Host response to EBV infection in X-linked lymphoproliferative disease results from mutations in an SH2-domain encoding gene
about
The DNA sequence of the human X chromosomeEpstein-Barr virus-negative boys with non-Hodgkin lymphoma are mutated in the SH2D1A gene, as are patients with X-linked lymphoproliferative disease (XLP)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 syndromeSLAM/SLAM interactions inhibit CD40-induced production of inflammatory cytokines in monocyte-derived dendritic cellsThe X-linked lymphoproliferative disease gene product SAP associates with PAK-interacting exchange factor and participates in T cell activationLatent membrane protein 2A of Epstein-Barr virus binds WW domain E3 protein-ubiquitin ligases that ubiquitinate B-cell tyrosine kinasesStructural basis for the interaction of the free SH2 domain EAT-2 with SLAM receptors in hematopoietic cellsSelective generation of functional somatically mutated IgM+CD27+, but not Ig isotype-switched, memory B cells in X-linked lymphoproliferative diseaseProgress and problems in understanding and managing primary Epstein-Barr virus infectionsXIAP deficiency: a unique primary immunodeficiency best classified as X-linked familial hemophagocytic lymphohistiocytosis and not as X-linked lymphoproliferative diseaseNTB-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 diseaseX-linked lymphoproliferative disease. 2B4 molecules displaying inhibitory rather than activating function are responsible for the inability of natural killer cells to kill Epstein-Barr virus-infected cellsThe X-linked lymphoproliferative syndrome gene product SH2D1A associates with p62dok (Dok1) and activates NF-kappa BSiglecs in the immune systemThe molecular pathology of primary immunodeficienciesResponses to Microbial Challenges by SLAMF ReceptorsSevere infectious diseases of childhood as monogenic inborn errors of immunityCytotoxic granule secretion by lymphocytes and its link to immune homeostasisHemophagocytic lymphohistiocytosis: an update on diagnosis and pathogenesisX-linked lymphoproliferative syndromes: brothers or distant cousins?NK Cell Influence on the Outcome of Primary Epstein-Barr Virus InfectionThe Host Cell Receptors for Measles Virus and Their Interaction with the Viral Hemagglutinin (H) ProteinThe cell surface expression of SAP-binding receptor CD229 is regulated via its interaction with clathrin-associated adaptor complex 2 (AP-2)Regulation of SLAM-mediated signal transduction by SAP, the X-linked lymphoproliferative gene productInteraction domains: from simple binding events to complex cellular behaviorDual 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)Macrophage activation syndrome: advances towards understanding pathogenesisCS1 (SLAMF7) inhibits production of proinflammatory cytokines by activated monocytesAssociation between SAP and FynT: Inducible SH3 domain-mediated interaction controlled by engagement of the SLAM receptorImpaired immune responses and prolonged allograft survival in Sly1 mutant miceNegative regulation of natural killer cell function by EAT-2, a SAP-related adaptorThe adaptor protein SAP directly associates with CD3ζ chain and regulates T cell receptor signaling.Genetic characterisation of spontaneous ankylosing arthropathy with unique inheritance from Fas-deficient strains of miceExpansion of murine gammaherpesvirus latently infected B cells requires T follicular help.Common variable immunodeficiency: etiological and treatment issues.SLAM-family receptors: immune regulators with or without SAP-family adaptors.
P2860
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P2860
Host response to EBV infection in X-linked lymphoproliferative disease results from mutations in an SH2-domain encoding gene
description
1998 nî lūn-bûn
@nan
1998 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
name
Host response to EBV infection ...... in an SH2-domain encoding gene
@ast
Host response to EBV infection ...... in an SH2-domain encoding gene
@en
Host response to EBV infection ...... in an SH2-domain encoding gene
@nl
type
label
Host response to EBV infection ...... in an SH2-domain encoding gene
@ast
Host response to EBV infection ...... in an SH2-domain encoding gene
@en
Host response to EBV infection ...... in an SH2-domain encoding gene
@nl
prefLabel
Host response to EBV infection ...... in an SH2-domain encoding gene
@ast
Host response to EBV infection ...... in an SH2-domain encoding gene
@en
Host response to EBV infection ...... in an SH2-domain encoding gene
@nl
P2093
P50
P3181
P356
P1433
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Host response to EBV infection ...... in an SH2-domain encoding gene
@en
P2093
A J Coffey
B H Behloradsky
C J Shaw-Smith
D R Bentley
P2888
P304
P3181
P356
10.1038/2424
P407
P577
1998-10-01T00:00:00Z
P6179
1022544887