• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

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.

DOI:10.1006/bbrc.1993.2584
PMID:8280119
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。

相似文献

1
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.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。
Biochem Biophys Res Commun. 1993 Dec 30;197(3):1049-55. doi: 10.1006/bbrc.1993.2584.
2
Altered mitochondrial function in fibroblasts containing MELAS or MERRF mitochondrial DNA mutations.含有线粒体脑肌病伴乳酸血症和卒中样发作(MELAS)或肌阵挛性癫痫伴破碎红纤维综合征(MERRF)线粒体DNA突变的成纤维细胞中线粒体功能的改变
Biochem J. 1996 Sep 1;318 ( Pt 2)(Pt 2):401-7. doi: 10.1042/bj3180401.
3
Analysis of cybrids harboring MELAS mutations in the mitochondrial tRNA(Leu(UUR)) gene.对线粒体tRNA(Leu(UUR))基因中携带MELAS突变的胞质杂种的分析。
Muscle Nerve Suppl. 1995;3:S119-23. doi: 10.1002/mus.880181424.
4
The mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episode syndrome-associated human mitochondrial tRNALeu(UUR) mutation causes aminoacylation deficiency and concomitant reduced association of mRNA with ribosomes.线粒体肌病、脑病、乳酸性酸中毒和卒中样发作综合征相关的人类线粒体tRNALeu(UUR)突变导致氨酰化缺陷,并伴随mRNA与核糖体的结合减少。
J Biol Chem. 2000 Jun 23;275(25):19198-209. doi: 10.1074/jbc.M908734199.
5
Defects in mitochondrial protein synthesis and respiratory chain activity segregate with the tRNA(Leu(UUR)) mutation associated with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes.线粒体蛋白合成和呼吸链活性缺陷与与线粒体肌病、脑病、乳酸性酸中毒和类卒中发作相关的tRNA(Leu(UUR))突变共分离。
Mol Cell Biol. 1992 Feb;12(2):480-90. doi: 10.1128/mcb.12.2.480-490.1992.
6
Fine mapping of mitochondrial RNAs derived from the mtDNA region containing a point mutation associated with MELAS.对源自包含与线粒体脑肌病伴乳酸血症和卒中样发作(MELAS)相关点突变的线粒体DNA(mtDNA)区域的线粒体RNA进行精细定位。
Nucleic Acids Res. 1993 Feb 11;21(3):657-62. doi: 10.1093/nar/21.3.657.
7
Codon-specific translational defect caused by a wobble modification deficiency in mutant tRNA from a human mitochondrial disease.人类线粒体疾病突变tRNA中摆动修饰缺陷导致的密码子特异性翻译缺陷
Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15070-5. doi: 10.1073/pnas.0405173101. Epub 2004 Oct 11.
8
Acquisition of the wobble modification in mitochondrial tRNALeu(CUN) bearing the G12300A mutation suppresses the MELAS molecular defect.携带G12300A突变的线粒体tRNALeu(CUN)中摆动修饰的获得抑制了MELAS分子缺陷。
Hum Mol Genet. 2006 Mar 15;15(6):897-904. doi: 10.1093/hmg/ddl007. Epub 2006 Jan 30.
9
A mitochondrial tRNA(Leu)(UUR) mutation at 3,256 associated with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).位于3256位点的线粒体tRNA(亮氨酸)(UUR)突变与线粒体肌病、脑病、乳酸性酸中毒和卒中样发作(MELAS)相关。
Biochem Mol Biol Int. 1994 Aug;33(6):1055-61.
10
Tissue distribution of mutant mitochondrial DNA in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS).
J Inherit Metab Dis. 1993;16(1):27-30. doi: 10.1007/BF00711311.

引用本文的文献

1
Post-transcriptional methylation of mitochondrial-tRNA differentially contributes to mitochondrial pathology.线粒体 tRNA 的转录后甲基化对线粒体病理学有不同的贡献。
Nat Commun. 2024 Oct 18;15(1):9008. doi: 10.1038/s41467-024-53318-x.
2
Mitochondrial haplotype mutation alleviates respiratory defect of MELAS by restoring taurine modification in tRNA with 3243A > G mutation.线粒体单倍型突变通过恢复 tRNA 中的牛磺酸修饰来减轻 MELAS 的呼吸缺陷,该修饰由 3243A>G 突变引起。
Nucleic Acids Res. 2023 Aug 11;51(14):7480-7495. doi: 10.1093/nar/gkad591.
3
Restoration of mitochondrial function through activation of hypomodified tRNAs with pathogenic mutations associated with mitochondrial diseases.
通过激活与线粒体疾病相关的致病性突变的低修饰 tRNA 来恢复线粒体功能。
Nucleic Acids Res. 2023 Aug 11;51(14):7563-7579. doi: 10.1093/nar/gkad139.
4
Insulin Resistance in Mitochondrial Diabetes.线粒体糖尿病中的胰岛素抵抗。
Biomolecules. 2023 Jan 7;13(1):126. doi: 10.3390/biom13010126.
5
The expanding world of tRNA modifications and their disease relevance.tRNA 修饰的扩展世界及其与疾病的相关性。
Nat Rev Mol Cell Biol. 2021 Jun;22(6):375-392. doi: 10.1038/s41580-021-00342-0. Epub 2021 Mar 3.
6
Human transfer RNA modopathies: diseases caused by aberrations in transfer RNA modifications.人类转移 RNA 修饰病:由转移 RNA 修饰异常引起的疾病。
FEBS J. 2021 Dec;288(24):7096-7122. doi: 10.1111/febs.15736. Epub 2021 Feb 16.
7
Mitochondrial dysfunction and its role in tissue-specific cellular stress.线粒体功能障碍及其在组织特异性细胞应激中的作用。
Cell Stress. 2018 Jul 13;2(8):184-199. doi: 10.15698/cst2018.07.147.
8
Mitochondrial transcript maturation and its disorders.线粒体转录本成熟及其紊乱
J Inherit Metab Dis. 2015 Jul;38(4):655-80. doi: 10.1007/s10545-015-9859-z. Epub 2015 May 28.
9
Unique features of animal mitochondrial translation systems. The non-universal genetic code, unusual features of the translational apparatus and their relevance to human mitochondrial diseases.动物线粒体翻译系统的独特特征。非通用遗传密码、翻译装置的不寻常特征及其与人类线粒体疾病的相关性。
Proc Jpn Acad Ser B Phys Biol Sci. 2010;86(1):11-39. doi: 10.2183/pjab.86.11.
10
Normal levels of wild-type mitochondrial DNA maintain cytochrome c oxidase activity for two pathogenic mitochondrial DNA mutations but not for m.3243A-->G.野生型线粒体DNA的正常水平可维持两种致病性线粒体DNA突变的细胞色素c氧化酶活性,但不能维持m.3243A→G突变的细胞色素c氧化酶活性。
Am J Hum Genet. 2007 Jul;81(1):189-95. doi: 10.1086/518901. Epub 2007 May 23.