Functional requirement for SAP in 2B4-mediated activation of human natural killer cells as revealed by the X-linked lymphoproliferative syndrome.
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Characterization of SH2D1A missense mutations identified in X-linked lymphoproliferative disease patientsA "three-pronged" binding mechanism for the SAP/SH2D1A SH2 domain: structural basis and relevance to the XLP syndromeNTB-A [correction of GNTB-A], a novel SH2D1A-associated surface molecule contributing to the inability of natural killer cells to kill Epstein-Barr virus-infected B cells in X-linked lymphoproliferative diseaseResponses to Microbial Challenges by SLAMF ReceptorsCytomegalovirus m154 hinders CD48 cell-surface expression and promotes viral escape from host natural killer cell controlStructure of Natural Killer Receptor 2B4 Bound to CD48 Reveals Basis for Heterophilic Recognition in Signaling Lymphocyte Activation Molecule FamilyX-linked lymphoproliferative syndromes: brothers or distant cousins?Influence of CRACC, a SLAM family receptor coupled to the adaptor EAT-2, on natural killer cell functionRegulation of SLAM-mediated signal transduction by SAP, the X-linked lymphoproliferative gene productDual functional roles for the X-linked lymphoproliferative syndrome gene product SAP/SH2D1A in signaling through the signaling lymphocyte activation molecule (SLAM) family of immune receptorsA spectrum of mutations in SH2D1A that causes X-linked lymphoproliferative disease and other Epstein-Barr virus-associated illnessesAssociation of the X-linked lymphoproliferative disease gene product SAP/SH2D1A with 2B4, a natural killer cell-activating molecule, is dependent on phosphoinositide 3-kinaseDifferential expression of SAP and EAT-2-binding leukocyte cell-surface molecules CD84, CD150 (SLAM), CD229 (Ly9) and CD244 (2B4)CD244 is expressed on dendritic cells and regulates their functionsEssential function for SAP family adaptors in the surveillance of hematopoietic cells by natural killer cellsUp on the tightrope: natural killer cell activation and inhibitionHigh expression of CD244 and SAP regulated CD8 T cell responses of patients with HTLV-I associated neurologic diseaseGenetic characterisation of spontaneous ankylosing arthropathy with unique inheritance from Fas-deficient strains of miceCD244 maintains the proliferation ability of leukemia initiating cells through SHP-2/p27kip1 signaling.Impaired humoral immunity in X-linked lymphoproliferative disease is associated with defective IL-10 production by CD4+ T cells.Molecular pathogenesis of EBV susceptibility in XLP as revealed by analysis of female carriers with heterozygous expression of SAP.On guard--activating NK cell receptors.Molecular dissection of 2B4 signaling: implications for signal transduction by SLAM-related receptors.Recognition of tumors by the innate immune system and natural killer cells.Comprehensive gene expression profiling reveals synergistic functional networks in cerebral vessels after hypertension or hypercholesterolemia.New aspects of natural-killer-cell surveillance and therapy of cancer.CRACC-CRACC interaction between Kupffer and NK cells contributes to poly I:C/D-GalN induced hepatitis.Adaptors as central mediators of signal transduction in immune cells.Molecular and immunological basis of X-linked lymphoproliferative disease.CD48 on hematopoietic progenitors regulates stem cells and suppresses tumor formation.SLAM Family Receptors Regulate Immunity with and without SAP-related AdaptorsPrimary hemophagocytic syndromes point to a direct link between lymphocyte cytotoxicity and homeostasis.Molecular and cellular pathogenesis of X-linked lymphoproliferative disease.X-linked lymphoproliferative disease due to SAP/SH2D1A deficiency: a multicenter study on the manifestations, management and outcome of the disease.The receptor Ly108 functions as a SAP adaptor-dependent on-off switch for T cell help to B cells and NKT cell development.A new self: MHC-class-I-independent natural-killer-cell self-tolerance.SAP regulates T cell-mediated help for humoral immunity by a mechanism distinct from cytokine regulation.Altered lymphocyte responses and cytokine production in mice deficient in the X-linked lymphoproliferative disease gene SH2D1A/DSHP/SAPNatural killer cell inhibitory receptors block actin cytoskeleton-dependent recruitment of 2B4 (CD244) to lipid rafts.2B4 acts as a non-major histocompatibility complex binding inhibitory receptor on mouse natural killer cells.
P2860
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P2860
Functional requirement for SAP in 2B4-mediated activation of human natural killer cells as revealed by the X-linked lymphoproliferative syndrome.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Functional requirement for SAP ...... lymphoproliferative syndrome.
@en
type
label
Functional requirement for SAP ...... lymphoproliferative syndrome.
@en
prefLabel
Functional requirement for SAP ...... lymphoproliferative syndrome.
@en
P2093
P1476
Functional requirement for SAP ...... lymphoproliferative syndrome.
@en
P2093
J H Phillips
K E Nichols
L L Lanier
S G Tangye
P304
P356
10.4049/JIMMUNOL.165.6.2932
P407
P577
2000-09-01T00:00:00Z