pubmed-article:20018762 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C1179435 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C0678640 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C1705248 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C1548799 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C1524073 | lld:lifeskim |
pubmed-article:20018762 | lifeskim:mentions | umls-concept:C0449432 | lld:lifeskim |
pubmed-article:20018762 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:20018762 | pubmed:dateCreated | 2010-1-18 | lld:pubmed |
pubmed-article:20018762 | pubmed:abstractText | Mitochondrial Ca(2+) efflux is linked to numerous cellular activities and pathophysiological processes. Although it is established that an Na(+)-dependent mechanism mediates mitochondrial Ca(2+) efflux, the molecular identity of this transporter has remained elusive. Here we show that the Na(+)/Ca(2+) exchanger NCLX is enriched in mitochondria, where it is localized to the cristae. Employing Ca(2+) and Na(+) fluorescent imaging, we demonstrate that mitochondrial Na(+)-dependent Ca(2+) efflux is enhanced upon overexpression of NCLX, is reduced by silencing of NCLX expression by siRNA, and is fully rescued by the concomitant expression of heterologous NCLX. NCLX-mediated mitochondrial Ca(2+) transport was inhibited, moreover, by CGP-37157 and exhibited Li(+) dependence, both hallmarks of mitochondrial Na(+)-dependent Ca(2+) efflux. Finally, NCLX-mediated mitochondrial Ca(2+) exchange is blocked in cells expressing a catalytically inactive NCLX mutant. Taken together, our results converge to the conclusion that NCLX is the long-sought mitochondrial Na(+)/Ca(2+) exchanger. | lld:pubmed |
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pubmed-article:20018762 | pubmed:language | eng | lld:pubmed |
pubmed-article:20018762 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20018762 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20018762 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20018762 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20018762 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20018762 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20018762 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20018762 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20018762 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20018762 | pubmed:month | Jan | lld:pubmed |
pubmed-article:20018762 | pubmed:issn | 1091-6490 | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:NolteChristia... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:SensiStefano... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:SeklerIsraelI | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:HershfinkelMi... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:SilvermanWill... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:Shoshan-Barma... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:KhananshviliD... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:FishmanDaniel... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:PaltyRazR | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:CaporaleTeres... | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:ParnisJuliaJ | lld:pubmed |
pubmed-article:20018762 | pubmed:author | pubmed-author:HerrmannSharo... | lld:pubmed |
pubmed-article:20018762 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20018762 | pubmed:day | 5 | lld:pubmed |
pubmed-article:20018762 | pubmed:volume | 107 | lld:pubmed |
pubmed-article:20018762 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20018762 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20018762 | pubmed:pagination | 436-41 | lld:pubmed |
pubmed-article:20018762 | pubmed:dateRevised | 2010-9-27 | lld:pubmed |
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pubmed-article:20018762 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20018762 | pubmed:articleTitle | NCLX is an essential component of mitochondrial Na+/Ca2+ exchange. | lld:pubmed |
pubmed-article:20018762 | pubmed:affiliation | Department of Physiology, and Zlotowski Center for Neuroscience, Ben-Gurion University of Negev, Beer-Sheva 84105, Israel. | lld:pubmed |
pubmed-article:20018762 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20018762 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |