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http://purl.uniprot.org/citations/10227994http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10227994http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10227994http://www.w3.org/2000/01/rdf-schema#comment"Activation-induced cell death of peripheral T cells results from the interaction between Fas and Fas ligand. Resting peripheral T cells are resistant to Fas-induced apoptosis and become susceptible only after their activation. We have investigated the molecular mechanism mediating the sensitization of resting peripheral T cells to Fas-mediated apoptosis following TCR stimulation. TCR activation decreases the steady state protein levels of FLIP (FLICE-like inhibitory protein), an inhibitor of the Fas signaling pathway. Reconstitution of intracellular FLIP levels by the addition of a soluble HIV transactivator protein-FLIP chimera completely restores resistance to Fas-mediated apoptosis in TCR primary T cells. Inhibition of IL-2 production by cyclosporin A, or inhibition of IL-2 signaling by rapamycin or anti-IL-2 neutralizing Abs prevents the decrease in FLIP levels and confers resistance to Fas-mediated apoptosis following T cell activation. Using cell cycle-blocking agents, we demonstrate that activated T cells arrested in G1 phase contain high levels of FLIP protein, whereas activated T cells arrested in S phase have decreased FLIP protein levels. These findings link regulation of FLIP protein levels with cell cycle progression and provide an explanation for the increase in TCR-induced apoptosis observed during the S phase of the cell cycle."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Algeciras-Schimnich A."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Algeciras-Schimnich A."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Griffith T.S."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Griffith T.S."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Lynch D.H."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Lynch D.H."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Paya C.V."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/author"Paya C.V."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/pages"5205-5211"xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/pages"5205-5211"xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/title"Cell cycle-dependent regulation of FLIP levels and susceptibility to Fas-mediated apoptosis."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/title"Cell cycle-dependent regulation of FLIP levels and susceptibility to Fas-mediated apoptosis."xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/volume"162"xsd:string
http://purl.uniprot.org/citations/10227994http://purl.uniprot.org/core/volume"162"xsd:string
http://purl.uniprot.org/citations/10227994http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10227994
http://purl.uniprot.org/citations/10227994http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10227994
http://purl.uniprot.org/citations/10227994http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/10227994
http://purl.uniprot.org/citations/10227994http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/10227994