Abstract
The ability to activate compensatory mechanisms in response to environmental stress is an important factor for survival and maintenance of cellular functions. A system that is often activated both in short and prolonged stress conditions is ubiquitin proteasome system (UPS). UPS is required to clear the cell from dysfunctional and altered proteins and is reported to increase during catabolic conditions. This increase contributes to the loss of contractile proteins and, when is exacerbated, to cachexia. Here I'll present the last data about UPS regulation, the role of UPS in protein turnover in skeletal muscles and the pathogenetic implications of deregulated UPS in muscle disorders.
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