INOSITOL 1,3,4,5-TETRAKISPHOSPHATE ACTIVATES AN ENDOTHELIAL CA2+-PERMEABLE CHANNEL
INOSITOL 1,3,4,5-TETRAKISPHOSPHATE ACTIVATES AN ENDOTHELIAL CA2+-PERMEABLE CHANNEL
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DOI：
10.1038/355356a0
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发表时间：
1992-01-23
期刊：
影响因子：
64.8
通讯作者：
CLAPHAM, DE
中科院分区：
文献类型：
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作者：
LUCKHOFF, A;CLAPHAM, DE
在大多数哺乳动物细胞中，受体介导的胞质游离钙离子浓度增加是由于细胞内储存的 Ca2+ 动员以及跨膜 Ca2+ 流入造成的。肌醇 1,4,5-三磷酸 (InsP3) 通过打开内质网 2-4 中的 Ca2+ 渗透通道，从细胞内储存 1 中释放钙。但 Ca2+ 进入非兴奋细胞的机制和调节仍然难以捉摸，因为进入途径尚未明确。在这里，我们描述了内皮细胞中新型肌醇 1,3,4,5-四磷酸 (InsP4) 和 Ca2+ 敏感的 Ca2+ 通透通道。我们发现，InsP4 会诱导 Ca2+ 流入腺泡细胞 5,6，当暴露于内皮细胞内向外斑块的细胞内表面时，会增强 Ca2+ 通透通道的活性。我们的结果表明一种分子机制可能对受体介导的 Ca2+ 进入很重要。
RECEPTOR-MEDIATED increases in the cytosolic free calcium ion concentration in most mammalian cells result from mobilization of Ca2+ from intracellular stores as well as transmembrane Ca2+ influx. Inositol 1,4,5-trisphosphate (InsP3) releases calcium from intracellular stores 1 by opening a Ca2+-permeable channel in the endoplasmic reticulum 2-4. But the mechanism and regulation of Ca2+ entry into nonexcitable cells has remained elusive because the entry pathway has not been defined. Here we characterize a novel inositol 1,3,4,5-tetrakisphosphate (InsP4) and Ca2+-sensitive Ca2+-permeable channel in endothelial cells. We find that InsP4, which induces Ca2+ influx into acinar cells 5,6, enhances the activity of the Ca2+-permeable channel when exposed to the intracellular surface of endothelial cell inside-out patches. Our results suggest a molecular mechanism which is likely to be important for receptor-mediated Ca2+ entry.