Disruption of striatal-enriched protein tyrosine phosphatase (STEP) function in neuropsychiatric disorders

被引:26
|
作者
Karasawa, Takatoshi [1 ]
Lombroso, Paul J. [2 ,3 ,4 ]
机构
[1] Aichi Human Serv Ctr, Inst Dev Res, Dept Mol Neurobiol, Kasugai, Aichi 4800392, Japan
[2] Yale Univ, Dept Neurobiol, Sch Med, New Haven, CT 06520 USA
[3] Yale Univ, Dept Psychiat, Sch Med, New Haven, CT 06520 USA
[4] Yale Univ, Ctr Child Study, Sch Med, New Haven, CT 06520 USA
关键词
Alzheimer's disease; Fragile X syndrome; Huntington's disease; Schizophrenia; STEP; Stroke; LONG-TERM POTENTIATION; IONOTROPIC GLUTAMATE RECEPTORS; ALZHEIMERS-DISEASE; SYNAPTIC PATHOLOGY; MOLECULAR CHARACTERIZATION; COGNITIVE IMPAIRMENTS; HUNTINGTONS-DISEASE; FOCAL ISCHEMIA; MESSENGER-RNAS; AMYLOID-BETA;
D O I
10.1016/j.neures.2014.08.018
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific tyrosine phosphatase that plays a major role in the development of synaptic plasticity. Recent findings have implicated STEP in several psychiatric and neurological disorders, including Alzheimer's disease, schizophrenia, fragile X syndrome, Huntington's disease, stroke/ischemia, and stress-related psychiatric disorders. In these disorders, STEP protein expression levels and activity are dysregulated, contributing to the cognitive deficits that are present. In this review, we focus on the most recent findings on STEP, discuss how STEP expression and activity are maintained during normal cognitive function, and how disruptions in STEP activity contribute to a number of illnesses. (C) 2014 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
引用
收藏
页码:1 / 9
页数:9
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