http://purl.uniprot.org/citations/18337558 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/18337558 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/18337558 | http://www.w3.org/2000/01/rdf-schema#comment | "In B lymphocytes, the B-cell adaptor for phosphatidylinositol 3-kinase (BCAP) facilitates signaling from the antigen receptor. Mice lacking BCAP have a predominantly immature pool of B cells with impaired immune function and increased susceptibility to apoptosis. Unexpectedly, we have found that natural killer (NK) cells from BCAP-deficient mice are more mature, more long-lived, more resistant to apoptosis, and exhibit enhanced functional activity compared with NK cells from wild-type mice. Surprisingly, these effects are evident despite a severe impairment of the immunoreceptor tyrosine-based activation motif-mediated Akt signaling pathway. The seemingly paradoxical phenotype reveals inherent differences in the signals controlling the final maturation of B cells and NK cells, which depend on positive and negative signals, respectively. Both enhanced interferon-gamma responses and augmented maturation of NK cells in BCAP-deficient mice are independent of available MHC class I ligands. Our data support a model in which blunting of BCAP-mediated activation signaling in developing NK cells promotes functionality, terminal maturation, and long-term survival."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2007-08-107847"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.org/dc/terms/identifier | "doi:10.1182/blood-2007-08-107847"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Campbell K.S."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Campbell K.S."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Fang M."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Fang M."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Kurosaki T."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Kurosaki T."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Yamazaki T."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Yamazaki T."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Macfarlane A.W. IV"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Macfarlane A.W. IV"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Sigal L.J."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/author | "Sigal L.J."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/name | "Blood"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/pages | "131-140"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/pages | "131-140"xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/title | "Enhanced NK cell development and function in BCAP-deficient mice."xsd:string |
http://purl.uniprot.org/citations/18337558 | http://purl.uniprot.org/core/title | "Enhanced NK cell development and function in BCAP-deficient mice."xsd:string |