皮膚表皮成長因子受容体は,アデノウイルスのE3領域によって暗号化された10,400MWのタンパク質によってダウン調節されます
C R Carlin1, A E Tollefson, H A Brady
1Institute for Molecular Virology, St. Louis University Medical Center, Missouri 63110.
Cell
|April 7, 1989
まとめ
人間のアデノウイルスは,感染中に表皮成長因子受容体 (EGF-Rs) を下調調節する. 特定のウイルスタンパク質がEGF-Rの内部化と分解を誘発し,新しい相互作用メカニズムを示唆しています.
科学分野:
- 細胞生物学 細胞生物学
- 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.
背景:
- Epidermal growth factor (EGF) のシグナル伝達には,受容体 (EGF-R) の内部化とリソソーム分解が含まれています.
- ウイルス感染症は,受容体密輸を含む宿主細胞のプロセスを調節することができます.
研究 の 目的:
- ヒトアデノウイルス感染中に表皮成長因子受容体 (EGF-R) のダウンレギュレーションのメカニズムを調査する.
- EGF-Rの調節に責任を負うウイルス遺伝子を特定する.
主な方法:
- グループCのヒトアデノウイルスの消去変異体を使用した.
- EGF-Rレベルと人身売買に対するウイルス遺伝子産物の影響を分析した.
- ウイルスのタンパク質とEGF-R.との間のシーケンスホモロジー分析を行った.
主要な成果:
- グループCのヒトアデノウイルスは,感染した細胞におけるEGF-Rのダウンレギュレーションを誘導する.
- E3トランスクリプションユニットは,EGF-Rの内部化と分解を司る10.4Kタンパク質をコードする.
- 10.4Kタンパク質はEGF-Rと配列の類似性を共有しており,ヘテロオリゴーマー形成を示唆しています.
結論:
- アデノウイルス感染症中のEGF-Rのダウンレギュレーションのための新しいメカニズムには,ウイルスのE3タンパク質が含まれています.
- ウイルスの10.4Kタンパク質は,EGF-Rと相互作用して,EGF-Rの分解を媒介する可能性があります.
- この相互作用は,ウイルスタンパク質と宿主受容体の間でヘテロオリゴメアの形成を伴う可能性があります.
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