| Literature DB >> 27702698 |
Abstract
The ubiquitin proteasome pathway (UPP) is essential for removing abnormal proteins and preventing accumulation of potentially toxic proteins within the neuron. UPP dysfunction occurs with normal aging and is associated with abnormal accumulation of protein aggregates within neurons in neurodegenerative diseases. Ischemia disrupts UPP function and thus may contribute to UPP dysfunction seen in the aging brain and in neurodegenerative diseases. Ubiquitin carboxy-terminal hydrolase L1 (UCHL1), an important component of the UPP in the neuron, is covalently modified and its activity inhibited by reactive lipids produced after ischemia. As a result, degradation of toxic proteins is impaired which may exacerbate neuronal function and cell death in stroke and neurodegenerative diseases. Preserving or restoring UCHL1 activity may be an effective therapeutic strategy in stroke and neurodegenerative diseases. Published by Elsevier B.V.Entities:
Keywords: Aging; Cerebral ischemia; Neurodegenerative disease; Ubiquitin; Ubiquitin carboxy-terminal hydrolase L1(UCHL1); Ubiquitin proteasome pathway (UPP)
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Year: 2016 PMID： 27702698 PMCID： PMC5250550 DOI： 10.1016/j.arr.2016.09.011
Source DB: PubMed Journal: Ageing Res Rev ISSN： 1568-1637 Impact factor: 10.895