SH2 domain-containing protein 1A

Nichols KE et al. (2005) Regulation of NKT cell development by SAP, the protein defective in XLP.

Morra M et al. (2001) Characterization of SH2D1A missense mutations identified in X-linked lymphoproliferative disease patients.

Latour S et al. (2001) Regulation of SLAM-mediated signal transduction by SAP, the X-linked lymphoproliferative gene product.

Sumazaki R et al. (2001) SH2D1A mutations in Japanese males with severe Epstein-Barr virus--associated illnesses.

Hwang PM et al. (2002) A "three-pronged" binding mechanism for the SAP/SH2D1A SH2 domain: structural basis and relevance to the XLP syndrome.

Li C et al. (2003) Dual functional roles for the X-linked lymphoproliferative syndrome gene product SAP/SH2D1A in signaling through the signaling lymphocyte activation molecule (SLAM) family of immune receptors.

Crotty S et al. (2003) SAP is required for generating long-term humoral immunity.

Chan B et al. (2003) SAP couples Fyn to SLAM immune receptors.

Parolini O et al. (2003) Differential methylation pattern of the X-linked lymphoproliferative (XLP) disease gene SH2D1A correlates with the cell lineage-specific transcription.

Sanzone S et al. (2003) SLAM-associated protein deficiency causes imbalanced early signal transduction and blocks downstream activation in T cells from X-linked lymphoproliferative disease patients.

Czar MJ et al. (2001) Altered lymphocyte responses and cytokine production in mice deficient in the X-linked lymphoproliferative disease gene SH2D1A/DSHP/SAP.

Pasquier B et al. (2005) Defective NKT cell development in mice and humans lacking the adapter SAP, the X-linked lymphoproliferative syndrome gene product.

Morra M et al. (2005) Defective B cell responses in the absence of SH2D1A.

Aoukaty A et al. (2005) Role for glycogen synthase kinase-3 in NK cell cytotoxicity and X-linked lymphoproliferative disease.

Veillette A et al. (2008) SAP expression in T cells, not in B cells, is required for humoral immunity.

Deenick EK et al. (2008) Immunology: Helpful T cells are sticky.

Qi H et al. (2008) SAP-controlled T-B cell interactions underlie germinal centre formation.

Nagy N et al. (2009) The proapoptotic function of SAP provides a clue to the clinical picture of X-linked lymphoproliferative disease.

Snow AL et al. (2009) Restimulation-induced apoptosis of T cells is impaired in patients with X-linked lymphoproliferative disease caused by SAP deficiency.

Recher M et al. (2013) Intronic SH2D1A mutation with impaired SAP expression and agammaglobulinemia.

Yin L et al. (1999) SH2D1A mutation analysis for diagnosis of XLP in typical and atypical patients.

Shapiro MB et al. (1987) RNA splice junctions of different classes of eukaryotes: sequence statistics and functional implications in gene expression.

None (1982) The CBA/N mouse strain: an experimental model illustrating the influence of the X-chromosome on immunity.

Thorley-Lawson DA et al. (1982) Epstein-Barr virus superinduces a new human B cell differentiation antigen (B-LAST 1) expressed on transformed lymphoblasts.

Coffey AJ et al. (1998) Host response to EBV infection in X-linked lymphoproliferative disease results from mutations in an SH2-domain encoding gene.

Sayos J et al. (1998) The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM.

Sumegi J et al. () The molecular genetics of X-linked lymphoproliferative (Duncan's) disease.

Tangye SG et al. (1999) Cutting edge: human 2B4, an activating NK cell receptor, recruits the protein tyrosine phosphatase SHP-2 and the adaptor signaling protein SAP.

Poy F et al. (1999) Crystal structures of the XLP protein SAP reveal a class of SH2 domains with extended, phosphotyrosine-independent sequence recognition.

Brandau O et al. (1999) Epstein-Barr virus-negative boys with non-Hodgkin lymphoma are mutated in the SH2D1A gene, as are patients with X-linked lymphoproliferative disease (XLP).

Ross MT et al. (2005) The DNA sequence of the human X chromosome.

Strahm B et al. (2000) Recurrent B-cell non-Hodgkin's lymphoma in two brothers with X-linked lymphoproliferative disease without evidence for Epstein-Barr virus infection.

Lappalainen I et al. (2000) Structural basis for SH2D1A mutations in X-linked lymphoproliferative disease.

Sylla BS et al. (2000) The X-linked lymphoproliferative syndrome gene product SH2D1A associates with p62dok (Dok1) and activates NF-kappa B.

Parolini S et al. (2000) X-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 cells.

Tangye SG et al. (2000) Functional requirement for SAP in 2B4-mediated activation of human natural killer cells as revealed by the X-linked lymphoproliferative syndrome.

Benoit L et al. (2000) Defective NK cell activation in X-linked lymphoproliferative disease.

Sumegi J et al. (2000) Correlation of mutations of the SH2D1A gene and epstein-barr virus infection with clinical phenotype and outcome in X-linked lymphoproliferative disease.

Arico M et al. (2001) Hemophagocytic lymphohistiocytosis due to germline mutations in SH2D1A, the X-linked lymphoproliferative disease gene.

Wu C et al. (2001) SAP controls T cell responses to virus and terminal differentiation of TH2 cells.