SNAP-25 in Neuropsychiatric Disorders

被引：88

作者：

Corradini, Irene

Verderio, Claudia

Sala, Mariaelvina

Wilson, Michael C. ^{[2
]}

Matteoli, Michela ^{[1
,3
]}

机构：

[1] Univ Milan, Inst Neurosci, Dept Med Pharmacol, CNR, I-20129 Milan, Italy

[2] Univ New Mexico, Hlth Sci Ctr, Dept Neurosci, Albuquerque, NM 87131 USA

[3] Fdn Don C Gnocchi, Ist Ricovero & Cura Carattere Sci, Milan, Italy

来源：

MECHANISMS OF EXOCYTOSIS | 2009年 / 1152卷

基金：

美国国家卫生研究院;

关键词：

SNAP-25; schizophrenia; epilepsy; ADHD; calcium channels; VOLTAGE-ACTIVATED CURRENTS; CALCIUM-CHANNELS; MOUSE MUTANT; LOCOMOTOR HYPERACTIVITY; DEFICIT; SCHIZOPHRENIA; MODEL; GENE; EPILEPSY; SNAP25;

D O I：

10.1111/j.1749-6632.2008.03995.x

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

SNAP-25 (synaptosomal-associated protein of 25 kDa) is a plasma membrane protein that, together with syntaxin and the synaptic vesicle protein VAMP/synaptobrevin, forms the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) docking complex for regulated exocytosis. SNAP-25 also modulates different voltage-gated calcium channels, representing therefore a multifunctional protein that plays essential roles in neurotransmitter release at different steps. Recent genetic studies of human populations and of some mouse models implicate alterations in SNAP-25 gene structure, expression, and/or function in contributing directly to these distinct neuropsychiatric and neurological disorders.

引用

页码：93 / 99

页数：7

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