14-3-3 proteins in neurodegeneration

被引：87
作者：
Steinacker, Petra [1 ]
Aitken, Alastair [2 ]
Otto, Markus [1 ]
机构：
[1] Univ Ulm, Dept Neurol, D-89081 Ulm, Germany
[2] Univ Edinburgh, ISB, Sch Biol Sci, Edinburgh EH9 3JR, Midlothian, Scotland
来源：
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY | 2011年 / 22卷 / 07期
关键词：
14-3-3; proteins; Neurodegeneration; Neurodegenerative diseases; GLIAL CYTOPLASMIC INCLUSIONS; NEUROFILAMENT MESSENGER-RNA; CEREBROSPINAL-FLUID; ALPHA-SYNUCLEIN; ALZHEIMERS-DISEASE; HUNTINGTONS-DISEASE; OXIDATIVE-STRESS; TAU-PROTEIN; MEDIATED NEURODEGENERATION; DIFFERENTIAL-DIAGNOSIS;
D O I：
10.1016/j.semcdb.2011.08.005
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Among the first reported functions of 14-3-3 proteins was the regulation of tyrosine hydroxylase (TH) activity suggesting a possible involvement of 14-3-3 proteins in Parkinson's disease. Since then the relevance of 14-3-3 proteins in the pathogenesis of chronic as well as acute neurodegenerative diseases, including Alzheimer's disease, polyglutamine diseases, amyotrophic lateral sclerosis and stroke has been recognized. The reported function of 14-3-3 proteins in this context are as diverse as the mechanism involved in neurodegeneration, reaching from basal cellular processes like apoptosis, over involvement in features common to many neurodegenerative diseases, like protein stabilization and aggregation, to very specific processes responsible for the selective vulnerability of cellular populations in single neurodegenerative diseases. Here, we review what is currently known of the function of 14-3-3 proteins in nervous tissue focussing on the properties of 14-3-3 proteins important in neurodegenerative disease pathogenesis. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码：696 / 704
页数：9
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