Biochemistry Department, Delta University for Science and Technology, Gamasaa, Egypt.
Adv Exp Med Biol. 2018;1088:235-248. doi: 10.1007/978-981-13-1435-3_10.
Many systemic diseases are featured by muscle atrophy. Cellular proteins are modified by covalent attachment to a small protein known as ubiquitin (Ub) through ubiquitination. This ubiquitination process serves as signal for protein turnover that leads to rapid muscle mass lack. This process is carried out through an enzymatic cascade, which includes three groups of enzymes termed ubiquitin E1 (activating enzyme), ubiquitin E2 (conjugating enzyme), and ubiquitin E3 (ligase). There are several ways of ubiquitin conjugation driving to ubiquitination of specific proteins through ubiquitin-proteasome system (UPS). A lot of UPS genes stated to be included in skeletal muscle atrophy. These genes do their effects by modifying different processes which affect muscle mass including myofibrillar protein degradation, myogenesis inhibition, and even modulation of autophagy as well as upstream regulatory pathways.
许多系统性疾病的特征是肌肉萎缩。细胞蛋白通过与一种称为泛素（Ub）的小蛋白的共价连接进行修饰。这种泛素化过程作为导致肌肉质量迅速丧失的蛋白质周转的信号。该过程通过酶级联反应进行，该反应包括三个酶组，称为泛素 E1（激活酶）、泛素 E2（连接酶）和泛素 E3（连接酶）。有几种泛素连接的方式通过泛素-蛋白酶体系统（UPS）导致特定蛋白质的泛素化。许多 UPS 基因被认为包含在骨骼肌萎缩中。这些基因通过修饰影响肌肉质量的不同过程发挥作用，包括肌原纤维蛋白降解、成肌抑制，甚至自噬的调节以及上游调节途径。
