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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
1999-10-26
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pubmed:abstractText |
Apoptosis of lymphocytes is triggered by different stimuli through the induced expression of Fas and Fas ligand (FasL). Using T cell activation-induced Fas/FasL expression as a model system, we observed a differential regulation of the induction of Fas and FasL. cAMP inhibited activation-induced apoptosis by an effective suppression of TCR-coupled FasL expres sion. In contrast, cAMP weakly interfered with activation-induced Fas expression, and the remaining Fas molecules on cAMP-treated T cells still mediated apoptosis. Among the major transcription elements on the FasL promoter, the activation of NF-kappaB, but not of NF-AT and AP-1, was suppressed by cAMP. The prominent role of NF-kappaB was further demonstrated by a better activation of the FasL promoter and an elevated expression of FasL induced by p65 (RelA) overexpression than those induced by AP-1 or NF-AT. Our results demonstrate the essential role of NF-kappaB for the expression of the death receptor ligand FasL, and suggest a direct link between NF-kappaB activation and the expression of FasL. NF-kappaB may be the common mediator in the induction of FasL through TCR activation and by various stress stimuli.
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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/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/FASLG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2948-56
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10508269-Antibodies, Monoclonal,
pubmed-meshheading:10508269-Antigens, CD3,
pubmed-meshheading:10508269-Antigens, CD95,
pubmed-meshheading:10508269-Antigens, Surface,
pubmed-meshheading:10508269-Apoptosis,
pubmed-meshheading:10508269-Cells, Cultured,
pubmed-meshheading:10508269-Cyclic AMP,
pubmed-meshheading:10508269-DNA Fragmentation,
pubmed-meshheading:10508269-Fas Ligand Protein,
pubmed-meshheading:10508269-G1 Phase,
pubmed-meshheading:10508269-Gene Expression Regulation,
pubmed-meshheading:10508269-Humans,
pubmed-meshheading:10508269-Jurkat Cells,
pubmed-meshheading:10508269-Ligands,
pubmed-meshheading:10508269-Lymphocyte Activation,
pubmed-meshheading:10508269-Membrane Glycoproteins,
pubmed-meshheading:10508269-NF-kappa B,
pubmed-meshheading:10508269-Promoter Regions, Genetic,
pubmed-meshheading:10508269-RNA, Messenger,
pubmed-meshheading:10508269-Tumor Cells, Cultured
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pubmed:year |
1999
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pubmed:articleTitle |
NF-kappa B-dependent Fas ligand expression.
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pubmed:affiliation |
Graduate Institute of Microbiology, National Taiwan University School of Medicine, Taipei, Taiwan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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