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Current Drug Targets

Editor-in-Chief

ISSN (Print): 1389-4501
ISSN (Online): 1873-5592

Protein Degradation Pathways after Brain Ischemia

Author(s): Pengfei Ge, Fan Zhang, Jingwei Zhao, Chunli Liu, Liankun Sun and Bingren Hu

Volume 13 , Issue 2 , 2012

Page: [159 - 165] Pages: 7

DOI: 10.2174/138945012799201694

Price: $65

Abstract

There are two major routes for clearance of aberrant cellular components: (i) the ubiquitin-proteasomal system (UPS); and (ii) the autophagy pathway. The UPS degrades individual abnormal proteins, whereas the autophagy pathway is the chief route for bulk degradation of large abnormal protein aggregates and aberrant organelles. Impairments of the protein degradation pathways are closely tied with many human diseases. Brain ischemia leads to protein misfolding and aggregation, resulting in overproduction of protein aggregate-associated organelles. Brain ischemia also damages protein degradation pathways. This chapter will discuss molecular mechanisms underlying the impairments of the UPS and autophagy pathways and how such impairments lead to multiple organelle failure and delayed neuronal death after brain ischemia.

Keywords: ubiquitin, microtubule-associated protein 1 light chain 3 (LC3), delayed neuronal death, autophagy, autophagosome, lysosome, protein aggregation, protein folding, organelle damage, global ischemia, focal ischemia


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