| pubmed-article:19133300 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19133300 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:19133300 | lifeskim:mentions | umls-concept:C0015161 | lld:lifeskim |
| pubmed-article:19133300 | lifeskim:mentions | umls-concept:C0006772 | lld:lifeskim |
| pubmed-article:19133300 | lifeskim:mentions | umls-concept:C0016126 | lld:lifeskim |
| pubmed-article:19133300 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:19133300 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:19133300 | pubmed:dateCreated | 2009-6-8 | lld:pubmed |
| pubmed-article:19133300 | 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. | lld:pubmed |
| pubmed-article:19133300 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19133300 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19133300 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19133300 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:19133300 | pubmed:issn | 0006-3002 | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:HaiechJacques... | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:KilhofferMari... | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:ZeniouMariaM | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:RanjevaRaoulR | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:MazarsChristi... | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:ChneiweissHer... | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:PigaultClaire... | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:BrièreChristi... | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:DagherRaniaR | lld:pubmed |
| pubmed-article:19133300 | pubmed:author | pubmed-author:FèveMarieM | lld:pubmed |
| pubmed-article:19133300 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19133300 | pubmed:volume | 1793 | lld:pubmed |
| pubmed-article:19133300 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19133300 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19133300 | pubmed:pagination | 1068-77 | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:meshHeading | pubmed-meshheading:19133300... | lld:pubmed |
| pubmed-article:19133300 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19133300 | pubmed:articleTitle | Calcium fingerprints induced by calmodulin interactors in eukaryotic cells. | lld:pubmed |
| pubmed-article:19133300 | pubmed:affiliation | UMR CNRS 7200, Université de Strasbourg, Faculté de Pharmacie 74, route du Rhin, F-67401 Illkirch, France. | lld:pubmed |
| pubmed-article:19133300 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19133300 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:801 | entrezgene:pubmed | pubmed-article:19133300 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19133300 | lld:entrezgene |
