期刊
TRENDS IN NEUROSCIENCES
卷 38, 期 1, 页码 26-35出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2014.09.003
关键词
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资金
- Canadian Institutes of Health Research (CIHR)
- Michael Smith Foundation for Health Research Postdoctoral Fellowship
- Bluma Tischler Postdoctoral Fellowship from the University of British Columbia
- CIHR Doctoral Award
- CIHR [MOP-84438, GPG-102165]
Autophagy is an important biological process that is essential for the removal of damaged organelles and toxic or aggregated proteins by delivering them to the lysosome for degradation. Consequently, autophagy has become a primary target for the treatment of neurodegenerative diseases that involve aggregating proteins. In Huntington disease (HD), an expansion of the polyglutamine (polyQ) tract in the N-terminus of the huntingtin (HTT) protein leads to protein aggregation. However, HD is unique among the neurodegenerative proteinopathies in that autophagy is not only dysfunctional but wild type (wt) HTT also appears to play several roles in regulating the dynamics of autophagy. Herein, we attempt to integrate the recently, described novel roles of wtHTT and altered autophagy in HD.
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