INOSITOL PHOSPHATE STRUCTURAL REQUISITES FOR CA2+ INFLUX
INOSITOL PHOSPHATE STRUCTURAL REQUISITES FOR CA2+ INFLUX
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DOI：
10.1152/ajpcell.1995.268.6.c1485
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发表时间：
1995-06-01
影响因子：
5.5
通讯作者：
WELSH, MJ
中科院分区：
文献类型：
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作者：
DELISLE, S;MAYR, GW;WELSH, MJ
为了了解肌醇磷酸（InsP）如何引起Ca 2+内流，我们注射了37个高度纯化的化合物，共含有49 InsP位置异构体到非洲爪蟾卵母细胞。8种InsP刺激Ca 2+内流是那些在释放细胞内Ca 2+方面具有最高效力的InsP，表明它们的共同靶点是肌醇1，4，5-三磷酸[Ins（1，4，5）P-3]受体。为了引起Ca 2+内流，这些InsP必须以比释放细胞内Ca 2+所需的最低浓度高得多的浓度注射。如此高的InsP浓度可以抑制持续振荡的细胞内Ca 2+释放。此外，我们发现InsPs不能引起进一步的细胞内Ca 2+释放过程中的Ca 2+内流。我们的数据与“容量性Ca 2+进入”假说一致，该假说指出InsP通过耗尽InsP敏感的细胞内Ca 2+库来刺激Ca 2+内流。在这种情况下，我们会建议，耗尽InsP敏感的细胞内Ca 2+商店，InsP可能必须以足够高的浓度存在，以覆盖振荡Ca 2+再填充机制的商店。
To understand how inositol phosphates (InsP) cause Ca2+ influx, we injected 37 highly purified compounds containing a total of 49 InsP positional isomers into Xenopus oocytes. The eight InsP that stimulated Ca2+ influx were those that had the highest potency at releasing intracellular Ca2+, indicating that their common target was the inositol 1,4,5-trisphosphate [Ins(1,4,5)P-3] receptor. To cause Ca2+ influx, these InsP had to be injected in a much higher concentration than the minimal concentration required to release intracellular Ca2+. Such high InsP concentrations could inhibit ongoing oscillatory intracellular Ca2+ release. In addition, we found that InsPs could not elicit further intracellular Ca2+ release during the course of Ca2+ influx. Our data are consistent with the ''capacitative Ca2+ entry'' hypothesis, which states that InsP stimulate Ca2+ influx by depleting the InsP-sensitive intracellular Ca2+ store. In this context, we would suggest that to deplete the InsP-sensitive intracellular Ca2+ store, InsP may have to be present in a sufficiently high concentration to override the oscillatory Ca2+-refilling mechanisms of the stores.