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从患有线粒体脑肌病伴乳酸血症和卒中样发作(MELAS)的患者引入到缺乏线粒体DNA(mtDNA)的HeLa细胞中的、在tRNA(Leu)(UUR)基因第3271位存在突变的mtDNA的积累,会导致线粒体呼吸功能的逐渐抑制。

Accumulation of mtDNA with a mutation at position 3271 in tRNA(Leu)(UUR) gene introduced from a MELAS patient to HeLa cells lacking mtDNA results in progressive inhibition of mitochondrial respiratory function.

作者信息

Hayashi J, Ohta S, Takai D, Miyabayashi S, Sakuta R, Goto Y, Nonaka I

机构信息

Institute of Biological Sciences, University of Tsukuba, Ibaraki, Japan.

出版信息

Biochem Biophys Res Commun. 1993 Dec 30;197(3):1049-55. doi: 10.1006/bbrc.1993.2584.

Abstract

A new mitochondrial DNA (mtDNA) mutation of tRNA(Leu)(UUR) at nucleotide position 3271 (MELAS3271) was determined to be involved in the pathogenic process of mitochondrial diseases MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) using intercellular transfer of patient-derived mtDNA to mtDNA-less HeLa cells (rho 0 HeLa cells). Cybrid clones containing imported mtDNA exclusively from a MELAS patient with MELAS3271 mtDNA were isolated, and the influence of MELAS3271 mtDNA on mitochondrial translation activity and mitochondrial respiratory complex I enzyme activity were examined. Accumulation of more than 87% MELAS3271 mutant mtDNA in the cybrid clones induced both low complex I activity and abnormal mtDNA-encoded polypeptide synthesis including at least complex I subunit ND6. suggesting involvement of the new MELAS-associated mutation in the pathogenesis.

摘要

通过将患者来源的线粒体DNA(mtDNA)细胞间转移至无mtDNA的HeLa细胞(ρ0 HeLa细胞),确定了核苷酸位置3271处tRNA(Leu)(UUR)的一种新的线粒体DNA(mtDNA)突变(MELAS3271)与线粒体疾病MELAS(线粒体肌病、脑病、乳酸性酸中毒和卒中样发作)的致病过程有关。分离出仅含有来自一名携带MELAS3271 mtDNA的MELAS患者的导入mtDNA的细胞杂交克隆,并检测了MELAS3271 mtDNA对线粒体翻译活性和线粒体呼吸复合体I酶活性的影响。细胞杂交克隆中超过87%的MELAS3271突变mtDNA的积累导致了低复合体I活性和异常的mtDNA编码多肽合成,包括至少复合体I亚基ND6,提示新的MELAS相关突变参与了发病机制。

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