抑圧から活性化への切り替え:マイクロRNAは,翻訳を上位調節することができる
Shobha Vasudevan1, Yingchun Tong, Joan A Steitz
1Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536, USA.
まとめ
マイクロRNA (miRNA) は,メッセンジャーRNA (mRNA) のAU豊富な元素 (AREs) に結合することによって,細胞サイクル停止中に遺伝子翻訳を活性化することができます. マイクロリボヌクレオプロテイン (miRNP) のこの活性化機能は,細胞増殖とともに振動するようです.
科学分野:
- 分子生物学は分子生物学である.
- 遺伝子規制 遺伝子規制
- トランスクリプション後のコントロール
背景:
- mRNA 3'UTRs内のAU豊富な元素 (AREs) とマイクロRNA標的サイトは,遺伝子発現を転写後的に調節する.
- 細胞サイクル停止の間,腫瘍死滅因子-アルファ (TNFalpha) のmRNAのAREsは,アルゴナウト (AGO) と脆弱なX精神遅延関連タンパク質1 (FXR1) を採用し,マイクロリボヌクレオプロテイン (miRNP) を形成します.
研究 の 目的:
- 翻訳活性化のためのAREsとタンパク質関連を誘導するマイクロRNAmiR369-3の役割を調査する.
- 他のマイクロRNAが細胞サイクル停止および増殖の間に同様の翻訳調節パターンを示すかどうかを判断する.
主な方法:
- miR369-3とAREおよび関連するタンパク質 (AGO,FXR1) の相互作用を調査した.
- 細胞サイクル停止と増殖の間にLet-7とmiRcxcr4によって標的mRNAの翻訳調節を分析した.
主要な成果:
- 人間のマイクロRNA miR369-3は,AREsへのAGOとFXR1の採用を指示し,mRNA翻訳を活性化します.
- Let-7とmiRcxcr4は,細胞サイクル停止時に標的mRNA翻訳を上位に調節するが,増殖細胞ではそれを抑制する.
- miRNPによる翻訳活性化は,細胞サイクル停止中に観察される一般的な機能です.
結論:
- マイクロRNA媒介による翻訳活性化は,細胞サイクル停止の際に重要なメカニズムです.
- マイクロRNA-リボヌクレオプロテイン (miRNP) 媒介による翻訳調節は,細胞サイクル全体で抑制と活性化との間の振動パターンを表しています.
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