneloup Claudine, Richard-Bulteau Hélène, Vignaud Alban, Baas Dominique, Defour Aurélia, Freyssenet Damien, Tanti Jean-François, Le-Marchand-Brustel Yannick, Ferrier Bernard, Conjard-Duplany Agnès, Romanino Klaas, Bauché Stéphanie, Hantaï Daniel, Mueller Matthias, Kozma Sara C, Thomas George, Rüegg Markus A, Ferry Arnaud, Pende Mario, Bigard Xavier, Koulmann Nathalie, Schaeffer Laurent, Gangloff Yann-Gaël
Abstract excerpt
Mammalian target of rapamycin (mTOR) is a key regulator of cell growth that associates with raptor and rictor to form the mTOR complex 1 (mTORC1) and mTORC2, respectively. Raptor is required for oxidative muscle integrity, whereas rictor is dispensable. In this study, we show that muscle-specific inactivation of mTOR leads to severe myopathy, resulting in premature death. mTOR-deficient muscles display metabolic...
Topics
- Adaptor Proteins, Signal Transducing
- Age Factors
- Animals
- Carrier Proteins
- Cells, Cultured
- Dystrophin
- Electroporation
- Energy Metabolism