Inositol phosphate structural requisites for Ca2+ influx

S. DeLisle, G. W. Mayr, M. J. Welsh

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


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)P3] 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.

Original languageEnglish (US)
Pages (from-to)C1485-C1491
JournalAmerican Journal of Physiology - Cell Physiology
Issue number6 37-6
StatePublished - Jan 1 1995


  • calcium
  • inositol 1,4,5-trisphosphate
  • signal transduction

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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