ソマティック・プロ・アポプトティック・シグナリングの逆行的な活性化によってゲートされたアクソン退化
David J Simon1, Jason Pitts1, Nicholas T Hertz1
1Laboratory of Brain Development and Repair, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Cell
|February 23, 2016
まとめ
細胞体はアクソンだけでなく アクソン退化も 積極的に制御しています 細胞体に逆行信号を誘発し,軸索の除去を開始します.
科学分野:
- 神経科学
- 細胞生物学
- 発達生物学
背景:
- 感覚軸索の発達には神経栄養因子に対する競争が伴う.
- 局所ニューロトロフィンの欠乏は通常,カスパースに依存する軸索変性を引き起こす.
- 既存のモデルは,軸索変性シグナル伝達が軸索自体の中に存在することを示唆しています.
研究 の 目的:
- ニューロトロフィン欠乏による軸索変異の調節における細胞体の役割を調査する.
- アクソン変性に関わる信号経路を解明する.
主な方法:
- 感覚軸索変性におけるシグナル伝達経路を調査した.
- 細胞体とアポプトシス機構の役割に焦点を当てた
主要な成果:
- 局所的な欠乏によるアクソン退化は,細胞体によって積極的に制御される.
- トロフィックサポーターの喪失は 細胞体に逆行信号を発信します
- 細胞体はプロアポプトティックなPumaをアップレギュレーションし,それは細胞体に限定されます.
- PumaはBcl-xLとBcl-wの阻害を克服し,アンテログラッドのプロデジェネレーションシグナリングを開始します.
結論:
- 細胞体は軸索の退化に 重要な門番です
- 欠乏した軸索からの逆行信号が体内アポプトシス経路を活性化します
- 細胞体はPumaのようなアンテログラード因子を介して軸索の除去をオーケストラします
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