pubmed-article:10952999 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0014239 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0014406 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0392747 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0443172 | lld:lifeskim |
pubmed-article:10952999 | lifeskim:mentions | umls-concept:C0699493 | lld:lifeskim |
pubmed-article:10952999 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10952999 | pubmed:dateCreated | 2000-9-28 | lld:pubmed |
pubmed-article:10952999 | pubmed:abstractText | To test the role of ER luminal environment in apoptosis, we generated HeLa cell lines inducible with respect to calreticulin and calnexin and investigated their sensitivity to drug-dependent apoptosis. Overexpression of calreticulin, an ER luminal protein, resulted in an increased sensitivity of the cells to both thapsigargin- and staurosporine-induced apoptosis. This correlated with an increased release of cytochrome c from the mitochondria. Overexpression of calnexin, an integral ER membrane protein, had no significant effect on drug-induced apoptosis. In contrast, calreticulin-deficient cells were significantly resistant to apoptosis and this resistance correlated with a decreased release of cytochrome c from mitochondria and low levels of caspase 3 activity. This work indicates that changes in the lumen of the ER amplify the release of cytochrome c from mitochondria, and increase caspase activity, during drug-induced apoptosis. There may be communication between the ER and mitochondria, which may involve Ca(2+) and play an important role in conferring cell sensitivity to apoptosis. Apoptosis may depend on both the presence of external apoptosis-activating signals, and, as shown in this study, on an internal factor represented by the ER. | lld:pubmed |
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pubmed-article:10952999 | pubmed:language | eng | lld:pubmed |
pubmed-article:10952999 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10952999 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10952999 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10952999 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10952999 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10952999 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10952999 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:10952999 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10952999 | pubmed:month | Aug | lld:pubmed |
pubmed-article:10952999 | pubmed:issn | 0021-9525 | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:NakamuraKK | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:MichalakMM | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:GreenD RDR | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:OpasMM | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:BurnsKK | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:BleackleyR... | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:Bossy-WetzelE... | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:GopingI SIS | lld:pubmed |
pubmed-article:10952999 | pubmed:author | pubmed-author:FadelM PMP | lld:pubmed |