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rdf:type |
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lifeskim:mentions |
umls-concept:C0007587,
umls-concept:C0007634,
umls-concept:C0012655,
umls-concept:C0017262,
umls-concept:C0040100,
umls-concept:C0185117,
umls-concept:C0441889,
umls-concept:C0591833,
umls-concept:C1413357,
umls-concept:C1539477,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2002-2-1
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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.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/CASP8 and FADD-Like Apoptosis...,
http://linkedlifedata.com/resource/pubmed/chemical/Camptothecin,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Cflar protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cycloheximide,
http://linkedlifedata.com/resource/pubmed/chemical/Doxorubicin,
http://linkedlifedata.com/resource/pubmed/chemical/Etoposide,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Mitomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Synthesis Inhibitors
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0014-4827
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pubmed:author |
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pubmed:copyrightInfo |
©2002 Elsevier Science (USA).
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
273
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
256-64
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11822881-Animals,
pubmed-meshheading:11822881-Antigens, CD95,
pubmed-meshheading:11822881-Apoptosis,
pubmed-meshheading:11822881-CASP8 and FADD-Like Apoptosis Regulating Protein,
pubmed-meshheading:11822881-Camptothecin,
pubmed-meshheading:11822881-Carrier Proteins,
pubmed-meshheading:11822881-Caspases,
pubmed-meshheading:11822881-Cell Membrane,
pubmed-meshheading:11822881-Cycloheximide,
pubmed-meshheading:11822881-Down-Regulation,
pubmed-meshheading:11822881-Doxorubicin,
pubmed-meshheading:11822881-Etoposide,
pubmed-meshheading:11822881-Fas Ligand Protein,
pubmed-meshheading:11822881-Gene Expression,
pubmed-meshheading:11822881-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:11822881-Membrane Glycoproteins,
pubmed-meshheading:11822881-Mice,
pubmed-meshheading:11822881-Mitomycin,
pubmed-meshheading:11822881-Protein Synthesis Inhibitors,
pubmed-meshheading:11822881-Thymoma,
pubmed-meshheading:11822881-Transcriptional Activation,
pubmed-meshheading:11822881-Transfection,
pubmed-meshheading:11822881-Tumor Cells, Cultured,
pubmed-meshheading:11822881-Up-Regulation
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pubmed:year |
2002
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pubmed:articleTitle |
Expression level of c-FLIP versus Fas determines susceptibility to Fas ligand-induced cell death in murine thymoma EL-4 cells.
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pubmed:affiliation |
Department of Bioengineering, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan. tkataoka@bio.titech.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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