BPV-1によってエンコードされた転写抑制剤は,E2トランザクティベーターと共通のカルボキシ端末ドメインを共有しています
Cell
|July 3, 1987
まとめ
研究者らは,細胞変容を阻害する,ボウインパピローマウイルス1型 (BPV-1) の調節因子を特定した. E2開いた読み取りフレームで暗号化されたこの負の作用因子は,ウイルスの遺伝子発現と変異を抑制します.
科学分野:
- ウイルス学 ウイルス学 ウイルス学
- 分子生物学は分子生物学である.
- がん研究 がん研究
背景:
- 牛のパピローマウイルス1型 (BPV-1) は,腫瘍を引き起こすことが知られている.
- ウイルスの遺伝子発現と調節は,BPV-1誘発の細胞変異に不可欠です.
研究 の 目的:
- BPV-1によってコード化された,負の作用を持つ転写制御因子を特定し,特徴づけること.
- BPV-1が自身の変換活動を調節するメカニズムを解明する.
主な方法:
- 機能的アッセイを通して,負の作用の要因を特定する.
- マウスC127細胞のBPV-1変異の分析.
- 抑制機能のプラズミドベースの発現.
- E2開いた読み取りフレームの3'ドメインへの抑制機能のマッピング.
主要な成果:
- BPV-1によって暗号化された負の作用の転写制御因子を特定しました.
- この因子は,特にマウスC127細胞のBPV-1媒介による変容を阻害する.
- この因子は,共有されたシス作用要素を通じて,BPV-1増強剤のE2トランザクティベーションを抑制する.
- 変換の阻害は,E2依存ウイルス遺伝子発現のダウンレギュレーションと相関する.
結論:
- BPV-1のE2開いた読み取りフレームは,陽性と陰性の両方をコードします.
- これらの規制要因は,共通のカーボキシ端末領域を共有しています.
- BPV-1は自己調節メカニズムを持ち,そのE2タンパク質を介して変換を制御します.
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