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ソマトスタチンは,タンパク質の脱リン酸化によってCa(2+) 活性化されたK+チャネルを刺激します

R E White¹, A Schonbrunn, D L Armstrong

¹Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.

|June 13, 1991

まとめ

ニューロペプチドであるソマトスタチンは,下垂体腫瘍細胞における大導電性カリウムチャネル (BK) を活性化します. この活性化は,直接的なイオンまたはGタンパク質の影響ではなく,タンパク質の脱リン酸化によって起こります.

科学分野:

神経内分泌学の神経内分泌学
細胞生理学細胞生理学
分子生物学は分子生物学である.

背景:

ソマトスタチンは,様々な組織における分泌を調節する神経ペプチドです.
pituitary腫瘍細胞では,ソマトスタチンは2つの pertussis toxin 敏感経路経由で分泌を抑制する.
1つの経路はアデニリルサイクラスを阻害し,もう1つは,Ca2+流入に影響するcAMP独立したメカニズムである.

研究の目的:

下垂体腫瘍細胞におけるソマトスタチンの作用の主な電気生理学的メカニズムを解明する.
ソマトスタチンの抑制作用に関与する特定のイオンチャンネルとシグナル伝達経路を特定する.

主な方法:

代謝的に健全な哺乳類の垂体下垂体腫瘍細胞からの電気生理学的記録.
ソマトスタチンがイオンチャネル活動に及ぼす影響の調査.
ソマトスタチンシグナル伝達におけるCa2+,cAMP,Gタンパク質の役割の分析.

主要な成果:

ソマトスタチンは,大導電性Ca2+と電圧活性化K+チャネル (BK) の活性を著しく増加させます.
このソマトスタチン誘発のBKチャネル活性化は,Ca2+,cAMP,またはGタンパク質からの直接的な影響とは無関係です.
主要なメカニズムは,タンパク質脱リン酸化を通してBKチャネル活動を刺激するソマトスタチンを含む.

結論:

下垂体腫瘍細胞におけるソマトスタチンの主要な電気生理学的効果は,BKチャネルの刺激である.
タンパク質の脱リン酸化は,BKチャネルに対するソマトスタチンの作用を媒介する重要なシグナルイベントとして特定されています.
この発見は,ソマトスタチンのこれまで未確認のcAMP独立メカニズムを明らかにしています.

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