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

By C. F. Bentzinger, Klaas Romanino, Dimitri Cloëtta, Shuo Lin, J. Mascarenhas, Filippo Oliveri, Jinyu Xia, E. Casanova, C. F. Costa, M. Brink and 3 more. Cell Metabolism, 2008

659 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/38a7e4b13a8f601151444f9273ce7b68bf459bf9

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In Cellular and Molecular Neuroscience

1. David M. Sabatini
2. Nahum Sonenberg
3. S. Schiaffino
4. C. Mammucari
5. M. Sandri

In Molecular Biology

1. David M. Sabatini
2. M. Laplante
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4. R. A. Saxton
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6. Craig B. Thompson
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8. M. Sandri

Citations in the corpus

• Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate (2012, background): “…1970; Tallal et al., 1970). mTORC1 has also been shown to have direct effects on promoting mitochondrial biogenesis, in part via a transcriptional complex that promotes the function of PGC-1a (Bentzinger et al., 2008; Cunningham et al., 2007; Ramanathan and Schreiber, 2009; Schieke et al., 2006).”
• mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “In agreement with this, deletion of RAPTOR in skeletal muscle leads to a defect in mitochondrial biogenesis and decreased oxidative capacit”
• Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, methodology): “Rictor null in muscle (HSA-Cre) Viable Reduced postnatal growth with severe myopathy and premature death [ 87 ]”
• Activation of a metabolic gene regulatory network downstream of mTOR complex 1. (2010, background): “Together with recent genetic approaches to understand the role of mTORC1 in integrated physiology (Bentzinger et al., 2008; Polak et al., 2008), we are gaining important insights into the contributions of mTORC1 to the metabolic reprogramming of cells in response to the physiological or pathological”
• Cellular and molecular mechanisms of muscle atrophy (2013, background): “…neonatal lethality Peng et al., 2003 mTOR Muscle-specific KO Dystrophic phenotype Risson et al., 2009 Raptor Muscle-specific KO Dystrophic phenotype Bentzinger et al., 2008 Rictor Muscle-specific KO No phenotype Bentzinger et al., 2008 Raptor + Rictor Muscle-specific double KO Dystrophic phenotype…”
• Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012, background): “Deletion of Rictor in muscle impairs phosphorylation of Akt S473, although the effect on glucose homeostasis has not been described (27).”
• mTOR signaling at a glance (2009, background): “Additionally, conditional deletion of Raptor in mouse skeletal muscle reduces the expression of genes involved in mitochondrial biogenesis (Bentzinger et al., 2008).”
• mTOR Signaling in Growth, Metabolism, and Disease. (2017, background): “This dramatic phenotype is also observed in muscle specific mTOR knockout mice, but not Rictor deficient mice, suggesting that the critical functions of mTOR in skeletal muscle are through mTORC1 (Bentzinger et al., 2008; Risson et al., 2009).”
• mTOR signaling in growth control and disease (2012, background): “In mice, muscle-specific loss of mTORC1 reduces muscle mass and oxidative function and leads to early death (Bentzinger et al., 2008).”
• mTOR Signaling in Growth, Metabolism, and Disease (2017, background): “This dramatic phenotype is also observed in muscle-specific mTOR knockout mice, but not Rictor-deficient mice, suggesting that the critical functions of mTOR in skeletal muscle are through mTORC1 (Bentzinger et al., 2008; Risson et al., 2009).”
• Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress (2010, background): “In murine skeletal muscle, the lack of raptor reduces the expression of genes involved inmitochondrial biogenesis and leads to a concomitant loss of oxidative capacity (Bentzinger et al., 2008).”
• mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation. (2013, background): “Consistent with a recent finding that a tissuespecific raptor knockout mouse exhibits decreased locomotor activity (Bentzinger et al., 2008; Polak et al., 2008), Ink1341 suppressed locomotor activity in WT mice, whereas this (D) Total mitochondrial respiration, ATP turnover, proton leak, and…”