ArticleMolecular and cellular biology2009
The mTORC2 complex regulates terminal differentiation of C2C12 myoblasts.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
- Mitochondrial Oxidative Stress and Mitophagy Activation Contribute to TNF-Dependent Impairment of Myogenesis.Antioxidants (Basel, Switzerland) · 2023Article
- Understanding the interplay of membrane trafficking, cell surface mechanics, and stem cell differentiation.Seminars in cell & developmental biology · 2023Review
- Mammalian Target of Rapamycin (mTOR) Signaling at the Crossroad of Muscle Fiber Fate in Sarcopenia.International journal of molecular sciences · 2022Review
- Time-resolved phosphoproteome and proteome analysis reveals kinase signaling on master transcription factors during myogenesis.iScience · 2022Article
- Perturbation of PI3K/Akt signaling affected autophagy modulation in dystrophin-deficient myoblasts.Cell communication and signaling : CCS · 2021Article
- Key Genes Regulating Skeletal Muscle Development and Growth in Farm Animals.Animals : an open access journal from MDPI · 2021Review
- Genetic interaction mapping and exon-resolution functional genomics with a hybrid Cas9-Cas12a platform.Nature biotechnology · 2020Article
- Effects of conditioned media from murine lung cancer cells and human tumor cells on cultured myotubes.American journal of physiology. Endocrinology and metabolism · 2020Article
- 6-Bromoindirubin-3'-oxime intercepts GSK3 signaling to promote and enhance skeletal muscle differentiation affecting miR-206 expression in mice.Scientific reports · 2019Article
- mTORC2 affects the maintenance of the muscle stem cell pool.Skeletal muscle · 2019Article
- [Rictor regulates mitochondrial calcium signaling in mouse embryo stem cell-derived cardiomyocytes].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Article
- Mitochondrial ROS-derived PTEN oxidation activates PI3K pathway for mTOR-induced myogenic autophagy.Cell death and differentiation · 2018Article
- Effect of 8-week leucine supplementation and resistance exercise training on muscle hypertrophy and satellite cell activation in rats.Physiological reports · 2018Article
- MYCN drives glutaminolysis in neuroblastoma and confers sensitivity to an ROS augmenting agent.Cell death & disease · 2018Article
- Reprogramming induced by isoliquiritigenin diminishes melanoma cachexia through mTORC2-AKT-GSK3β signaling.Oncotarget · 2017Article
- Heterogeneous nuclear ribonucleoprotein M associates with mTORC2 and regulates muscle differentiation.Scientific reports · 2017Article
- Involvement of Rictor/mTORC2 in cardiomyocyte differentiation of mouse embryonic stem cellsInternational journal of biological sciences · 2017Article
- Negative regulation of initial steps in skeletal myogenesis by mTOR and other kinases.Scientific reports · 2016Article
- From Nutrient to MicroRNA: a Novel Insight into Cell Signaling Involved in Skeletal Muscle Development and Disease.International journal of biological sciences · 2016Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Rapamycin, a selective inhibitor of mTORC1 signaling, blocks terminal myoblast differentiation. We found that downregulation of rictor, a component of the mTORC2 complex, but not downregulation of raptor, a component of the mTORC1 complex, prevented terminal differentiation (fusion) of C2C12 myoblasts. Both rapamycin and rictor downregulation suppressed the phosphorylation of AKT(S(473)), and rapamycin treatment of C2C12 myoblasts disrupted the mTORC2 complex. Importantly, downregulation of rictor inhibited TORC2 signaling without inhibiting mTORC1 signaling, suggesting that inhibition of mTORC1 by rapamycin may not be the cause of arrested differentiation. In support of this, expression of a phosphomimetic mutant AKT(S473D) in rictor-deficient cells rescued myoblast fusion even in the presence of rapamycin. mTORC2 signaling to AKT appears necessary for downregulation of the Rho-associated kinase (ROCK1) that occurs during myogenic differentiation. Rapamycin treatment prevented ROCK1 inactivation during differentiation, while suppression of ROCK1 activity during differentiation and myoblast fusion was restored through expression of AKT(S473D), even in the presence of rapamycin. Further, the ROCK inhibitor Y-27632 restored terminal differentiation in rapamycin-treated myoblasts. These results provide the first evidence of a specific role for mTORC2 signaling in terminal myogenic differentiation.
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