異なったウイルス誘導性増強剤の要素間の転写シネジズムメカニズム
1Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, Massachusetts 02138.
Cell
|September 10, 1993
まとめ
高流動性グループタンパク質HMG I(Y) は,インターフェロンベータ遺伝子調節に不可欠です. 転写因子NF-kappa Bとの相互作用を促進し,転写因子2 (ATF-2) を活性化することによって,ウイルス誘導性要素PRDIIとPRDIVの活性を強化します.
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
- 免疫学 免疫学とは
背景:
- ヒトのインターフェロンベータ遺伝子プロモーターには,ウイルス誘導性調節要素が含まれています.
- 陽性調節領域II (PRDII) の活動には,高流動性グループタンパク質HMG I(Y) と転写因子NF-kappa Bが必要です.
研究 の 目的:
- PRDIVの活動におけるHMG I(Y) の役割を調査する.PRDIVはPRDIIと連携する規制要素である.
- HMG I(Y) がトランスクリプションのシナジーに寄与する分子メカニズムを解明する.
主な方法:
- タンパク質とDNAの相互作用を研究するための電泳運動シフトアッセイ (EMSA).
- 共同免疫プレシピテーションは,タンパク質とタンパク質の相互作用を分析するための測定法です.
- ウイルス誘導に対するレギュレータ要素の活性分析.
主要な成果:
- HMG I(Y) は,PRDIVの活動に不可欠であり,PRDIIと連携して働く.
- HMG I(Y) は,活性化転写因子2 (ATF-2) の結合と,ATF-2とc-Jun.を含む誘導性複合体の組み立てを促進する.
- HMG I(Y) はATF-2のレウシンジッパー/ベース領域と直接相互作用し,ATF-2はNF-カッパBと相互作用する.
結論:
- HMG I(Y) は,PRDIIとPRDIVのトランスクリプションの連携を確立する上で重要な構造的役割を果たしています.
- HMG I(Y) は,NF-kappa BとATF-2の相互作用を促進し,それによってそれらの活動を促進し,または拘束します.
- このメカニズムは,インターフェロンベータ遺伝子のウイルス誘導性発現に不可欠です.
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