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http://purl.uniprot.org/citations/10588860http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10588860http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10588860http://www.w3.org/2000/01/rdf-schema#comment"We have characterized a phosphoprotein protein with a death effector domain that has a novel bifunctional role in programmed cell death. The 15-kDa phosphoprotein enriched in astrocytes (PEA-15) inhibits Fas-mediated apoptosis and increases tumor necrosis factor receptor-1 (TNF-R1)-mediated apoptosis in the same cell type in a ligand-dependent manner. Phosphorylation appears to play a role in its differential effects, since point mutations at one or both phosphorylation consensus sites within PEA-15 destroy its effect on Fas-mediated, but not TNF-R1-mediated, apoptosis. Furthermore, the differential effect is evident at the level of caspase-8 activity which is inhibited via Fas activation, but increased via TNF-R1 activation upon PEA-15 expression. These results show that PEA-15 provides a potential mechanism during development for distinguishing between diverse extracellular death-inducing signals that culminate either in apoptosis or in survival."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.org/dc/terms/identifier"doi:10.1006/dbio.1999.9510"xsd:string
http://purl.uniprot.org/citations/10588860http://purl.org/dc/terms/identifier"doi:10.1006/dbio.1999.9510"xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/author"Blau H.M."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/author"Blau H.M."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/author"Estelles A."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/author"Estelles A."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/author"Charlton C.A."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/author"Charlton C.A."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/name"Dev. Biol."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/name"Dev. Biol."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/pages"16-28"xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/pages"16-28"xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/title"The phosphoprotein protein PEA-15 inhibits Fas- but increases TNF-R1-mediated caspase-8 activity and apoptosis."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/title"The phosphoprotein protein PEA-15 inhibits Fas- but increases TNF-R1-mediated caspase-8 activity and apoptosis."xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/volume"216"xsd:string
http://purl.uniprot.org/citations/10588860http://purl.uniprot.org/core/volume"216"xsd:string
http://purl.uniprot.org/citations/10588860http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10588860
http://purl.uniprot.org/citations/10588860http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/10588860
http://purl.uniprot.org/citations/10588860http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/10588860
http://purl.uniprot.org/citations/10588860http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/10588860