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http://purl.uniprot.org/citations/11717445http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11717445http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11717445http://www.w3.org/2000/01/rdf-schema#comment"A role for caspase-10, previously implicated in the autoimmune lymphoproliferative syndrome, in death receptor signaling has not been directly shown. Here we show that caspase-10 can function independently of caspase-8 in initiating Fas- and tumor necrosis factor-related apoptosis-inducing ligand-receptor-mediated apoptosis. Moreover, Fas crosslinking in primary human T cells leads to the recruitment and activation of caspase-10. Fluorescent resonance energy transfer analysis indicates that the death-effector domains of caspase-8 and -10 both interact with the death-effector domain of FADD. Nonetheless, we find that caspase-8 and -10 may have different apoptosis substrates and therefore potentially distinct roles in death receptor signaling or other cellular processes."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.org/dc/terms/identifier"doi:10.1073/pnas.241358198"xsd:string
http://purl.uniprot.org/citations/11717445http://purl.org/dc/terms/identifier"doi:10.1073/pnas.241358198"xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Wong W."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Wong W."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Lenardo M.J."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Lenardo M.J."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Chun H.J."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Chun H.J."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Spencer D.M."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/author"Spencer D.M."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/pages"13884-13888"xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/pages"13884-13888"xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/title"Caspase-10 is an initiator caspase in death receptor signaling."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/title"Caspase-10 is an initiator caspase in death receptor signaling."xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/volume"98"xsd:string
http://purl.uniprot.org/citations/11717445http://purl.uniprot.org/core/volume"98"xsd:string