检索结果-南通市图书馆

Micro RNA-124 slows down the progression of Huntington's disease by promoting neurogenesis in the striatum

Neural Regeneration Research 2015年第5期10卷 786-791页

作者： Tian Liu wooseok im Inhee Mook-Jung Manho Kim Department of Biomedical Sciences Seoul National University College of Medicine Department of Neurology Biomedical Research InstituteSeoul National University Hospital Department of Biochemistry Seoul National University College of Medicine Protein Metabolism Medical Research Center College of MedicineSeoul National University

MicroRNA-124 contributes to neurogenesis through regulating its targets, but its expression both in the brain of Huntington＇s disease mouse models and patients is decreased. However, the effects of microRNA-124 on the progression of Huntington＇s disease have not been reported. Results from this study showed that microRNA-124 increased the latency to fall for each R6/2 Hunting- ton＇s disease transgenic mouse in the rotarod test. 5-Bromo-2＇-deoxyuridine （BrdU） staining of the striatum shows an increase in neurogenesis. In addition, brain-derived neurotrophic factor and peroxisome proliferator-activated receptor gamma coactivator 1-alpha protein levels in the striatum were increased and SRY-related HMG box transcription factor 9 protein level was de- creased. These findings suggest that microRNA-124 slows down the progression of Huntington＇s disease possibly through its important role in neuronal differentiation and survival.

关键词： nerve regeneration microRNA-124 neurogenesis neuronal survival Huntington'sdisease SRY-related HMG box transcription factor 9 brain-derived neurotrophic factor peroxisomeproliferator-activated receptor gamma coactivator 1-alpha mutant huntingtin

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Downregulated miR-18b-5p triggers apoptosis by inhibition of calcium signaling and neuronal cell differentiation in transgenic SOD1(G93A)mice and SOD1(G17S and G86S)ALS patients

引用

Translational Neurodegeneration 2020年第3期9卷 323-343页

作者： Ki Yoon Kim Yu Ri Kim Kyung Won Choi Mijung Lee Somyung Lee wooseok im Je-Young Shin Jin Young Kim Yoon Ho Hong Manho Kim Jong-ll Kim Jung-Joon Sung Department of Neurology Seoul National University Hospital 28 yongon-DongChongno-guSeoul 110-744Republic of Korea Division of Mass Spectrometry Research Korea Basic Science InstituteDaejunRepublic of Korea Department of Neurology Seoul National University Seoul Metropolitan Government Boramae Medical G enterSeoulRepublic of Korea Department of Biochemistry and Molecular Biology Seoul National University College of MedicineSeoulRepublic of Korea

Background:MicroRNAs(miRNAs)are endogenous non-coding RNAS that regulate gene expression at the post-transcriptional level and are key modulators in neurodegenerative *** miRNAs play an important role in amyotrophic lateral sclerosis(ALS);however,the pathogenic mechanisms of deregulated miRNAS are still ***:We aimed to assess the dysfunction of RNAS or miRNAs in fALS(SOD1 mutations).We compared the RNA-seq of subcellular fractions in NSC-34 WT(hSOD1)and MT(hSOD1(G93A))cells to find altered RNAs or *** identified that Hif1a and Mef2c were upregulated,and Mctp1 and Rarb were downregulated in the cytoplasm of NSC-34 MT ***:SOD1 mutations decreased the level of *** Hif1a which is the target for miR-18b increased Mef2c expression as a transcription ***2c upregulated miR-206 as a transcription *** of Mctp1 and Rarb,which are targets of miR-206,induced intracellular Ca^2+ levels and reduced cell differentiation,*** miR-18b-5p pathway was also observed in G93A Tg mice,fALS(G86S)patient,and iPSC-derived motor neurons from fALS(G17S)***:Our data indicate that SOD1 mutation decreases miR-18b-5p,which sequentially regulates Hif1a,Mef2c,miR-206,Mctp1 and Rarb in fALS-linked SOD1 *** results provide new insights into the downregulation of miR-18b-5p-dependent pathogenic mechanisms of ALS.

关键词： miRNAs Hif1a Mef2c Mctp1 Rarb

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：