中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2015, 27(4): 462-470
组蛋白去乙酰化酶在突触可塑性及神经退行性疾病中的作用
阮杭泽, 郭 霞, 祁羡杰, 沈万华*
(杭州师范大学浙江省器官发育与再生技术研究重点实验室,杭州 310036)
摘 要:突触可塑性是学习与记忆的分子机制之一。表观遗传调控在突触可塑性过程中起着重要作用。通过组蛋白去乙酰化酶和组蛋白乙酰化酶对组蛋白进行修饰是其中一种主要方式。组蛋白乙酰化修饰可以激活转录、活化相应位点和信号分子,影响突触可塑性。组蛋白去乙酰化酶抑制剂在治疗神经退行性疾病的过程中,发现可以增强突触可塑性,改善记忆损伤。因此,现就组蛋白去乙酰化酶在突触可塑性中的作用机制及其与相关神经退行性疾病发生发展的联系进行综述。
 
The role of histone deacetylases in synaptic plasticity and neurodegenerative disorders
RUAN Hang-Ze, GUO Xia, QI Xian-Jie, SHEN Wan-Hua*
(Zhejiang Key Laboratory of Organ Development and Rengeneration, Hangzhou Normal University, Hangzhou 310036, China)
Abstract: It is thought that synaptic plasticity is one of the key mechanisms of learning and memory. Epigenetic mechanisms such as histone modification play a vital role in synaptic plasticity. Histone modification is regulated by histone deacetylases (HDACs) and histone acetyltransferases (HATs), which are the major pathways in regulation of gene expression. Histone acetylation can activate gene transcription and change synaptic plasticity. Non-specific pharmacological inhibition of the histone deacetylase (HDACi) has been used to treat neurodegenerative diseases, which can enhance synaptic plasticity and improve memory impairment. Thus, this review will discuss the role of HDACs in the synaptic plasticity and neurodegenerative disorders.
 
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