エフリンBsは,ニューロンの移動を調節するReelin経路の重要な構成要素です

Aycan Sentürk¹, Sylvia Pfennig, Alexander Weiss

¹Frankfurt Institute for Molecular Life Sciences and Institute of Cell Biology and Neuroscience, Goethe University Frankfurt, Max-von-Laue-Str. 9, D-60438, Frankfurt am Main, Germany.

Nature

|April 5, 2011

まとめ

エフリンBタンパク質は,発達中の脳におけるニューロン移動を誘導するリリン信号伝達に不可欠です. エフリンBsを活性化することで,リーリン欠乏に関連した移住欠陥を修正することができます.

科学分野:

神経科学は神経科学である.
発達生物学発達生物学について
分子生物学は分子生物学である.

背景:

協調されたニューロン移動は,脳の機能にとって不可欠です.
リーリン (RELN) タンパク質とその受容体 (VLDLR,ApoER2) は,ニューロン移動を誘導し,その損失がリセンセファリーやその他の神経学的障害を引き起こす.
Reelinシグナル伝達の正確な分子機構は,ほとんど不明のままである.

研究の目的:

Reelinシグナル伝達とニューロン移動におけるエフリンBタンパク質の役割を調査する.
脳の発達におけるエフリンBsとリーリンを結びつける分子メカニズムを解明する.

主な方法:

複合マウスミュータント (Reln(+/-); Efnb3(-/-),Reln(+/-); Efnb2(-/-)) とトリプルエフリンBノックアウトの遺伝子解析.
エフリンBsへのリリンの結合と受容体複合体の形成を研究する生化学的分析.
Dab1のリン酸化と救出実験の分析.

主要な成果:

エフリンBタンパク質はReelinと遺伝的に相互作用し,Reelinのシグナル伝達に不可欠です.
リエリンはエフリンBsと結合し,VLDLRとApoER2と結合し,Dab1のリン酸化を引き起こします.
エフリンB機能の喪失は,リーリン誘発のDab1リン酸化を損なう.
エフリンBの活性化により,リーリン欠乏に関連するニューロン移動の欠陥を救済する.

結論:

エフリンBタンパク質は,リーリン受容体とシグナル伝達経路の重要な構成要素です.
エフリンBsは,神経系の発達中に神経細胞の移動を制御する上で重要な役割を果たします.
エフリンB経路を標的にすることは,リーリンシグナル伝達欠陥に関連した神経学的疾患の治療の可能性を提供します.

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