细胞生物学
自噬
蛋白质稳态
α-突触核蛋白
泛素连接酶
帕金
粒体自噬
路易体
癌症研究
蛋白质降解
品脱1
黑质
突触核蛋白
程序性细胞死亡
作者
Christopher A. Ross,Cecile M. Pickart
标识
DOI:10.1016/j.tcb.2004.10.006
摘要
During the past decade, it has become apparent that a set of ostensibly unrelated neurodegenerative diseases, including Parkinson's disease and Huntington's disease, shares striking molecular and cell biology commonalities. Each of the diseases involves protein misfolding and aggregation, resulting in inclusion bodies and other aggregates within cells. These aggregates often contain ubiquitin, which is the signal for proteolysis by the 26S proteasome, and chaperone proteins that are involved in the refolding of misfolded proteins. The link between the ubiquitin–proteasome system and neurodegeneration has been strengthened by the identification of disease-causing mutations in genes coding for several ubiquitin–proteasome pathway proteins in Parkinson's disease. However, the exact molecular connections between these systems and pathogenesis remain uncertain and controversial. In this article, we summarize the state of current knowledge, focusing on important unresolved questions.
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