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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2002-11-26
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pubmed:abstractText |
Although the physiological relevance of mitochondrial Ca2+ homeostasis is widely accepted, no information is yet available on the molecular identity of the proteins involved in this process. Here we analyzed the role of the voltage-dependent anion channel (VDAC) of the outer mitochondrial membrane in the transmission of Ca2+ signals between the ER and mitochondria by measuring cytosolic and organelle [Ca2+] with targeted aequorins and Ca2+-sensitive GFPs. In HeLa cells and skeletal myotubes, the transient expression of VDAC enhanced the amplitude of the agonist-dependent increases in mitochondrial matrix Ca2+ concentration by allowing the fast diffusion of Ca2+ from ER release sites to the inner mitochondrial membrane. Indeed, high speed imaging of mitochondrial and cytosolic [Ca2+] changes showed that the delay between the rises occurring in the two compartments is significantly shorter in VDAC-overexpressing cells. As to the functional consequences, VDAC-overexpressing cells are more susceptible to ceramide-induced cell death, thus confirming that mitochondrial Ca2+ uptake plays a key role in the process of apoptosis. These results reveal a novel function for the widely expressed VDAC channel, identifying it as a molecular component of the routes for Ca2+ transport across the mitochondrial membranes.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10318833,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10330407,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10487752,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10500161,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10570154,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10655583,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10713963,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-10716996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11080247,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11080249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11080251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11256942,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11259441,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11387204,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11387331,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11485562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11733937,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11739410,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-11980717,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-2157230,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-450112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-7634331,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-7770772,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-8235595,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-8413629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-8647283,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-8900151,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-8910409,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9017601,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9049249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9346910,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9615439,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9624056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9724635,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9732284,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9804816,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9878054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12438411-9925820
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pubmed:language |
eng
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorescent Dyes,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/N-acetylsphingosine,
http://linkedlifedata.com/resource/pubmed/chemical/Porins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Sphingosine,
http://linkedlifedata.com/resource/pubmed/chemical/Voltage-Dependent Anion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein,
http://linkedlifedata.com/resource/pubmed/chemical/fura-2-am
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pubmed:status |
MEDLINE
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pubmed:author |
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
613-24
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pubmed:dateRevised |
2009-11-18
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pubmed:articleTitle |
Recombinant expression of the voltage-dependent anion channel enhances the transfer of Ca2+ microdomains to mitochondria.
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pubmed:affiliation |
Department of Experimental and Diagnostic Medicine, Section of General Pathology, Telethon Center for Cell Imaging and Interdisciplinary Center for the Study of Inflammation, University of Ferrara, Via Borsari 46, I-44100 Ferrara, Italy.
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