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Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
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ESCRT-IIIは,MLKLのダウンストリームで,ネクロプトシス細胞死とその結果を調節する
Yi-Nan Gong1, Cliff Guy1, Hannes Olauson2
1Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Cell
|April 8, 2017
まとめ
受容体相互作用タンパク質キナーゼ3 (RIPK3) は混合系キナーゼ型 (MLKL) を活性化し,死滅時に細胞膜の破壊を引き起こします. ESCRT-III装置は,プラズマ膜の完全性を管理し,CD8+T細胞の反応を促進します.
科学分野:
- 細胞生物学
- 免疫学
- 生物化学
背景:
- 受容体相互作用タンパク質キナーゼ3 (RIPK3) は混合系キナーゼ型 (MLKL) を活性化させ,制御性ネクロスの形態であるネクロプトーシスを引き起こします.
- ネクロプトーシスは,プラズマ膜 (PM) の破壊によって特徴付けられます.
研究 の 目的:
- MLKLの活性化と死滅の過程における一連の出来事を調査する.
- ESCRT-IIIメカニズムの死滅における役割とその結果について説明する.
主な方法:
- 細胞の死滅を観察した研究
- カルシウム流入とフォスファティジルセリンの暴露の分析
- ESCRT-III機構の役割を調査する.
主要な成果:
- MLKLの活性化により,PMの整合性が失われる前に,カルシウム流入とフォスファティジルセリンの露出が引き起こされます.
- MLKLの活性化により,露出したフォスファディチルセリンの流出プラズマ膜"泡"が生成されます.
- ESCRT-III装置は,バブル形成に不可欠であり,プラズマ膜の整合期間を調節する.
- 死体におけるESCRT- IIIの作用は,ケモカイン発現とCD8+T細胞のクロスプライミングを促進する.
結論:
- ESCRT-III機構は,死滅時に血の完全性を管理する上で重要な役割を果たします.
- T細胞の活性化を含む免疫反応にESCRT-III媒介のプロセスが寄与する.
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