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pubmed-article:8395025pubmed:dateCreated1993-9-21lld:pubmed
pubmed-article:8395025pubmed:abstractTextIn non-excitable cells, release of Ca2+ from the inositol 1,4,5-trisphosphate (InsP3)-sensitive store can activate Ca2+ entry. Very little is known about the signal mechanism relating store emptying to plasma membrane Ca2+ influx. It has been suggested that the signal may be either a diffusible messenger like an inositol phosphate, or the InsP3 receptor itself, which, by physically coupling to some component of Ca2+ entry in the plasma membrane, may link store release to Ca2+ entry. The nature of the Ca2+ entry pathway is also unclear. Only in mast cells has a very selective Ca2+ current been observed after store emptying. Activation of exogenous 5-hydroxytryptamine (5-HT) receptors expressed in Xenopus oocytes or direct injection of InsP3 evokes Ca2+ entry activated by InsP3 pool depletion. Here we investigate the nature of this influx pathway and find a current activated by pool depletion. This has an unusual selectivity in that it is more permeable to Ca2+ ions than to other divalent cations (Ba2+, Sr2+ or Mn2+). Moreover, a K+ permeability is also stimulated after pool depletion. The activation of this store depletion current involves both a phosphatase and an unidentified diffusible messenger. Both the Ca2+ entry pathway and the activating factors found here may be relevant to pool-depleted Ca2+ entry in a variety of non-excitable cells.lld:pubmed
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pubmed-article:8395025pubmed:pagination814-8lld:pubmed
pubmed-article:8395025pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:8395025pubmed:articleTitleDepletion of InsP3 stores activates a Ca2+ and K+ current by means of a phosphatase and a diffusible messenger.lld:pubmed
pubmed-article:8395025pubmed:affiliationMax-Planck-Institute for Biophysical Chemistry, Department of Membrane Biophysics, Göttingen, Germany.lld:pubmed
pubmed-article:8395025pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8395025pubmed:publicationTypeIn Vitrolld:pubmed
pubmed-article:8395025pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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