Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy
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
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.
Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways
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
- BiologyInternational Journal of Biochemistry and Cell…
- 1 October 2005
IKKbeta/NF-kappaB activation causes severe muscle wasting in mice.
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
Agrin Acts via a MuSK Receptor Complex
IKKβ/NF-κB Activation Causes Severe Muscle Wasting in Mice