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首页> 外文期刊>Molecular syndromology >Hippocampal Characteristics and Invariant Sequence Elements Distribution of GLRA2 and GLRA3 C-to-U Editing
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Hippocampal Characteristics and Invariant Sequence Elements Distribution of GLRA2 and GLRA3 C-to-U Editing

机译：GLRA2和GLRA3 C-U编辑的海马特征和不变序列元素分布

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Glycine receptor α2 and α3 subunit (GLRA2/GLRA3) high-affinity variants, of which the subjacent amino acid substitutions issue from C-to-U RNA editing, are thought to influence tonic inhibition and pathophysiology. In light of the detection of GLRA3 {"type":"entrez-nucleotide","attrs":{"text":"NM_006529","term_id":"557786115","term_text":"NM_006529"}}NM_006529:r.1157C>U and GLRA2 {"type":"entrez-nucleotide","attrs":{"text":"NM_002063","term_id":"169646714","term_text":"NM_002063"}}NM_002063:r.1416C>U exchanges in hippocampus explants of temporal lobe epilepsy patients, we now examine the healthy situation and relate it to the epileptic situation by ascertaining controls in a legitimate reanalysis. The GLRA2 and GLRA3 editing events that would ultimately result in a glycine receptor with increased affinity occur in the postmortem nonepileptic hippocampus. Most notably, their relative amounts do not significantly differ from those in increased damaged hippocampus explants, whereas curbed relative amounts in epileptic explants without cell loss come out statistically significant. Local sequence alignment reveals invariant sequence stretches consistent in GLRA2/ GLRA3 and other edited transcripts that coincide with known APOB sequence elements. Concerning the essential mooring element, GLRA2/GLRA3 comply strictly only with the motif's 5′ part. While this lack of canonical mooring elements and uncertain action of the famous deaminase APOBEC1 suggest a specific regulation of GLRA2/GLRA3 editing, its reduction in the less-damaged epileptic hippocampus could be attributed to anomalous epileptic neurogenesis.
机译：甘氨酸受体α2和α3亚基（GLRA2 / GLRA3）高亲和力变异体（其下部氨基酸取代由C-to-U RNA编辑产生）被认为会影响补品抑制和病理生理。鉴于检测到GLRA3 {“ type”：“ entrez-nucleotide”，“ attrs”：{“ text”：“ NM_006529”，“ term_id”：“ 557786115”，“ term_text”：“ NM_006529”}} NM_006529： r.1157C> U和GLRA2 {“ type”：“ entrez-nucleotide”，“ attrs”：{“ text”：“ NM_002063”，“ term_id”：“ 169646714”，“ term_text”：“ NM_002063”}} NM_002063： r.1416C>颞叶癫痫患者海马外植体中的U交换，我们现在检查健康状况，并通过在合法的再分析中确定对照将其与癫痫状况相关联。 GLRA2和GLRA3编辑事件最终会导致死后非癫痫性海马体发生甘氨酸受体的亲和力增加。最值得注意的是，它们的相对数量与受损海马外植体数量增加没有显着差异，而在没有细胞丢失的情况下，抑制的癫痫外植体的相对数量具有统计学意义。局部序列比对揭示了在GLRA2 / GLRA3和与已知APOB序列元件一致的其他编辑的转录本中一致的不变序列延伸。关于必要的系泊元件，GLRA2 / GLRA3仅严格遵守图案的5'部分。尽管缺乏典型的系泊元件以及著名的脱氨酶APOBEC1的不确定作用提示了GLRA2 / GLRA3编辑的特定调控，但其对较少受损的癫痫海马的减少可能归因于异常的癫痫神经发生。

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