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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
36
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pubmed:dateCreated |
1993-1-21
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pubmed:abstractText |
Mechanisms controlling Ca2+ fluxes through the plasma membrane of lymphocytes have been characterized in a human T-cell clone and in the Jurkat T-cell line. Due to endogenous buffers, about 1/125 of the Ca2+ ions that enter the cell are free. Ca2+ fluxes were estimated from the variations in intracellular Ca2+ concentration ([Ca2+]i) elicited by concentration jumps in extracellular Ca2+ ([Ca2+]o). Thapsigargin was used to inhibit Ca2+ uptake into intracellular stores and to stimulate Ca2+ entry. Ca2+ extrusion was strictly due to the activity of plasma membrane Ca(2+)-ATPases since there was no detectable Na+/Ca2+ exchange activity in these cells. The rate of Ca2+ extrusion was mainly influenced by [Ca2+]i and less by [Ca2+]o but was insensitive to cell depolarization. In depolarized cells, thapsigargin-induced Ca2+ influx was reduced to 10% of the value measured in normally polarized cells, suggesting that depolarization not only reduces the electrochemical gradient for Ca2+ ions, but also inhibits Ca2+ permeation. When Ca2+ ions enter the cell, they bind to a site inside the channel, with a Kd of 3.3 mM. Stimulation of clonal T-cells with low concentrations of either anti-CD3 antibodies or thapsigargin elicited Ca2+ oscillations. Both the amplitude and the frequency of CD3-induced Ca2+ oscillations were sensitive to [Ca2+]o. These oscillations were immediately interrupted when extracellular Ca2+ was removed. The properties of Ca2+ oscillations in T lymphocytes suggest that they are mainly due to variations of Ca2+ influx, modulated by variations in [Ca2+]i.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Transporting ATPases,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
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 |
Dec
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
267
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25864-72
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:1464601-Antibodies, Monoclonal,
pubmed-meshheading:1464601-Antigens, CD3,
pubmed-meshheading:1464601-Calcium,
pubmed-meshheading:1464601-Calcium-Transporting ATPases,
pubmed-meshheading:1464601-Clone Cells,
pubmed-meshheading:1464601-Egtazic Acid,
pubmed-meshheading:1464601-Fura-2,
pubmed-meshheading:1464601-Humans,
pubmed-meshheading:1464601-Kinetics,
pubmed-meshheading:1464601-Membrane Potentials,
pubmed-meshheading:1464601-Oscillometry,
pubmed-meshheading:1464601-T-Lymphocytes,
pubmed-meshheading:1464601-Terpenes,
pubmed-meshheading:1464601-Thapsigargin,
pubmed-meshheading:1464601-Time Factors,
pubmed-meshheading:1464601-Tumor Cells, Cultured
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pubmed:year |
1992
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pubmed:articleTitle |
Calcium fluxes in T lymphocytes.
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pubmed:affiliation |
Laboratoire de Neurobiologie, Centre National de la Recherche Scientifique (CNRS) URA 295, Ecole Normale Supérieure, Paris, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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