60SリボソームサブユニットからのL13aの規制された放出は,トランスクリプト特異的な翻訳制御のメカニズムとして機能する
Barsanjit Mazumder1, Prabha Sampath, Vasudevan Seshadri
1Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Cell
|October 22, 2003
まとめ
新しいトランスレーションサイレンシングメカニズムにより,リボソームタンパク質L13aが,リン酸化により,セルロプラズミンmRNAに結合することを明らかにした.
科学分野:
- 分子生物学は分子生物学である.
- 細胞生物学 細胞生物学
- バイオケミストリー バイオケミストリー
背景:
- トランスクリプト特異的翻訳制御は,mRNAの未翻訳領域 (UTR) を結合するタンパク質に依存する.
- インターフェロン・ガンマ活性化翻訳阻害剤 (GAIT) システムは,転写後の遺伝子発現を調節する.
研究 の 目的:
- リボソームタンパク質L13aを含む新しいトランスレーションサイレンシングメカニズムの解明.
- セルロプラズミン (Cp) mRNA翻訳の調節におけるL13aの役割を調査する.
主な方法:
- Cp3'-UTR結合タンパク質を特定するための遺伝子スクリーニング.
- リコンビナントL13aを用いたインビトロ翻訳アッセイ.
- インターフェロン-ガンマ刺激とL13aのリン酸化とリボソームサブユニット放出の分析を含むインビボ試験.
主要な成果:
- 人間のリボソームタンパク質L13aは,Cp mRNAのGAITとして特定されました.
- リコンビナントL13aはCp mRNAの翻訳を in vitroで阻害しました.
- インターフェロン-ガンマ誘導によるL13aのリン酸化と60Sリボソームサブユニットからの放出.
- 放出されたL13aは,Cp mRNA 3'-UTR GAIT要素に特異的に結合し,翻訳を静止する.
結論:
- リボソームは,翻訳を調節する調節タンパク質の貯蔵庫として機能する.
- リボソームタンパク質L13aの調節された放出は,トランスレーションサイレンシングの重要なメカニズムです.
- この発見は,タンパク質合成を超えて,リボソームタンパク質の既知の機能を拡張します.
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