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一个线粒体肌病家系中线粒体tRNA(Leu)(UUR)基因的新型点突变。

A novel point mutation in the mitochondrial tRNA(Leu)(UUR) gene in a family with mitochondrial myopathy.

作者信息

Goto Y, Tojo M, Tohyama J, Horai S, Nonaka I

机构信息

Division of Ultrastructural Research, National Center of Neurology and Psychiatry, Tokyo, Japan.

出版信息

Ann Neurol. 1992 Jun;31(6):672-5. doi: 10.1002/ana.410310617.

Abstract

A T-to-C transition mutation at nucleotide position 3,250 in the mitochondrial tRNA(Leu)(UUR) gene was present in a family with mitochondrial myopathy. Two of three muscle biopsies examined had complex I (NADH-ubiquinone oxidoreductase) deficiency. Heteroplasmy of wild and mutant mitochondrial DNA was detected by Nae I digestion of the polymerase chain reaction products with a modified primer. This was found in blood or muscle samples or both from all seven members examined. Similar to the 3,243 mutation in most patients with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes), the new mutation site was located in the dihydrouridine loop and embedded in the binding region of mitochondrial transcription termination factor. Elucidation of the effects of this mutation may help clarify the role of mitochondrial tRNAs and transcription termination.

摘要

线粒体肌病家族中线粒体tRNA(Leu)(UUR)基因第3250位核苷酸处存在T到C的转换突变。所检查的三块肌肉活检样本中有两块存在复合体I(NADH-泛醌氧化还原酶)缺陷。通过用改良引物对聚合酶链反应产物进行Nae I酶切,检测到野生型和突变型线粒体DNA的异质性。在所检查的所有七名成员的血液或肌肉样本或两者中均发现了这种情况。与大多数线粒体肌病、脑病、乳酸酸中毒和卒中样发作(MELAS)患者的3243突变类似,新的突变位点位于二氢尿嘧啶环,且嵌入线粒体转录终止因子的结合区域。阐明该突变的影响可能有助于明确线粒体tRNA和转录终止的作用。

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