Inactivating mutations in an SH2 domain-encoding gene in X-linked lymphoproliferative syndrome
about
Epstein-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 activationStructural 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 BResponses 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 homeostasisT-regulatory cells in primary immune deficienciesX-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 two SH2-domain-containing inositol 5-phosphatases SHIP1 and SHIP2 are coexpressed in human T lymphocytesRegulation 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)CS1 (SLAMF7) inhibits production of proinflammatory cytokines by activated monocytesAssociation between SAP and FynT: Inducible SH3 domain-mediated interaction controlled by engagement of the SLAM receptorNegative 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.Expansion of murine gammaherpesvirus latently infected B cells requires T follicular help.SLAM-family receptors: immune regulators with or without SAP-family adaptors.Impaired humoral immunity in X-linked lymphoproliferative disease is associated with defective IL-10 production by CD4+ T cells.Signaling lymphocytic activation molecule (SLAM)/SLAM-associated protein pathway regulates human B-cell tolerance.Defective B cell responses in the absence of SH2D1AA novel ICOS-independent, but CD28- and SAP-dependent, pathway of T cell-dependent, polysaccharide-specific humoral immunity in response to intact Streptococcus pneumoniae versus pneumococcal conjugate vaccine.Treatment strategies for Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH).Molecular pathogenesis of EBV susceptibility in XLP as revealed by analysis of female carriers with heterozygous expression of SAP.A two-gene signature, SKI and SLAMF1, predicts time-to-treatment in previously untreated patients with chronic lymphocytic leukemia.On guard--activating NK cell receptors.
P2860
Q22010776-55C45D85-5435-44CD-9D9F-A08CCD802AC7Q24291489-3DF65FE1-BF62-44AB-9A60-FA856798CFD9Q24292245-D11C96A6-ABF1-457E-A967-2EBF61B1C016Q24297438-692F1917-1956-4CA3-A271-07BA64364119Q24303904-2ACB07D3-5D89-4CFE-B379-4E10DEA0C907Q24535874-20E4E06A-01A0-4A4A-9020-D08B4F859DC3Q24536218-2F5FDA79-7033-4EA1-9137-AA5A408CF036Q24597706-68D59859-5FDF-4BEB-9DAC-38984C66C034Q24610800-E405E09C-E2D2-418D-AC3D-C58DD61E51CEQ24675566-494F9FBE-4840-4F9C-A609-930EFC8E5A39Q24676168-10E4486E-DD10-48C1-84C5-B87E3B53378AQ24681336-FCA0F0B2-67F9-4043-8432-286D056E74F8Q26772707-45B2985D-2E46-4FCB-82F1-2CD2D7FE4779Q26775891-DEB60439-B482-438F-AA91-EFD775AF4ACEQ26776499-059C5720-D72D-4B0A-97B1-DCB0C1276C3BQ26862699-7C738325-9E06-4367-9B7B-892F2DD0B773Q27690253-8C51B144-FA1F-4CBA-A1AF-8D9029622FD7Q28069456-975B6B0F-489F-43D5-9E70-5D962D5CB81CQ28069519-1FEBA8B6-1567-418C-A009-FFA5CF57469BQ28144847-F8D695FA-D667-483A-922C-44F9B3852B4FQ28209604-E60D469A-BC71-4A48-B21D-EF31D1C3F7D8Q28209614-183F00EE-4E11-403F-9128-73695E7BCE34Q28216360-80418DBD-ABB9-4974-B4DF-FB9577B82F66Q28216635-848F0FEE-C2AF-4211-B001-F78436D8154AQ28216840-60BF6EE3-1FBE-4320-ABA1-BC3E6FDCBEE0Q28271106-38C8C55B-E037-45FD-9F3E-D995FB5AC934Q28291155-3F5B93AD-AC94-47D7-B46C-77EFFC32449DQ28585941-453B1511-20BA-45F8-915E-10BC52D1403AQ28593740-0AD8ABD3-4434-4E2D-9A48-5FE0D6CA25F7Q30010025-7F7943E8-6AD8-40CA-BC23-ED54FBFF8984Q33553789-98C144C5-8E83-421C-A9BD-806C371804F8Q33693795-7DD143D2-D121-4775-A508-7AA05B9E7051Q33700550-FEA6F82B-977F-4323-8D8F-035E819F743AQ33829714-78ED1D6C-DEF7-4969-B444-B087F1F0E234Q33935159-59D487AF-F8BE-4634-8639-08B3CF726545Q33944575-F377DA3B-4A91-4635-8B8C-A35706465BC9Q34024242-6C35CCDD-0204-4EAF-8166-AD3991B7236CQ34070452-CB22596C-E2DE-4E56-B619-D38B92E66968Q34110002-337C2A1D-ED5A-4851-905A-687F5948B53BQ34117069-19D180BB-2D89-4EAF-8C2B-5E232C655696
P2860
Inactivating mutations in an SH2 domain-encoding gene in X-linked lymphoproliferative syndrome
description
1998 nî lūn-bûn
@nan
1998 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի նոյեմբերին 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
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@ast
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@en
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@nl
type
label
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@ast
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@en
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@nl
prefLabel
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@ast
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@en
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@nl
P2093
P2860
P3181
P356
P1476
Inactivating mutations in an S ...... d lymphoproliferative syndrome
@en
P2093
A J Buckler
C Genovese
D E Housman
D P Harkin
K A Kolquist
P2860
P304
P3181
P356
10.1073/PNAS.95.23.13765
P407
P577
1998-11-10T00:00:00Z