| pubmed-article:16824596 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C0033085 | lld:lifeskim |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C0014239 | lld:lifeskim |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C1550548 | lld:lifeskim |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C1555714 | lld:lifeskim |
| pubmed-article:16824596 | lifeskim:mentions | umls-concept:C1705654 | lld:lifeskim |
| pubmed-article:16824596 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:16824596 | pubmed:dateCreated | 2006-12-12 | lld:pubmed |
| pubmed-article:16824596 | pubmed:abstractText | In this study the relationship between the efficiency of endoplasmic reticulum (ER) Ca2+ refilling and the extent of Ca2+ entry was investigated in endothelial cells. ER and mitochondrial Ca2+ concentration were measured using genetically encoded Ca2+ sensors, while the amount of entering Ca2+ was controlled by varying either the extracellular Ca2+ or the electrical driving force for Ca2+ by changing the plasma membrane potential. In the absence of an agonist, ER Ca2+ replenishment was fully accomplished even if the Ca2+ concentration applied was reduced from 2 to 0.5mM. A similar strong efficiency of ER Ca2+ refilling was obtained under condition of plasma membrane depolarization. However, in the presence of histamine, ER Ca2+ refilling depended on mitochondrial Ca2+ transport and was more susceptible to membrane depolarization. Store-operated Ca2+ entry (SOCE), was strongly reduced under low Ca2+ and depolarizing conditions but increased if ER Ca2+ uptake was blocked or if ER Ca2+ was released continuously by IP(3). A correlation of the kinetics of ER Ca2+refilling with cytosolic Ca2+ signals revealed that termination of SOCE is a rapid event that is not delayed compared to ER refilling. Our data indicate that ER refilling occurs in priority to, and independently from the cytosolic Ca2+ elevation upon Ca2+ entry and that this important process is widely achieved even under conditions of diminished Ca2+entry. | lld:pubmed |
| pubmed-article:16824596 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16824596 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16824596 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16824596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16824596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16824596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16824596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16824596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16824596 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16824596 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16824596 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:16824596 | pubmed:issn | 0143-4160 | lld:pubmed |
| pubmed-article:16824596 | pubmed:author | pubmed-author:GraierW FWF | lld:pubmed |
| pubmed-article:16824596 | pubmed:author | pubmed-author:MalliRR | lld:pubmed |
| pubmed-article:16824596 | pubmed:author | pubmed-author:FriedelKK | lld:pubmed |
| pubmed-article:16824596 | pubmed:author | pubmed-author:TrenkerMM | lld:pubmed |
| pubmed-article:16824596 | pubmed:author | pubmed-author:HunkovaMM | lld:pubmed |
| pubmed-article:16824596 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16824596 | pubmed:volume | 41 | lld:pubmed |
| pubmed-article:16824596 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16824596 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16824596 | pubmed:pagination | 63-76 | lld:pubmed |
| pubmed-article:16824596 | pubmed:dateRevised | 2010-12-3 | lld:pubmed |
| pubmed-article:16824596 | pubmed:meshHeading | pubmed-meshheading:16824596... | lld:pubmed |
| pubmed-article:16824596 | pubmed:meshHeading | pubmed-meshheading:16824596... | lld:pubmed |
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| pubmed-article:16824596 | pubmed:meshHeading | pubmed-meshheading:16824596... | lld:pubmed |
| pubmed-article:16824596 | pubmed:meshHeading | pubmed-meshheading:16824596... | lld:pubmed |
| pubmed-article:16824596 | pubmed:meshHeading | pubmed-meshheading:16824596... | lld:pubmed |
| pubmed-article:16824596 | pubmed:meshHeading | pubmed-meshheading:16824596... | lld:pubmed |
| pubmed-article:16824596 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:16824596 | pubmed:articleTitle | Ca2+ refilling of the endoplasmic reticulum is largely preserved albeit reduced Ca2+ entry in endothelial cells. | lld:pubmed |
| pubmed-article:16824596 | pubmed:affiliation | Institute of Molecular Biology and Biochemistry, Center of Molecular Medicine, Molecular and Cellular Physiology Research Unit (MCPRU), Medical University Graz, Harrachgasse 21/III, A-8010 Graz, Austria. | lld:pubmed |
| pubmed-article:16824596 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16824596 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16824596 | lld:pubmed |
