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Association of methylation profiles of mitochondrial genes with schizophrenia

机译:分层精神分裂症线粒体基因甲基化谱的缔合

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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,如癫痫发作,痴呆,共济失调,线粒体脑膜病变(如MELARS)。精神分裂症中线粒体基因的甲基化谱可能有助于解释精神分裂症症状的表型,如厌氧,虚弱,疲劳和阴性症状。已经提出了线粒体的功能障碍是精神分裂症的疾病机制之一。线粒体基因的差异表达基因谱意味着蛋白质 - 蛋白质相互作用的调节机制。线粒体相关基因的启动区甲基化如NDUFS6,ATP5H,NDUFA10,NDUFA6和NDUFv1在线粒体亚基复合物功能障碍中起重要作用。它表明线粒体复合物I复合物,特别是NADH:奥基醌氧化还原酶(EC 1.6.5.3)γ亚基可以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基因组序列的甲基化谱可能是精神分裂症发病机制的关键因素。

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