| pubmed-article:14644092 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14644092 | lifeskim:mentions | umls-concept:C1621443 | lld:lifeskim |
| pubmed-article:14644092 | lifeskim:mentions | umls-concept:C0030013 | lld:lifeskim |
| pubmed-article:14644092 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:14644092 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:14644092 | lifeskim:mentions | umls-concept:C1627358 | lld:lifeskim |
| pubmed-article:14644092 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:14644092 | pubmed:dateCreated | 2003-12-3 | lld:pubmed |
| pubmed-article:14644092 | pubmed:abstractText | Signalling through the death receptor CD95 induces apoptosis by formation of a signalling complex at the cell membrane and subsequent caspase-8 and caspase-3-activation. Treatment of Jurkat T cells with protonophores across the mitochondrial membrane such as 2,4-dinitrophenol (DNP) enhances the death-inducing capacity of CD95. In this study, we show that this enhancement is due to the specific acceleration of caspase-8-processing and activation at the CD95-receptor. DNP-treatment did not affect NF-kappaB-induction by CD95. Immunoprecipitation experiments showed that the amounts of the adapter FADD/MORT1 and pro-caspase-8 at the CD95-receptor were not altered by DNP. Subcellular fractionation studies revealed that the amount of mature caspase-8 but not pro-caspase at the membrane was increased following CD95-stimulation in the presence of DNP. As a consequence of caspase-activation, c-FLIP-levels in the cytosol decreased. In Jurkat cells overexpressing c-FLIPS, DNP was still able to enhance caspase-activation. The enhancing capacity of DNP was seen in some cell lines (Jurkat, CEM and HeLa) but not in SKW6 cells and was also found in mitogen-stimulated human T cells. Furthermore, the enhancement extended to TRAIL-induced caspase-activation. Thus, a mechanism exists by which caspase-8-activation can be accelerated at death receptors and this mechanism can be triggered by targeting mitochondrial oxidative phosphorylation. | lld:pubmed |
| pubmed-article:14644092 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14644092 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14644092 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14644092 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:14644092 | pubmed:issn | 0161-5890 | lld:pubmed |
| pubmed-article:14644092 | pubmed:author | pubmed-author:WagnerHermann... | lld:pubmed |
| pubmed-article:14644092 | pubmed:author | pubmed-author:VierJulianeJ | lld:pubmed |
| pubmed-article:14644092 | pubmed:author | pubmed-author:HäckerGeorgG | lld:pubmed |
| pubmed-article:14644092 | pubmed:author | pubmed-author:GerhardMonika... | lld:pubmed |
| pubmed-article:14644092 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14644092 | pubmed:volume | 40 | lld:pubmed |
| pubmed-article:14644092 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14644092 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14644092 | pubmed:pagination | 661-70 | lld:pubmed |
| pubmed-article:14644092 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:14644092 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14644092 | pubmed:articleTitle | Enhancement of death-receptor induced caspase-8-activation in the death-inducing signalling complex by uncoupling of oxidative phosphorylation. | lld:pubmed |
| pubmed-article:14644092 | pubmed:affiliation | Institute for Medical Microbiology, Immunology and Hygiene, Technische Universität München, Trogerstrasse 9, D-81675 Munich, Germany. | lld:pubmed |
| pubmed-article:14644092 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14644092 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:14644092 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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