InIBに依存するリステリアの内部化は,メット受容体チロシンキナーゼによって媒介されます
1Department of Medical Genetics and Microbiology, University of Toronto, Ontario, Canada.
Cell
|November 18, 2000
まとめ
Listeria monocytogenesの表面タンパク質InlBは,宿主メット受容体チロシンキナーゼ (RTK) をハイジャックし,細菌の侵入を促進する. この研究は,InlB媒介による哺乳類の細胞への侵入に不可欠な細胞受容体であるMetを特定しています.
科学分野:
- 微生物学 微生物学とは
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- Listeria monocytogenesは,宿主細胞に侵入する細胞内病原体です.
- 表面タンパク質InlBは,細菌が哺乳類の細胞に侵入するのを促進する.
- InlB媒介によるエントリーの特定の宿主細胞受容体は,以前は知られていなかった.
研究 の 目的:
- InlBがバクテリアの侵入に利用する細胞表面受容体を特定する.
- InlBが侵入を媒介するメカニズムを解明する.
- InlBとその宿主受容体との相互作用を特徴付ける.
主な方法:
- 哺乳類の細胞をInlBタンパク質とL. monocytogenes感染で治療する.
- レセプターチロシンキナーゼ (RTK) であるメットのチロシンリン酸化の分析.
- Met陽性とMet欠乏性の細胞系を用いた実験.
主要な成果:
- InlBがMetと結合すると,チロシンリン酸化と上皮細胞の分散を誘導し,ヘパトサイト成長因子 (HGF) に似ています.
- Metは,L. monocytogenesのInlB依存性エントリーに不可欠であることが判明しました.
- InlBは,新しいメットアゴニストとして機能します.
結論:
- Metは,Listeria monocytogenesのInlB媒介の侵入に必要な細胞受容体である.
- InlBは,宿主メット受容体のチロシンキナーゼ経路を利用して,細菌の侵入を容易にします.
- これは,宿主-病原体相互作用と細菌の侵入の新しいメカニズムを特定します.
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