Source:http://linkedlifedata.com/resource/pubmed/id/19133300
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2009-6-8
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pubmed:abstractText |
Calcium (Ca2+) is a ubiquitous second messenger which promotes cell responses through transient changes in intracellular concentrations. The prominent role of Ca2+ in cell physiology is mediated by a whole set of proteins constituting a Ca2+-signalling toolkit involved in Ca2+-signal generation, deciphering and arrest. The different Ca2+-signalosomes deliver Ca2+-signals with spatial and temporal dynamics to control the function of specific cell types. Among the intracellular proteins involved in Ca2+-signal deciphering, calmodulin (CaM) plays a pivotal role in controlling Ca2+-homeostasis and downstream Ca2+-based signalling events. Due to its ubiquitous expression in eukaryotic cells and the variety of proteins it interacts with, CaM is central in Ca2+-signalling networks. For these reasons, it is expected that disrupting or modifying CaM interactions with its target proteins will affect Ca2+-homeostasis and cellular responses. The resulting calcium response will vary depending on which interactions between CaM and target proteins are altered by the molecules and on the specific Ca2+-toolkit expressed in a given cell, even in the resting state. In the present paper, the effect of six classical CaM interactors (W5, W7, W12, W13, bifonazole and calmidazolium) was studied on Ca2+-signalling in tumor initiating cells isolated from human glioblastoma (TG1) and tobacco cells (BY-2) using the fluorescent Ca2+-sensitive Indo-1 dye and aequorin, respectively. Various Ca2+-fingerprints were obtained depending both on the CaM interactor used and the cell type investigated. These data demonstrate that interaction between the antagonists and CaM results in a differential inhibition of CaM-dependent proteins involved in Ca2+-signal regulation. In addition, the distinct Ca2+-fingerprints in tobacco and human tumor initiating glioblastoma cells induced by a given CaM interactor highlight the specificity of the Ca2+-signalosome in eukaryotic cells.
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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/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calmodulin,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Imidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/W 12,
http://linkedlifedata.com/resource/pubmed/chemical/bifonazole,
http://linkedlifedata.com/resource/pubmed/chemical/calmidazolium
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0006-3002
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pubmed:author |
pubmed-author:BrièreChristianC,
pubmed-author:ChneiweissHervéH,
pubmed-author:DagherRaniaR,
pubmed-author:FèveMarieM,
pubmed-author:HaiechJacquesJ,
pubmed-author:KilhofferMarie-ClaudeMC,
pubmed-author:MazarsChristianC,
pubmed-author:PigaultClaireC,
pubmed-author:RanjevaRaoulR,
pubmed-author:ZeniouMariaM
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pubmed:issnType |
Print
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pubmed:volume |
1793
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1068-77
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pubmed:meshHeading |
pubmed-meshheading:19133300-Anisotropy,
pubmed-meshheading:19133300-Calcium,
pubmed-meshheading:19133300-Calcium Signaling,
pubmed-meshheading:19133300-Calmodulin,
pubmed-meshheading:19133300-Cell Line,
pubmed-meshheading:19133300-Enzyme Inhibitors,
pubmed-meshheading:19133300-Eukaryotic Cells,
pubmed-meshheading:19133300-Humans,
pubmed-meshheading:19133300-Imidazoles,
pubmed-meshheading:19133300-Molecular Structure,
pubmed-meshheading:19133300-Spectrometry, Fluorescence,
pubmed-meshheading:19133300-Sulfonamides,
pubmed-meshheading:19133300-Tobacco
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pubmed:year |
2009
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pubmed:articleTitle |
Calcium fingerprints induced by calmodulin interactors in eukaryotic cells.
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pubmed:affiliation |
UMR CNRS 7200, Université de Strasbourg, Faculté de Pharmacie 74, route du Rhin, F-67401 Illkirch, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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