Decreased mTORC1 activation and subsequent decreases in muscle protein synthesis, coupled with increased FOXO nuclear localization, increased transcription of atrophy - related genes, with up - regulated caspase 3 activation and muscle
protein ubiquitylation provide a possible mechanism contributing to skeletal muscle loss in response to periods of negative energy balance.
Not exact matches
A
protein that is inactive in the absence of additional modification (s), such as phosphorylation or
ubiquitylation.
Enhanced
ubiquitylation and accelerated degradation of the dopamine transporter mediated by
protein kinase C. Journal of Biological Chemistry, 280 (42), 35617 — 35624.
As such, it appears that the insulin / IGF - PI 3K pathway not only regulates myofibrillar cleavage through caspase 3, but also the
ubiquitylation of the resulting
protein fragments via modification of ubiquitin - ligase expression.