pubmed-article:15860671 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C0026764 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C0574895 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:15860671 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:15860671 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:15860671 | pubmed:dateCreated | 2005-8-4 | lld:pubmed |
pubmed-article:15860671 | pubmed:abstractText | Multiple myeloma (MM) is an as-yet incurable B-cell malignancy. Increased survival in vitro is a hallmark of MM cells, implying that a therapeutic potential may lie in circumventing antiapoptotic signals. We have previously reported that interferons (IFNs) sensitize MM cells to Fas/CD95-mediated apoptosis. In the present study, we explore the mechanism underlying this effect. In a wide screening of apoptosis-related genes, Apo2L/TRAIL (tumor necrosis factor [TNF]-related apoptosis inducing ligand) and Fas were identified as IFN targets. Sensitization to Fas-mediated apoptosis by IFNs was not affected by blocking Apo2L/TRAIL, suggesting that Apo2L/TRAIL is not a key mediator in this process. In contrast, we found that an elevated Fas expression was functionally linked to increased susceptibility to Fas-mediated apoptosis. This was further supported by the finding that IFN treatment enhanced Fas-mediated caspase-8 activation, one of the earliest signaling events downstream receptor activation. In addition, IFN treatment attenuated the interleukin 6 (IL-6)-dependent activation of signal transducer and activator of transcription 3 (Stat3), interfering with a known survival pathway in MM that has previously been linked with resistance to Fas-mediated apoptosis. Taken together, our results show that IFN-induced up-regulation of Fas sensitizes MM cells to Fas-mediated apoptosis and suggest that attenuation of Stat3 activation may be a potentially important event in this process. | lld:pubmed |
pubmed-article:15860671 | pubmed:language | eng | lld:pubmed |
pubmed-article:15860671 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860671 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:15860671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15860671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860671 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:15860671 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15860671 | pubmed:month | Aug | lld:pubmed |
pubmed-article:15860671 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:NilssonKennet... | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:ObergFredrikF | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:OsterborgAnde... | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:StrömbergThom... | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:DimbergLina... | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:DimbergAnna... | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:IvarssonKarol... | lld:pubmed |
pubmed-article:15860671 | pubmed:author | pubmed-author:Jernberg... | lld:pubmed |
pubmed-article:15860671 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15860671 | pubmed:day | 15 | lld:pubmed |
pubmed-article:15860671 | pubmed:volume | 106 | lld:pubmed |
pubmed-article:15860671 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15860671 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15860671 | pubmed:pagination | 1346-54 | lld:pubmed |
pubmed-article:15860671 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:15860671 | pubmed:meshHeading | pubmed-meshheading:15860671... | lld:pubmed |
pubmed-article:15860671 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15860671 | pubmed:articleTitle | Ectopic and IFN-induced expression of Fas overcomes resistance to Fas-mediated apoptosis in multiple myeloma cells. | lld:pubmed |
pubmed-article:15860671 | pubmed:affiliation | Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden. | lld:pubmed |
pubmed-article:15860671 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15860671 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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