| http://purl.uniprot.org/citations/12031969 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12031969 | http://www.w3.org/2000/01/rdf-schema#comment | "Ca(2+) may trigger programmed cell death (apoptosis) and regulate death-specific enzymes. Therefore, the development of strategies to control Ca(2+) homeostasis may represent a potential approach to prevent or enhance cell apoptosis. To test this hypothesis, the plasma membrane Na/Ca exchanger (NCX1.7 isoform) was stably overexpressed in insulin-secreting tumoral cells. NCX1.7 overexpression increased apoptosis induced by endoplasmic reticulum (ER) Ca(2+)-ATPase inhibitors, but not by agents increasing intracellular calcium concentration ([Ca(2+)](i)), through the opening of plasma membrane Ca(2+)-channels. NCX1.7 overexpression reduced the rise in [Ca(2+)](i) induced by all agents, depleted ER Ca(2+) stores, sensitized the cells to Ca(2+)-independent proapoptotic signaling pathways, and reduced cell proliferation by approximately 40%. ER Ca(2+) stores depletion was accompanied by the activation of the ER-specific caspase (caspase-12), and the activation was enhanced by ER Ca(2+)-ATPase inhibitors. Hence, Na/Ca exchanger overexpression, by depleting ER Ca(2+) stores, triggers the activation of caspase-12 and increases apoptotic cell death. By increasing apoptosis and decreasing cell proliferation, overexpression of Na/Ca exchanger may represent a new potential approach in cancer gene therapy. On the other hand, our results open the way to the development of new strategies to control cellular Ca(2+) homeostasis that could, on the contrary, prevent the process of apoptosis that mediates, in part, beta-cell autoimmune destruction in type 1 diabetes."xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.org/dc/terms/identifier | "doi:10.2337/diabetes.51.6.1815"xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/author | "Diaz-Horta O."xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/author | "Herchuelz A."xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/author | "Kamagate A."xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/author | "Van Eylen F."xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/pages | "1815-1824"xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/title | "Na/Ca exchanger overexpression induces endoplasmic reticulum-related apoptosis and caspase-12 activation in insulin-releasing BRIN-BD11 cells."xsd:string |
| http://purl.uniprot.org/citations/12031969 | http://purl.uniprot.org/core/volume | "51"xsd:string |
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