貯蔵されたCa2+のエントリー:分泌物のような結合モデルの証拠
R L Patterson1, D B van Rossum, D L Gill
1Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore 21201, USA.
Cell
|September 11, 1999
まとめ
この研究では,エンドプラズマ網膜 (ER) とプラズマ膜 (PM) が物理的,可逆的なメカニズムを通じて通信することを明らかにしました. アクチン細胞骨格の再編成は,このカルシウム (Ca2+) 信号伝達経路を混乱させるが,その正常な機能は回復することができる.
科学分野:
- 細胞生物学 細胞生物学
- カルシウムシグナル伝達
- 膜のダイナミクス
背景:
- エンドプラズマ網膜 (ER) のカルシウム (Ca2+) 貯蔵庫とプラズマ膜 (PM) のCa2+チャネルを結びつける正確なメカニズムは,まだ完全に理解されていません.
- 貯蔵式カルシウム入力 (SOCE) は,ER Ca2+貯蔵庫とPMチャネル間の通信によって規制される重要なプロセスです.
研究 の 目的:
- ER Ca2+ 貯蔵庫と PM Ca2+ 経路の結合を媒介する細胞骨格,特にアクチン繊維の役割を調査する.
- カルシウムシグナル伝達のためのERとPMの間の通信の物理的基礎を解明する.
主な方法:
- アクチンフィラメントの破壊と再分布を含む細胞骨格の改変を用いて,ER-PM結合を調査した.
- これらの改変がCa2+の入り口と,イノシトール1,4,5-トリスホスファート媒介の貯蔵放出に及ぼす影響を観察した.
主要な成果:
- アクチン細胞骨格の分解は,ER-PM結合に影響を与えなかった.
- F-アクチンの細胞皮質への再配分は,イノシトール1,4,5-トリスホスファート誘発のCa2+の放出に影響を与えることなく,結合を妨害し,Ca2+の侵入を防ぐため,ERを移動させた.
- アクチン皮質層形成の逆転により,ER-PMの接近性と結合が回復しました.
結論:
- ERとPMの間のカルシウム信号結合は,密接で可逆的な相互作用を含む物理的,分泌のようなメカニズムによって媒介されます.
- アクチン細胞骨格は,カルシウムの侵入のためにERとPMの接近と機能的結合を調節する上で重要な役割を果たします.
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