Na+,K(+) -ATPASEの細胞表面分布をポリラ化された上皮細胞で調節するメカニズム
R W Hammerton1, K A Krzeminski, R W Mays
1Department of Molecular and Cellular Physiology, Stanford University School of Medicine, CA 94305-5426.
Science (New York, N.Y.)
|November 8, 1991
まとめ
偏極化した上皮細胞は,タンパク質を標的とするだけでなく,選択的な酵素の保持と損失を通じて,ナトリウム,カリウム,アデノシン・トリフォスファターゼ (Na+,K,K,K+) -ATPASE) の分布を維持する. これは,健康と病気におけるイオン輸送に影響を与えます.
科学分野:
- 細胞生物学 細胞生物学
- 生理学 生理学とは
- バイオケミストリー バイオケミストリー
背景:
- 偏極化された上皮細胞は,ベクトル輸送に不可欠なドメイン特異のタンパク質局所化を示します.
- ナトリウム・カリウム・アデノシン・トリフォスファタゼ (Na+,K(+) -ATPase) は,細胞機能に不可欠な重要なイオンポンプである.
研究 の 目的:
- ポラライズされた上皮細胞におけるNa+,K(+) -ATPaseの制限された膜分布を生成するメカニズムを調査する.
- Na+,K(+) -ATPase局所化のためのタンパク質ターゲティングとタンパク質保持/無活性化モデルを区別する.
主な方法:
- Madin-Darby犬腎臓 (MDCK) の上皮細胞をモデルシステムとして利用した.
- 異なる膜領域におけるNa+,K(+) -ATPaseの分布と活性を実験的に評価した.
- 新しく合成されたNa+,K(+) -ATPaseサブユニットの運命を調査した.
主要な成果:
- Na+,K(+) -ATPaseの活動は,好ましくは基礎側膜領域に留まっていました.
- 活性酵素は選択的に不活性化され,アピカル膜領域から失われました.
- ゴルギから新たに合成されたNa+,K(+) -ATPaseのベクトル標的化は,基礎側部局在化の主なメカニズムではなかった.
結論:
- 極化性表皮細胞におけるNa+,K(+) -ATPaseの制限された分布は,直接的な取引によるものではなく,合成後の調節 (保持および不活性化) に起因する.
- これらのメカニズムを理解することは,上皮機能とイオン輸送欠陥に関連する疾患状態を理解するために不可欠です.
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