Sustained activation of mTORC1 in skeletal muscle inhibits constitutive and starvation-induced autophagy and causes a severe, late-onset myopathy.
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The beneficial role of proteolysis in skeletal muscle growth and stress adaptationSkeletal muscle autophagy: a new metabolic regulatorAutophagy is essential to support skeletal muscle plasticity in response to endurance exerciseA model of muscle atrophy based on live microscopy of muscle remodelling in Drosophila metamorphosis.Transcriptional and epigenetic regulation of autophagy in agingPathophysiological concepts in the congenital myopathies: blurring the boundaries, sharpening the focusmiR-199a impairs autophagy and induces cardiac hypertrophy through mTOR activationRhabdomyolysis-Associated Mutations in Human LPIN1 Lead to Loss of Phosphatidic Acid Phosphohydrolase Activity.Antioxidant supplement inhibits skeletal muscle constitutive autophagy rather than fasting-induced autophagy in mice.Identification and Small Molecule Inhibition of an Activating Transcription Factor 4 (ATF4)-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy.Macronutrient composition of the diet affects the feeding-mediated down regulation of autophagy in muscle of rainbow trout (O. mykiss).External physical and biochemical stimulation to enhance skeletal muscle bioengineeringRegulation of autophagy and the ubiquitin-proteasome system by the FoxO transcriptional network during muscle atrophyMuscle-specific 4E-BP1 signaling activation improves metabolic parameters during aging and obesity.Sustained activation of mTORC1 in macrophages increases AMPKα-dependent autophagy to maintain cellular homeostasisResveratrol induces autophagy by directly inhibiting mTOR through ATP competition.Alterations to mTORC1 signaling in the skeletal muscle differentially affect whole-body metabolismMultiple amino acid sensing inputs to mTORC1.Serine 302 Phosphorylation of Mouse Insulin Receptor Substrate 1 (IRS1) Is Dispensable for Normal Insulin Signaling and Feedback Regulation by Hepatic S6 Kinase.Four-week rapamycin treatment improves muscular dystrophy in a fukutin-deficient mouse model of dystroglycanopathyGlycolytic-to-oxidative fiber-type switch and mTOR signaling activation are early-onset features of SBMA muscle modified by high-fat dietMechanisms of skeletal muscle aging: insights from Drosophila and mammalian modelsTSC but not PTEN loss in starving cones of retinitis pigmentosa mice leads to an autophagy defect and mTORC1 dissociation from the lysosome.Hyperactivation of mammalian target of rapamycin complex 1 (mTORC1) promotes breast cancer progression through enhancing glucose starvation-induced autophagy and Akt signaling.AMPK activation of muscle autophagy prevents fasting-induced hypoglycemia and myopathy during aging"Get the Balance Right": Pathological Significance of Autophagy Perturbation in Neuromuscular DisordersTargeting deregulated AMPK/mTORC1 pathways improves muscle function in myotonic dystrophy type I.Modulation of mTOR signaling as a strategy for the treatment of Pompe disease.Mammalian target of rapamycin signaling in cardiac physiology and disease.Signaling pathways controlling skeletal muscle massDifferential control of muscle mass in type 1 and type 2 diabetes mellitus.Autophagy as a Potential Target for Sarcopenia.mTOR Signaling in Growth, Metabolism, and Disease.Autophagy is required and protects against apoptosis during myoblast differentiation.AKT/PKB Signaling: Navigating the Network.The fine tuning of metabolism, autophagy and differentiation during in vitro myogenesis.Looking at the metabolic consequences of the colchicine-based in vivo autophagic flux assayDual function of the PI3K-Akt-mTORC1 axis in myelination of the peripheral nervous system.Glycine restores the anabolic response to leucine in a mouse model of acute inflammation.Identification of mechanically regulated phosphorylation sites on tuberin (TSC2) that control mechanistic target of rapamycin (mTOR) signaling.
P2860
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P2860
Sustained activation of mTORC1 in skeletal muscle inhibits constitutive and starvation-induced autophagy and causes a severe, late-onset myopathy.
description
2013 nî lūn-bûn
@nan
2013 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
name
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@ast
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@en
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@nl
type
label
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@ast
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@en
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@nl
prefLabel
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@ast
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@en
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@nl
P2093
P1433
P1476
Sustained activation of mTORC1 ...... a severe, late-onset myopathy.
@en
P2093
Klaas Romanino
Lionel A Tintignac
Maitea Guridi
Markus A Rüegg
Michael Sinnreich
Nathalie Rion
Perrine Castets
Sabrina Di Fulvio
Stephan Frank
P304
P356
10.1016/J.CMET.2013.03.015
P577
2013-04-18T00:00:00Z