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  1. 0 資料タイプ別
  2. 03 紀要論文
  1. 250 大学院医歯学総合研究科(医)
  2. 20 紀要
  3. 02 新潟医学会雑誌
  4. 第112巻第9号

歯状核赤核・淡蒼球ルイ体萎縮症蛋白の伸長ポリグルタミン鎖のアデノウイルスベクターを用いた発現による神経細胞障害機構の解析

http://hdl.handle.net/10191/46201
http://hdl.handle.net/10191/46201
917b03c7-5061-40d7-bb6b-0347a9e36c70
名前 / ファイル ライセンス アクション
112(9)_563-572.pdf 112(9)_563-572.pdf (1.6 MB)
Item type 紀要論文 / Departmental Bulletin Paper(1)
公開日 2017-02-07
タイトル
タイトル 歯状核赤核・淡蒼球ルイ体萎縮症蛋白の伸長ポリグルタミン鎖のアデノウイルスベクターを用いた発現による神経細胞障害機構の解析
タイトル
言語 en
タイトル 歯状核赤核・淡蒼球ルイ体萎縮症蛋白の伸長ポリグルタミン鎖のアデノウイルスベクターを用いた発現による神経細胞障害機構の解析
言語
言語 jpn
キーワード
主題Scheme Other
主題 DRPLA
キーワード
主題Scheme Other
主題 CAG trinucleotid disease
キーワード
主題Scheme Other
主題 adenovirus
キーワード
主題Scheme Other
主題 COS-TPC method
キーワード
主題Scheme Other
主題 neuronal PC12
キーワード
主題Scheme Other
主題 歯状核赤核淡蒼球ルイ体萎縮症
キーワード
主題Scheme Other
主題 CAGリピート病
キーワード
主題Scheme Other
主題 アデノウイルスベクター
キーワード
主題Scheme Other
主題 COS-TPC法
キーワード
主題Scheme Other
主題 分化型PC12
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ departmental bulletin paper
その他のタイトル
その他のタイトル Adenovirus-mediated Expression of Truncated DRPLA Protein Containing an Expanded Polyglutamine Stretch Results in Intranuclear Inclusion in Neuronal PC12
著者 佐藤, 晶

× 佐藤, 晶

WEKO 104684

佐藤, 晶

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著者別名
識別子 104685
識別子Scheme WEKO
姓名 Sato, Aki
抄録
内容記述タイプ Abstract
内容記述 Dentatorubtal-pallidoluysian atrophy (DRPLA) is an autosomal dominant neurodegenerative disorder caused by unstable expansion of a CAG trinucleotide repeat of DRPLA, gene on chromospme 12p13.31. Although recent investigations suggest that mutant proteins with expanded polyglutamine stretches exert gain of toxic functions to neuronal cells, molecular mechanisms of the toxicity to neuronal cells remain unclear. To elucidate molecular mechanisms of neurodegeneration caused by expanded CAG repeats in DRPLA, we established an efficient expression system of truncated DRPLA proteins with normal or expanded polyglutamine stretches, Using COS/TPC method, we constructed adenovirus vectors containing truncated DRPLA cDNA coding for normal or expaneded polyglutamine stretches (19 or 82 glutamines) and the flanking regions. Using these adenovirus vectors, truncated DRPLA proteins with normal or expanded polyglutatnine stretchs were expressed in neuronal PC12 cells and human cultured skin fibroblasts. Formation of aggregate bodeis were observed in cells expressing the truncated DRPLA protein with the expanded polyglutamine stretch, but not in cells expressing that with the normal stretch. In neuronal PC12 cells, more than 97 %, of cells showed intranuclear inclusions at 3 days after infection, while only 36.0±29.6 % of fibroblasts had intranuclear inclusios at 4 days after infection. Numbers of apoptotic cells were higher in cells expressing the expanded polyglutamine stretch than in those expressing the normal polyglutamine stretch, especially in neuronal PC12. The results showed neuronoal PC12 cells are more vulnerable to mutant DRPLA proteins than fibroblasts. This expression system of truncated wild type and mutant DRPLA proteins is proved to be a useful system to analyze the toxicity of mutant proteins containing expanded polyglutamine stretches in neuronal cells.
書誌情報 新潟医学会雑誌
en : 新潟医学会雑誌

巻 112, 号 9, p. 563-572, 発行日 1998-09
出版者
出版者 新潟医学会
ISSN
収録物識別子タイプ ISSN
収録物識別子 00290440
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AN00182415
著者版フラグ
値 publisher
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