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Role of MeCP2, DNA methylation, and HDACs in regulating synapse function

机译:MeCP2,DNA甲基化和HDAC在调节突触功能中的作用

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Over the past several years there has been intense effort to delineate the role of epigenetic factors, including methyl-CpG-binding protein 2, histone deacetylases, and DNA methyltransferases, in synaptic function. Studies from our group as well as others have shown that these key epigenetic mechanisms are critical regulators of synapse formation, maturation, as well as function. Although most studies have identified selective deficits in excitatory neurotransmission, the latest work has also uncovered deficits in inhibitory neurotransmission as well. Despite the rapid pace of advances, the exact synaptic mechanisms and gene targets that mediate these effects on neurotransmission remain unclear. Nevertheless, these findings not only open new avenues for understanding neuronal circuit abnormalities associated with neurodevelopmental disorders but also elucidate potential targets for addressing the pathophysiology of several intractable neuropsychiatric disorders.Keywords: HDAC, DNA methylation, MeCP2, Neurotransmission, Synaptic plasticity
机译:在过去的几年中,人们一直在努力研究表观遗传因素在突触功能中的作用,包括甲基CpG结合蛋白2,组蛋白脱乙酰基酶和DNA甲基转移酶。我们小组以及其他小组的研究表明,这些关键的表观遗传机制是突触形成,成熟以及功能的关键调节因子。尽管大多数研究已经确定了兴奋性神经传递的选择性缺陷,但最新的研究也发现了抑制性神经传递的缺陷。尽管进展迅速,但是尚不清楚介导这些对神经传递的影响的确切突触机制和基因靶标。然而,这些发现不仅为了解与神经发育障碍相关的神经元回路异常开辟了新途径,而且为解决几种难治性神经精神疾病的病理生理学提供了潜在的靶标。关键词:HDAC,DNA甲基化,MeCP2,神经传递,突触可塑性

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