Review: The ubiquitin-proteasome system: contributions to cell death or survival in neurodegeneration

被引：0

作者：

Rogers, N. ^{[1
]}

Paine, S. ^{[1
]}

Bedford, L. ^{[1
]}

Layfield, R. ^{[1
]}

机构：

[1] Univ Nottingham, Sch Med, Queens Med Ctr, Sch Biomed Sci, Nottingham NG7 2UH, England

来源：

NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY | 2010年 / 36卷 / 02期

关键词：

neurodegeneration; Parkinson's disease; proteasome; ubiquitin; FAMILIAL PARKINSONS-DISEASE; ALPHA-SYNUCLEIN PHOSPHORYLATION; CHAPERONE-MEDIATED AUTOPHAGY; TERMINAL HYDROLASE L1; LEWY BODIES; ALZHEIMERS-DISEASE; TYROSINE-HYDROXYLASE; AGGRESOME FORMATION; PROTEOLYTIC STRESS; DROSOPHILA MODEL;

D O I：

10.1111/j.1365-2990.2009.01063.x

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

The significance of the accumulation of ubiquitin-positive intraneuronal inclusions in the brains of those affected with different neurodegenerative diseases is currently unclear. While one interpretation is that the disease mechanism(s) involves dysfunction of an ubiquitin-mediated process, such as the ubiquitin-proteasome system, the inclusions are also found in surviving neurones, suggesting a possible neuroprotective role. Here we review recent evidence in support of these seemingly opposing notions gleaned from cell and animal models as well as investigations of patient samples, with particular emphasis on studies relevant to Parkinson's disease.

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页码：113 / 124

页数：12

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