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通透化肝细胞中由肌醇1,4,5-三磷酸刺激引起的量子化Ca2+动员。

Quantal Ca2+ mobilization stimulated by inositol 1,4,5-trisphosphate in permeabilized hepatocytes.

作者信息

Oldershaw K A, Nunn D L, Taylor C W

机构信息

Department of Pharmacology, University of Cambridge, U.K.

出版信息

Biochem J. 1991 Sep 15;278 ( Pt 3)(Pt 3):705-8. doi: 10.1042/bj2780705.

Abstract

In several cell types, including hepatocytes, submaximal concentrations of Ins(1,4,5)P3 stimulate an initial rapid mobilization of intracellular Ca2+ stores that is followed by either no further Ca2+ release or very much slower release. Further additions of Ins(1,4,5)P3 then evoke further Ca2+ mobilization. Such 'incremental' responses [Meyer & Stryer (1990) Proc. Natl. Acad. Sci. U.S.A. 87, 3841-3845] could result from all-or-nothing emptying of stores that differ in their sensitivities to Ins(1,4,5)P3 or from partial emptying of stores that are more uniformly sensitive, but unable to release all of their Ca2+ because the response to Ins(1,4,5)P3 rapidly attenuates. By measuring unidirectional 45Ca2+ efflux from intracellular stores stimulated with Ins(1,4,5)P3 under conditions where they continue to sequester 40Ca2+, we provide evidence suggesting that Ins(1,4,5)P3 stimulates all-or-nothing emptying of stores that differ in their sensitivities to Ins(1,4,5)P3, a quantal response pattern.

摘要

在包括肝细胞在内的几种细胞类型中,亚最大浓度的肌醇-1,4,5-三磷酸(Ins(1,4,5)P3)会刺激细胞内钙库最初快速释放钙离子,随后要么不再有钙离子释放,要么释放速度非常缓慢。进一步添加Ins(1,4,5)P3会引发更多的钙离子动员。这种“增量”反应[迈耶尔和斯特里尔(1990年),《美国国家科学院院刊》87卷,3841 - 3845页]可能是由于对Ins(1,4,5)P3敏感性不同的钙库全部排空或部分排空所致,其中部分排空的钙库对Ins(1,4,5)P3的敏感性较为一致,但由于对Ins(1,4,5)P3的反应迅速减弱,无法释放其所有的钙离子。通过在细胞内钙库持续摄取40Ca2+的条件下,测量由Ins(1,4,5)P3刺激引起的单向45Ca2+流出,我们提供的证据表明,Ins(1,4,5)P3刺激对Ins(1,4,5)P3敏感性不同的钙库全部排空,这是一种量子反应模式。

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