Gong Bing, Leznik Elena
Taub Institute for Research on Alzheimer's disease and the Aging Brain, Department of Pathology, Columbia University, New York, New York, USA.
Drug News Perspect. 2007 Jul-Aug;20(6):365-70. doi: 10.1358/dnp.2007.20.6.1138160.
Impairment of the ubiquitin-proteasome system (UPS) results in the failure to remove and degrade misfolded proteins and consequently causes the accumulation of misfolded proteins in the cell. The aberrant interactions between misfolded proteins and normal intracellular proteins are thought to underlie the pathogenesis in many neurodegenerative diseases. Ubiquitin C-terminal hydrolase L1 (UCH-L1) is an important component of the UPS. Its major function is related to mono-ubiquitin recycling and thereby, sustaining protein degradation. Mutations of the UCH-L1 gene and alterations of its proteins' activity have been found to associate with several neurodegenerative disorders. In this review, we will discuss a link between UCH-L1 and Parkinson's, Huntington's and Alzheimer's diseases. We will also present a potential strategy for the treatment of Alzheimer's disease by boosting endogenous UCH-L1 activity.
泛素-蛋白酶体系统(UPS)功能受损会导致无法清除和降解错误折叠的蛋白质,从而致使错误折叠的蛋白质在细胞内积累。错误折叠的蛋白质与正常细胞内蛋白质之间的异常相互作用被认为是许多神经退行性疾病发病机制的基础。泛素C末端水解酶L1(UCH-L1)是UPS的重要组成部分。其主要功能与单泛素循环有关,从而维持蛋白质降解。已发现UCH-L1基因突变及其蛋白质活性改变与多种神经退行性疾病相关。在本综述中,我们将讨论UCH-L1与帕金森病、亨廷顿舞蹈症和阿尔茨海默病之间的联系。我们还将提出一种通过提高内源性UCH-L1活性来治疗阿尔茨海默病的潜在策略。