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甘氨酸受体——基因组与蛋白质组之间的桥梁:RNA 编辑和剪接的功能意义。

Glycine Receptors Caught between Genome and Proteome - Functional Implications of RNA Editing and Splicing.

机构信息

INSERM U952 Paris, France.

出版信息

Front Mol Neurosci. 2009 Nov 9;2:23. doi: 10.3389/neuro.02.023.2009. eCollection 2009.

DOI:10.3389/neuro.02.023.2009
PMID:19936314
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2779093/
Abstract

Information processing in the brain requires a delicate balance between excitation and inhibition. Glycine receptors (GlyR) are involved in inhibitory mechanisms mainly at a synaptic level, but potential novel roles for these receptors recently emerged due to the discovery of posttranscriptional processing. GLR transcripts are edited through enzymatic modification of a single nucleotide leading to amino acid substitution within the neurotransmitter binding domain. RNA editing produces gain-of-function receptors well suited for generation and maintenance of tonic inhibition of neuronal excitability. As neuronal activity deprivation in early stages of development or in epileptic tissue is detrimental to neurons and because RNA editing of GlyR is up-regulated in temporal lobe epilepsy patients with a severe course of disease a pathophysiological role of these receptors emerges. This review contains a state-of-the-art discussion of (patho)physiological implications of GlyR RNA editing.

摘要

大脑中的信息处理需要兴奋和抑制之间的微妙平衡。甘氨酸受体(GlyR)参与抑制机制,主要在突触水平,但由于转录后加工的发现,这些受体最近出现了潜在的新作用。GLR 转录本通过单个核苷酸的酶修饰进行编辑,导致神经递质结合域内的氨基酸取代。RNA 编辑产生功能获得性受体,非常适合产生和维持神经元兴奋性的紧张抑制。由于发育早期或癫痫组织中的神经元活动剥夺对神经元有害,并且 GlyR 的 RNA 编辑在疾病严重程度较高的颞叶癫痫患者中上调,因此这些受体的病理生理作用出现了。这篇综述包含了对 GlyR RNA 编辑的(病理)生理意义的最新讨论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/7e8d57303228/fnmol-02-023-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/b12819597ed1/fnmol-02-023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/540b4026b8c3/fnmol-02-023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/8861a76b103e/fnmol-02-023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/7e8d57303228/fnmol-02-023-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/b12819597ed1/fnmol-02-023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/540b4026b8c3/fnmol-02-023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/8861a76b103e/fnmol-02-023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00d9/2779093/7e8d57303228/fnmol-02-023-g004.jpg

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