Pathogens can tamper with the ubiquitin-proteasome system to cripple the cell’s defenses. For instance, ubiquitination and proteasomal degradation of p53, initiated by a Human Papillomavirus protein , or stabilization of Ikb-a by Yersinia deubiquitinases have been described. The continuing discovery of new deubiquitinating proteases in viruses broadly hints at how important it is for these pathogens to seize control of posttranslational modifications in host cells. Here, we focus on cysteine proteases of the CE clan , as defined by the MEROPS database. The MPred group had lower body mass and muscle mass than the FR group, demonstrating a greater catabolic effect of glucocorticoids compared to food CHIR-99021 restriction alone. The difference in muscle mass cannot be explained either by protein synthesis or by muscle hydration, which did not differ among groups, Nor can the differences in muscle loss be attributed to activity of the branched-chain amino acid transamination and oxidation enzymes, which were similarly increased in both FR and MPred muscles. Another potential reason for the greater catabolic effect in Mpred group is greater muscle protein catabolism in MPred than FR. This is supported by earlier studies showing that during fasting or energy restriction muscle protein synthesis and breakdown decrease , whereas in response to glucocorticoids markers of protein breakdown and proteolytic pathways are elevated. It has been repeatedly shown that glucocorticoid-stimulated muscle protein breakdown is mediated primarily through ubiquitin-proteasome-dependent proteolysis and other calcium-dependent protein degradation pathways.Correspondingly, the activity of DCN neurons in adult rodents consists of pauses, most likely caused by PC inhibition, mixed with transient periods of fast bursting. The effectiveness of disinhibition to create a rebound spike depends on the synchronicity of the disinhibition, which we recently demonstrated to be significant among nearby PCs , and on the level of preceding inhibition. Because the inactivation of calcium channels expressed in the DCN neurons is strongly voltage dependent in the relevant potential range , these channels are very sensitive to even small changes in inhibitory input. Consequently, the level of inhibition preceding the rebound spike exerts a very strong effect on the amplitude of the rebound spike. We hypothesize that regular patterns encode a specific level of inhibition in their firing rate and, as such, approximate a perfect firing rate code , which should be completely regular. When regular patterns from convergent PCs coincide, the summed inhibition will be relatively constant over the duration of the patterns and, consequently, keep the level of inactivation of calcium channels steady. Thereby, the firing rates of regular spike patterns in afferent PCs will control the amplitude of any rebound spike that follows in the next second.