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由肌醇-3,4,5,6-四磷酸门控的钙离子流入NIH/3T3成纤维细胞。

Ca2+ influx gated by inositol-3,4,5,6-tetrakisphosphate in NIH/3T3 fibroblasts.

作者信息

Hashii M, Hirata M, Ozaki S, Nozawa Y, Higashida H

机构信息

Department of Biophysics, Kanazawa University School of Medicine, Japan.

出版信息

Biochem Biophys Res Commun. 1994 May 16;200(3):1300-6. doi: 10.1006/bbrc.1994.1592.

Abstract

The functional role of three inositol tetrakisphosphate isomers on Ca2+ influx was examined by intracellular application in NIH/3T3 mouse fibroblasts. Infusion of inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), inositol-1,3,4,6- tetrakisphosphate, and inositol-3,4,5,6-tetrakisphosphate (Ins(3,4,5,6)P4) from the patch pipette into the cytoplasm produced a transient increase in cytoplasmic free Ca2+ concentration by fura-2 recording in extracellular Ca(2+)-dependent fashion. Stimulation of NIH/3T3 cells with bradykinin increased the levels of Ins(1,3,4,5)P4 and Ins(3,4,5,6)P4. These results suggest that mouse fibroblast cells possess a Ca2+ influx pathway gated with naturally occurring inositol tetrakisphosphates in response to stimulation with bradykinin.

摘要

通过在NIH/3T3小鼠成纤维细胞中进行细胞内注射,研究了三种肌醇四磷酸异构体对Ca2+内流的功能作用。从膜片吸管向细胞质中注入肌醇-1,3,4,5-四磷酸(Ins(1,3,4,5)P4)、肌醇-1,3,4,6-四磷酸和肌醇-3,4,5,6-四磷酸(Ins(3,4,5,6)P4),通过fura-2记录以细胞外Ca(2+)依赖的方式使细胞质游离Ca2+浓度产生短暂升高。用缓激肽刺激NIH/3T3细胞会增加Ins(1,3,4,5)P4和Ins(3,4,5,6)P4的水平。这些结果表明,小鼠成纤维细胞拥有一条Ca2+内流途径,该途径在缓激肽刺激下由天然存在的肌醇四磷酸门控。

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