| pubmed-article:11822881 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0012655 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0040100 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C1413357 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:11822881 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:11822881 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11822881 | pubmed:dateCreated | 2002-2-1 | lld:pubmed |
| pubmed-article:11822881 | pubmed:abstractText | The caspase-8 inhibitor c-FLIP blocks death receptor-mediated cell death and plays an essential role in the regulation of lymphocyte homeostasis and the immune escape of tumors. The murine thymoma cell line EL-4 was resistant to Fas ligand (FasL)-induced apoptosis by constitutive expression of FLIP (L). Cycloheximide downregulated the expression of FLIP (L) and markedly sensitized EL-4 cells to FasL-induced apoptosis. In contrast, DNA-damaging agents sensitized EL-4 cells to FasL-induced cell death via an increase of cell-surface Fas without any influence on FLIP (L) expression. Enforced expression of transfected Fas rendered EL-4 cells highly susceptible to FasL-induced cell death. These findings demonstrate that susceptibility to FasL-induced cell death mainly depends on the expression level of c-FLIP versus cell-surface Fas. | lld:pubmed |
| pubmed-article:11822881 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11822881 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11822881 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11822881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11822881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11822881 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11822881 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11822881 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11822881 | pubmed:issn | 0014-4827 | lld:pubmed |
| pubmed-article:11822881 | pubmed:author | pubmed-author:NagaiKazuoK | lld:pubmed |
| pubmed-article:11822881 | pubmed:author | pubmed-author:KataokaTakaoT | lld:pubmed |
| pubmed-article:11822881 | pubmed:author | pubmed-author:TschoppJürgJ | lld:pubmed |
| pubmed-article:11822881 | pubmed:author | pubmed-author:ItoMikaM | lld:pubmed |
| pubmed-article:11822881 | pubmed:author | pubmed-author:BuddRalph CRC | lld:pubmed |
| pubmed-article:11822881 | pubmed:copyrightInfo | ©2002 Elsevier Science (USA). | lld:pubmed |
| pubmed-article:11822881 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11822881 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:11822881 | pubmed:volume | 273 | lld:pubmed |
| pubmed-article:11822881 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11822881 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11822881 | pubmed:pagination | 256-64 | lld:pubmed |
| pubmed-article:11822881 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11822881 | pubmed:meshHeading | pubmed-meshheading:11822881... | lld:pubmed |
| pubmed-article:11822881 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11822881 | pubmed:articleTitle | Expression level of c-FLIP versus Fas determines susceptibility to Fas ligand-induced cell death in murine thymoma EL-4 cells. | lld:pubmed |
| pubmed-article:11822881 | pubmed:affiliation | Department of Bioengineering, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan. tkataoka@bio.titech.ac.jp | lld:pubmed |
| pubmed-article:11822881 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11822881 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11822881 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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