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肌醇1,3,4,5-四磷酸增加了肌醇1,4,5-三磷酸介导的钙离子瞬变的持续时间。

Inositol 1,3,4,5-tetrakisphosphate increases the duration of the inositol 1,4,5-trisphosphate-mediated Ca2+ transient.

作者信息

Joseph S K, Hansen C A, Williamson J R

出版信息

FEBS Lett. 1987 Jul 13;219(1):125-9. doi: 10.1016/0014-5793(87)81203-6.

DOI:10.1016/0014-5793(87)81203-6
PMID:3496245
Abstract

The effect of Ins 1,3,4,5-P4 on the intracellular Ca2+ mobilization produced by Ins 1,4,5-P3 has been examined in permeabilized hepatocytes. Ins 1,3,4,5-P4 did not affect the magnitude of the Ins 1,4,5-P3-mediated Ca2+ release but did inhibit re-accumulation of the released Ca2+ back into intracellular stores. This effect was not mimicked by Ins 1,3,4-P3. In hepatocytes, the re-uptake phase of the response results from Ins 1,4,5-P3 hydrolysis. Measurements using labeled substrates indicate that Ins 1,3,4,5-P4 inhibits the hydrolysis of Ins 1,4,5-P3 and vice versa. Since the removal of the 5-phosphate on Ins 1,4,5-P3 and Ins 1,3,4,5-P4 is a common step in the disposal of both compounds, it is suggested that one of the biological effects of Ins 1,3,4,5-P4 may be to slow hydrolysis of Ins 1,4,5-P3 and thereby prolong the duration of a Ca2+ transient.

摘要

已在通透化肝细胞中研究了肌醇1,3,4,5 -四磷酸(Ins 1,3,4,5 -P4)对肌醇1,4,5 -三磷酸(Ins 1,4,5 -P3)所产生的细胞内钙离子动员的影响。Ins 1,3,4,5 -P4不影响Ins 1,4,5 -P3介导的钙离子释放幅度,但确实抑制了释放的钙离子重新积累回细胞内储存库。Ins 1,3,4 -P3未模拟出这种效应。在肝细胞中,反应的再摄取阶段源于Ins 1,4,5 -P3的水解。使用标记底物的测量表明,Ins 1,3,4,5 -P4抑制Ins 1,4,5 -P3的水解,反之亦然。由于去除Ins 1,4,5 -P3和Ins 1,3,4,5 -P4上的5 -磷酸是这两种化合物代谢的共同步骤,因此有人提出Ins 1,3,4,5 -P4的生物学效应之一可能是减缓Ins 1,4,5 -P3的水解,从而延长钙离子瞬变的持续时间。

相似文献

1
Inositol 1,3,4,5-tetrakisphosphate increases the duration of the inositol 1,4,5-trisphosphate-mediated Ca2+ transient.肌醇1,3,4,5-四磷酸增加了肌醇1,4,5-三磷酸介导的钙离子瞬变的持续时间。
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