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Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy
TLDR
Two genes encode ubiquitin ligases that are potential drug targets for the treatment of muscle atrophy, and mice deficient in either MAFbx orMuRF1 were found to be resistant to atrophy.
Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo
TLDR
It is concluded that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of this pathway can oppose muscle atrophy induced by disuse.
The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors.
TLDR
Akt is not only capable of activating prosynthetic pathways, as previously demonstrated, but is simultaneously and dominantly able to suppress catabolic pathways, allowing it to prevent glucocorticoid and denervation-induced muscle atrophy.
Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways
TLDR
It is shown that Akt promotes hypertrophy by activating downstream signalling pathways previously implicated in activating protein synthesis: the pathways downstream of mammalian target of rapamycin (mTOR) and the pathway activated by phosphorylating and thereby inhibiting glycogen synthase kinase 3 (GSK3).
Skeletal muscle hypertrophy and atrophy signaling pathways.
  • D. Glass
  • Biology, Medicine
    The international journal of biochemistry & cell…
  • 1 October 2005
TLDR
Recent progress in the understanding of molecular signalling, which governs skeletal muscle atrophy and hypertrophy, and the known instances of cross-regulation between the two systems are focused on.
IKKbeta/NF-kappaB activation causes severe muscle wasting in mice.
TLDR
Denervation- and tumor-induced muscle loss were substantially reduced and survival rates improved by NF-kappaB inhibition in MISR mice, consistent with a critical role for NF- kappaB in the pathology of muscle wasting and establishing it as an important clinical target for the treatment of muscle atrophy.
The Receptor Tyrosine Kinase MuSK Is Required for Neuromuscular Junction Formation In Vivo
TLDR
It is indicated that MuSK responds to a critical nerve-derived signal (agrin), and in turn activates signaling cascades responsible for all aspects of synapse formation, including organization of the postsynaptic membrane, synapse-specific transcription, and presynaptic differentiation.
IKKβ/NF-κB Activation Causes Severe Muscle Wasting in Mice
TLDR
Denervation- and tumor-induced muscle loss were substantially reduced and survival rates improved by NF-kappaB inhibition in MISR mice, consistent with a critical role for NF- kappaB in the pathology of muscle wasting and establishing it as an important clinical target for the treatment of muscle atrophy.
Agrin Acts via a MuSK Receptor Complex
TLDR
It is demonstrated that agrin acts via a receptor complex that includes MuSK as well as a myotube-specific accessory component, which is a receptor tyrosine kinase localized to the motor endplate.
Differentiation stage-specific inhibition of the Raf-MEK-ERK pathway by Akt.
TLDR
The stage-specific inhibitory action of Akt correlated with its stage- specific ability to form a complex with Raf, suggesting the existence of differentially expressed mediators of an inhibitory Akt-Raf complex.
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