期刊
AUTOPHAGY
卷 5, 期 5, 页码 747-+出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.5.5.8704
关键词
polyglutamine; Huntington disease; huntingtin; proteasome; autophagy; rho-associated kinase; ROCK
类别
Enhancing the degradation of mutant protein is one of the most investigated approaches in experimental therapy of the polyglutamine-related disorders such as Huntington disease (HD). Inhibition of rho-associated kinases (ROCKs) reduced the aggregation and levels of mutant huntingtin in cellular models of HD via activation of the ubiquitin proteasome system (UPS) and macroautophagy. This unique effect makes the Rho/ROCK pathway and its downstream effectors attractive therapeutic targets for polyglutamine-related diseases.
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