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RNA結合蛋白質が細胞シグナルに応答して制御する翻訳とmRNA分解との連携機構
https://kindai.repo.nii.ac.jp/records/20625
https://kindai.repo.nii.ac.jp/records/2062533b89063-ece0-4a49-99eb-2c1df2dbee28
名前 / ファイル | ライセンス | アクション |
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16H04745seika.pdf (192.8 kB)
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Item type | 研究報告書 / Research Paper(1) | |||||
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公開日 | 2020-03-12 | |||||
タイトル | ||||||
言語 | ja | |||||
タイトル | RNA結合蛋白質が細胞シグナルに応答して制御する翻訳とmRNA分解との連携機構 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | The coupling mechanism of translation and mRNA degradation regulated by RNA binding protein in response to cell signals | |||||
著者 |
藤原, 俊伸
× 藤原, 俊伸× 三嶋, 雄一郎× 足達, 俊吾 |
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言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
主題 | 翻訳制御, mRNP, mRNA分解 | |||||
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 | |||||
著者(英) | ||||||
en | ||||||
FUJIWARA, Toshinobu | ||||||
著者(英) | ||||||
en | ||||||
MISHIMA, Yuichiro | ||||||
著者(英) | ||||||
en | ||||||
ADACHI, shungo | ||||||
著者 所属 | ||||||
近畿大学薬学部; 教授 | ||||||
著者 所属 | ||||||
京都産業大学総合生命科学部; 准教授 | ||||||
著者所属(翻訳) | ||||||
Kindai University | ||||||
著者 役割 | ||||||
研究代表者 | ||||||
著者 役割 | ||||||
研究分担者 | ||||||
著者 役割 | ||||||
研究協力者 | ||||||
版 | ||||||
出版タイプ | NA | |||||
出版タイプResource | http://purl.org/coar/version/c_be7fb7dd8ff6fe43 | |||||
出版者 名前 | ||||||
出版者 | 近畿大学 | |||||
書誌情報 |
科学研究費助成事業研究成果報告書 (2018) p. 1-6, 発行日 2019 |
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リンクURL | ||||||
内容記述タイプ | Other | |||||
内容記述 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16H04745/ | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 研究成果の概要(和文):ARE結合タンパク質であるZFP36LやZFL36L1は、標的mRNA上にCCR4-NOT複合体をリクルートし、脱アデニル化を介したmRNA分解を惹起し、遺伝子発現を負に調節する。本研究では、AREを有するInterleukin-6 (IL-6) の3'-UTRを組み込んだレポーターmRNAとZFL36L1を過剰発現させた細胞抽出液を用いたin vitro実験系を構築し、解析を行なった。その結果、ZFL36L1がmiRISC同様に脱アデニル化非依存的に翻訳を抑制すること、さらにmiRISCと異なり翻訳開始複合体の形成は阻害せず翻訳を抑制することが明らかとなった。研究成果の概要(英文):We show that ZFP36L1 represses translation initiation, and demonstrate that this effect is independent of deadenylation mediated by the ARE. Strikingly, ZFP36L1-mediated translation repression nevertheless requires interaction between ZFP36L1 and CNOT1. Moreover, the eIF4F complex remains bound to the mRNA even in the presence of ZFP36L1. These observations imply that ZFP36L1-mediated repression of translation initiation differs fundamentally from the mechanism used by miRISC. Moreover, we find that translational repression by ZFP36L1 is also independent of 4EHP, despite this being a key factor for translation repression by ZFP36L. Collectively, our results highlight surprising diversity of regulatory mechanisms used by ARE-BPs and factors that interact with the CCR4/NOT co-factor complex. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究種目:基盤研究(B); 研究期間:2016~2018; 課題番号:16H04745; 研究分野:翻訳制御; 科研費の分科・細目: | |||||
資源タイプ(WEKO2) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Research Paper | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | application/pdf |