The role of E3 ubiquitin ligases in synapse function in the healthy and diseased brain
The role of E3 ubiquitin ligases in synapse function in the healthy and diseased brain
复制标题
E3泛素连接酶在健康和患病脑突触功能中的作用
DOI：
10.1016/j.mcn.2021.103602
复制
发表时间：
2021-02-17
影响因子：
3.5
通讯作者：
Stegmueller, Judith
中科院分区：
文献类型：
--
作者：
Kawabe, Hiroshi;Stegmueller, Judith
泛素化是控制蛋白质降解和蛋白质静止的关键翻译后修饰。底物特异性是由E3泛素连接酶家族决定的，该家族由哺乳动物基因组中的600多个基因编码。一些E3基因的功能获得或丧失导致神经变性或神经发育障碍，影响突触功能。这意味着突触底物的特异性泛素化对正常神经元网络至关重要。本文将对泛素化调控突触发生和突触传递的研究历史、现状和面临的挑战进行综述。
Ubiquitination is a key posttranslational modification for the controlled protein degradation and proteostasis. The substrate specificity is determined by a family of E3 ubiquitin ligases, which are encoded by more than 600 genes in the mammalian genome. Gain- or loss-of-function of a number of E3 genes results in neurodegeneration or neurodevelopmental disorders, affecting synapse function. This implies that the specific ubiquitination of synaptic substrates are of crucial importance for the normal neuronal network. In this review, we will summarize the history, current topics, and challenges in the field of ubiquitination-dependent regulations of synaptogenesis and synaptic transmission.