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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1999-5-19
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pubmed:databankReference |
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pubmed:abstractText |
Programmed cell death is a process required for the normal development of an organism. One of the best understood apoptotic pathways occurs in T lymphocytes and is mediated by Fas/Fas ligand (FasL) interaction. During studies of apoptosis induced by T cell-receptor engagement, we identified ALG-4F, a truncated transcript that prevents T cell-receptor-induced FasL upregulation and cell death. Overexpression of full-length ALG-4 induced transcription of FasL and, consequently, apoptosis. These results indicate that ALG-4 is necessary and sufficient for FasL expression. Fas/FasL interaction initiates cell death in many other systems, and its dysregulation is a mechanism by which several pathologic conditions arise. Understanding the molecular mechanisms of FasL regulation could be very useful in elucidating how these diseases develop and in identifying potential therapeutic targets.
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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/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/FASLG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1078-8956
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
542-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:10229231-Amino Acid Sequence,
pubmed-meshheading:10229231-Apoptosis,
pubmed-meshheading:10229231-Apoptosis Regulatory Proteins,
pubmed-meshheading:10229231-Caspases,
pubmed-meshheading:10229231-Fas Ligand Protein,
pubmed-meshheading:10229231-Genes, Reporter,
pubmed-meshheading:10229231-Humans,
pubmed-meshheading:10229231-Jurkat Cells,
pubmed-meshheading:10229231-Membrane Glycoproteins,
pubmed-meshheading:10229231-Membrane Proteins,
pubmed-meshheading:10229231-Molecular Sequence Data,
pubmed-meshheading:10229231-NF-kappa B,
pubmed-meshheading:10229231-Promoter Regions, Genetic,
pubmed-meshheading:10229231-Receptors, Antigen, T-Cell,
pubmed-meshheading:10229231-Sequence Homology, Amino Acid,
pubmed-meshheading:10229231-T-Lymphocytes,
pubmed-meshheading:10229231-Transcription, Genetic,
pubmed-meshheading:10229231-Up-Regulation
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pubmed:year |
1999
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pubmed:articleTitle |
Regulation of Fas ligand expression and cell death by apoptosis-linked gene 4.
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pubmed:affiliation |
T-cell Apoptosis Unit, Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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