アデノウイルスE1Aタンパク質による転写因子IIICの活性化
W K Hoeffler1, R Kovelman, R G Roeder
1Laboratory of Biochemistry and Molecular Biology, Rockefeller University, New York, New York 10021.
Cell
|June 17, 1988
まとめ
アデノウイルスE1Aは,転写因子IIIC (TFIIIC) を変えてRNAポリメラーゼIIIの転写を活性化します. TFIIICのリン酸化により,より活性な形態が作られ,ウイルス感染中に遺伝子発現が強化されます.
科学分野:
- 分子生物学は分子生物学である.
- ウイルス学 ウイルス学 ウイルス学
- 遺伝子規制 遺伝子規制
背景:
- アデノウイルスE1Aタンパク質は,RNAポリメラーゼIII遺伝子の転写を刺激することが知られている.
- 以前の研究では,トランスクリプション因子IIIC (TFIIIC) に責任因子を局所化した.
研究 の 目的:
- アデノウイルスE1A媒介の転写に関与するTFIIICの特定の形態を調査する.
- TFIIICの活動を規制するメカニズムを解明する.
主な方法:
- TFIIICの染色学的な分離により,異なる形状に分けられる.
- VA遺伝子-タンパク質複合体を分析するためのゲルシフトアッセイ.
- In vitroトランスクリプションアッセイは,トランスクリプションの活動を測定するものです.
- TFIIICのフォームの相互変換を評価するために,フォスファターゼ処理を行います.
主要な成果:
- 2つの分離可能なTFIIICの形態が特定され,VA遺伝子-タンパク質複合体を形成する能力によって異なる.
- より活発なTFIIIC形態は,より迅速なプロモーター結合と塩への抵抗性の増加と関連していました.
- E1A発現または血清濃度の上昇は,活性TFIIIC形態のレベルを高めました.
- TFIIICの総濃度は,ウイルス感染中に一定でした.
結論:
- アデノウイルスE1AによるRNAポリメラーゼIII遺伝子の転写活性化は,TFIIICの異なる形態によって媒介されます.
- TFIIICのリン酸化は,TFIIICの活動を制御する重要な規制メカニズムです.
- このリン酸化イベントは,ウイルスの遺伝子発現におけるTFIIICの役割を強化する.
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