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Ras-Erk-ETS-シグナル伝達経路は長寿のための薬物のターゲットです

Cathy Slack¹, Nazif Alic², Andrea Foley²

¹Institute of Healthy Ageing, Department of Genetics, Evolution, and Environment, University College London, Darwin Building, Gower Street, London WC1E 6BT, UK; Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9b, 50931 Cologne, Germany.

|June 30, 2015

まとめ

科学者は,Ras-Erk-ETS経路を阻害することで,フルーツハエの寿命を延長することがわかった. 前部オープン (Aop) を含むこの経路は,ヒトのアンチエイジング薬の潜在的なターゲットを提供します.

科学分野:

分子生物学は分子生物学である.
遺伝学遺伝学とは
老化に関する研究.

背景:

老化メカニズムを理解することは,人間の健康にとって極めて重要です.
インスリン/IGF-1シグナル伝達 (IIS) 経路は,老化に関連しています.
薬理学的介入は,潜在的に老化プロセスを調節することができます.

研究の目的:

ドロソフィラの老化の分子メカニズムを特定する.
Ras-Erk-ETSシグナル伝達の老化における役割を調査する.
寿命延長のためのこの経路の薬理学的ターゲティングを探求する.

主な方法:

ドロソフィラのRas,Erk,およびAnterior open (Aop) の遺伝子操作.
縮小されたIISのダウンストリームでの寿命延長の分析.
Ras-Erk-ETS阻害剤であるトラメチニブを成虫に投与する.

主要な成果:

Rasの阻害は寿命延長に十分である.
減少したRasまたはErkの活動は,寿命を直接延長します.
ETS抑制器Aopは,寿命の延長に中心的な役割を果たしています.
トラメチニブの大人発症投与は寿命を延ばします.

結論:

Ras-Erk-ETS経路は,ドロソフィラの老化の重要な調節因子である.
Ras-Erk-ETSシグナリングを阻害することは,寿命延長のための実行可能な戦略です.
この経路は,哺乳類におけるアンチエイジング介入の有望な薬理学的標的である.

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