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タンパク質合成系への作用からみたN-アセチルシステインの抗精神病作用機序の解明
https://doi.org/10.24517/00056728
https://doi.org/10.24517/000567285ed2249c-84de-418b-88e9-ffa2d8ce2cc5
名前 / ファイル | ライセンス | アクション |
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ME-PR-NISHIKAWA-H-kaken 2016-4p.pdf (313.5 kB)
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Item type | 報告書 / Research Paper(1) | |||||
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公開日 | 2020-01-27 | |||||
タイトル | ||||||
タイトル | タンパク質合成系への作用からみたN-アセチルシステインの抗精神病作用機序の解明 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Elucidating the mechanism of the effects of N-acetyl cysteine on animal models of mental disorders | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
ID登録 | ||||||
ID登録 | 10.24517/00056728 | |||||
ID登録タイプ | JaLC | |||||
著者別表示 |
Nishikawa, Hiromi
× Nishikawa, Hiromi |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域医学系 | |||||
書誌情報 |
平成27(2015)年度 科学研究費補助金 若手研究(B) 研究成果報告書 en : 2015 Fiscal Year Final Research Report 巻 2014-04-01 - 2016-03-31, p. 4p., 発行日 2016-05-23 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | コカイン依存症動物モデルで予想される側坐核での細胞内システィンの欠乏からtRNAのチオール化抑制を予測し、それを触媒するMOCS3の発現量についてウエスタン法で検討したが、発現確認できなかった。またシスティンを合成の律速段階とするグルタチオンの量はコカインの影響を受けていなかった。メチオニンからのシスティン供給に関与する酵素についても活性をに有意な差を認めなかった。従って、慢性コカイン投与でシスチン-グルタミン酸交換体の機能障害が起きても、細胞内システィンの供給は代償されていると考えられた。一方、N-アセチルシスティンの急性投与は慢性コカイン動物でのシナプス構成タンパク質の分解を促進した。 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | It was predicted that protein synthesis would be attenuated in the nucleus accumbent (NAc) of chronic cocaine-treated rats due to intracellular cysteine shortage -induced attenuation of thiolation of tRNA which resulted from dysfunction of cystine-glutamate anti porter (xCT). However, the existence of MOCS3, which is supposed to catalyst tRNA violation, was not confirmed. In addition, the amount of total glutathione, which demands cysteine for its synthesis, was not affected by cocaine, Another intracellular cysteine supplying pathway from methionine owing to the enzymatic activity of cystathionine beta synthase was also less likely, because its activity was not altered by cocaine. Thus, it is concluded that intracellular cysteine was supplied by unknown pathway besides via xCT, and the basel levels of protein synthesis was not affected in the NAc by repeated cocaine treatment. On the other hand , N-acteyl-cysteine robustly promoted protein degradation in chronic cocaine-treated rats. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:26860920, 研究期間(年度):2014-04-01 - 2016-03-31 | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 出典:研究課題「タンパク質合成系への作用からみたN-アセチルシステインの抗精神病作用機序の解明」課題番号26860920 (KAKEN:科学研究費助成事業データベース(国立情報学研究所)) (https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-26860920/26860920seika/)を加工して作成 |
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著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/search/?qm=70534155 | |||||
関連名称 | https://kaken.nii.ac.jp/search/?qm=70534155 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-26860920/ | |||||
関連名称 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-26860920/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-26860920/26860920seika/ | |||||
関連名称 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-26860920/26860920seika/ |