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Association of Methylation Profiles of Mitochondrial Genes with Schizophrenia

机译:线粒体基因甲基化谱与精神分裂症的关系

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Mitochondrial dysfunction manifests common central nervous system disorders such as seizures, dementia, ataxia, mitochondrial encephalomyopathy (such as MELARS). Methylation profiles of mitochondrial genes in schizophrenia may help to explain the phenotype of schizophrenic symptoms such as anhedonia, weakness, fatigue and negative symptoms. The dysfunction of mitochondria has been suggested to be one of the disease mechanism for schizophrenia. The differential expression genes profile of mitochondrial genes implicates modulation mechanism of protein-protein interactions. Methylation in the promotor region of mitochondrial related genes such as NDUFS6, ATP5H, NDUFA10, NDUFA6 and NDUFV1 play the important role in dysfunction of mitochondrial subunit complex. It indicates the mitochondrial complex I complex, especially NADH: ubiquinone oxidoreductase (EC 1.6.5.3) gamma subunit could be the potential biomarker for schizophrenia. These results suggested that methylation profile of the genomic sequence in the promoter region of mitochondrial genes might be a crucial factor of pathogenesis for schizophrenia.
机译:线粒体功能障碍表现出常见的中枢神经系统疾病,例如癫痫发作,痴呆,共济失调,线粒体脑病(例如MELARS)。精神分裂症中线粒体基因的甲基化特征可能有助于解释精神分裂症症状的表型,如精神病,无力,疲倦和阴性症状。线粒体功能障碍已被认为是精神分裂症的发病机制之一。线粒体基因的差异表达基因谱牵涉蛋白质-蛋白质相互作用的调节机制。线粒体相关基因(例如NDUFS6,ATP5H,NDUFA10,NDUFA6和NDUFV1)的启动子区域的甲基化在线粒体亚基复合体功能障碍中起重要作用。它表明线粒体复合物I复合物,尤其是NADH:泛醌氧化还原酶(EC 1.6.5.3)γ亚基可能是精神分裂症的潜在生物标志物。这些结果表明线粒体基因的启动子区域中的基因组序列的甲基化配置文件可能是精神分裂症发病机理的关键因素。

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