Signal-transduction networks and the regulation of muscle protein degradation.
Protein degradation in muscle functions in maintaining normal physiological homeostasis and adapting to new homeostatic states, and is required for muscle wasting or atrophy in various pathological states. The interplay between protein synthesis and degradation to maintain homeostasis is complex and responds to a variety of autocrine and intercellular signals from neuronal inputs, hormones, cytokines, growth factors and other regulatory molecules. The intracellular events that connect extracellular signals to the molecular control of protein degradation are incompletely understood, but likely involve interacting signal-transduction networks rather than isolated pathways. We review some examples of signal-transduction systems that regulate protein degradation, including effectors of proteolysis inducing factor (PIF), insulin and insulin-like growth factor (IGF) and their receptors, and fibroblast growth factor (FGF) and its receptors.
Szewczyk
Nathaniel J
NJ
Department of Biological Sciences, University of Pittsburgh, 304 Langley Hall, Pittsburgh, PA 15260, USA.
Jacobson
Lewis A
LA
D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D017173:Caenorhabditis elegans; D005346:Fibroblast Growth Factors / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008954:Models, Biological; D009124:Muscle Proteins / Q000378:metabolism* / Q000502:physiology; D009133:Muscular Atrophy / Q000378:metabolism; D011509:Proteoglycans; D015398:Signal Transduction / Q000502:physiology*
D001798:Blood Proteins; D007328:Insulin; D009124:Muscle Proteins; D011509:Proteoglycans; C042057:proteolysis-inducing peptide; D005346:Fibroblast Growth Factors; D007334:Insulin-Like Growth Factor I