Skeletal muscle-specific ablation of raptor, but not of rictor, causes metabolic changes and results in muscle dystrophy

Mammalian target of rapamycin (mTOR) is a central controller of cell growth. mTOR assembles into two distinct multiprotein complexes called mTOR complex 1 (mTORC1) and mTORC2. Here we show that the mTORC1 component raptor is critical for muscle function and prolonged survival. In contrast, muscles lacking the mTORC2 component rictor are indistinguishable from wild-type controls. Raptor-deficient muscles become progressively dystrophic, are impaired in their oxidative capacity, and contain increased glycogen stores, but they express structural components indicative of oxidative muscle fibers.

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Bentzinger, C. F., et al. (2008). Skeletal muscle-specific ablation of raptor, but not of rictor, causes metabolic changes and results in muscle dystrophy. Cell metabolism. https://doi.org/10.1016/j.cmet.2008.10.002

@article{BEN2008,
  author       = {Bentzinger, C. F. and Rueegg, M. A. and others},
  title        = {{Skeletal muscle-specific ablation of raptor, but not of rictor, causes metabolic changes and results in muscle dystrophy}},
  journal      = {Cell metabolism},
  year         = {2008},
  doi          = {10.1016/j.cmet.2008.10.002},
  note         = {PMID: 19046572},
}

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Barton, O. (2026). Oliver's mTOR Atlas (record BEN2008) [Data set]. https://mtor-atlas.org/study/BEN2008/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_BEN2008,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record BEN2008},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/BEN2008/},
  doi          = {10.5281/zenodo.22059963}
}