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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6358
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pubmed:dateCreated |
1992-2-20
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pubmed:abstractText |
In many cell types, receptor-mediated Ca2+ release from internal stores is followed by Ca2+ influx across the plasma membrane. The sustained entry of Ca2+ is thought to result partly from the depletion of intracellular Ca2+ pools. Most investigations have characterized Ca2+ influx indirectly by measuring Ca(2+)-activated currents or using Fura-2 quenching by Mn2+, which in some cells enters the cells by the same influx pathway. But only a few studies have investigated this Ca2+ entry pathway more directly. We have combined patch-clamp and Fura-2 measurements to monitor membrane currents in mast cells under conditions where intracellular Ca2+ stores were emptied by either inositol 1,4,5-trisphosphate, ionomycin, or excess of the Ca2+ chelator EGTA. The depletion of Ca2+ pools by these independent mechanisms commonly induced activation of a sustained calcium inward current that was highly selective for Ca2+ ions over Ba2+, Sr2+ and Mn2+. This Ca2+ current, which we term ICRAC (calcium release-activated calcium), is not voltage-activated and shows a characteristic inward rectification. It may be the mechanism by which electrically nonexcitable cells maintain raised intracellular Ca2+ concentrations and replenish their empty Ca2+ stores after receptor stimulation.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1,2-bis(2-aminophenoxy)ethane-N,N,N'...,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Cations, Divalent,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Ionomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Terpenes,
http://linkedlifedata.com/resource/pubmed/chemical/Thapsigargin
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0028-0836
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
23
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pubmed:volume |
355
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
353-6
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1309940-Animals,
pubmed-meshheading:1309940-Calcium,
pubmed-meshheading:1309940-Calcium Channel Blockers,
pubmed-meshheading:1309940-Calcium Channels,
pubmed-meshheading:1309940-Cations, Divalent,
pubmed-meshheading:1309940-Cell Membrane Permeability,
pubmed-meshheading:1309940-Cells, Cultured,
pubmed-meshheading:1309940-Egtazic Acid,
pubmed-meshheading:1309940-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:1309940-Ionomycin,
pubmed-meshheading:1309940-Mast Cells,
pubmed-meshheading:1309940-Membrane Potentials,
pubmed-meshheading:1309940-Rats,
pubmed-meshheading:1309940-Terpenes,
pubmed-meshheading:1309940-Thapsigargin
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pubmed:year |
1992
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pubmed:articleTitle |
Depletion of intracellular calcium stores activates a calcium current in mast cells.
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pubmed:affiliation |
Max-Planck-Institut für biophysikalische Chemie, Göttingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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