Associated Papers
Accurate affinity models for SH2 domains from peptide binding assays and free-energy regression.
Gagoski D et al.
Protein Science : a Publication of the Protein Society, 2025
Accurate sequence-to-affinity models for SH2 domains from multi-round peptide binding assays coupled with free-energy regression.
Gagoski D et al.
Biorxiv : the Preprint Server for Biology, 2025
Hemophagocytic Lymphohistiocytosis Gene Variants in Severe Aplastic Anemia and Their Impact on Hematopoietic Cell Transplantation Outcomes.
Rafati M et al.
Transplantation and Cellular Therapy, 2024
Analysis of the FLVR motif of SHIP1 and its importance for the protein stability of SH2 containing signaling proteins.
Ehm PAH et al.
Cellular Signalling, 2019
2B4 dysfunction in XLP1 NK cells: More than inability to control EBV infection.
Pende D et al.
Clinical Immunology (orlando, Fla.), 2019
X-linked Lymphoproliferative Disease Type 1 in a Patient With the p.Gly93Asp SH2D1A Gene Mutation and Hemophagocytic Lymphohistiocytosis.
de la Varga-Martínez R et al.
Journal of Pediatric Hematology/oncology, 2017
Inhibitory 2B4 contributes to NK cell education and immunological derangements in XLP1 patients.
Meazza R et al.
European Journal of Immunology, 2017
The value of DNA storage and pedigree analysis in rare diseases: a 17-year-old boy with X-linked lymphoproliferative disease (XLP) caused by a de novo SH2D1A mutation.
Overwater E et al.
European Journal of Pediatrics, 2014
Diagnosing XLP1 in patients with hemophagocytic lymphohistiocytosis.
Meazza R et al.
The Journal of Allergy and Clinical Immunology, 2014
A unique clinical presentation of X-linked lymphoproliferative syndrome with a novel mutation in SH2D1A and review of the literature.
Eckrich MJ et al.
Journal of Pediatric Hematology/oncology, 2011
Regulation of NKT cell development by SAP, the protein defective in XLP.
Nichols KE et al.
Nature Medicine, 2005
Molecular and cellular pathogenesis of X-linked lymphoproliferative disease.
Nichols KE et al.
Immunological Reviews, 2005
The SAP and SLAM families in immune responses and X-linked lymphoproliferative disease.
Engel P et al.
Nature Reviews. Immunology, 2003
Molecular and immunological basis of X-linked lymphoproliferative disease.
Latour S et al.
Immunological Reviews, 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.
Li C et al.
The Journal of Biological Chemistry, 2003
A spectrum of mutations in SH2D1A that causes X-linked lymphoproliferative disease and other Epstein-Barr virus-associated illnesses.
Sumegi J et al.
Leukemia & Lymphoma, 2002
A "three-pronged" binding mechanism for the SAP/SH2D1A SH2 domain: structural basis and relevance to the XLP syndrome.
Hwang PM et al.
The Embo Journal, 2002
Characterization of SH2D1A missense mutations identified in X-linked lymphoproliferative disease patients.
Morra M et al.
The Journal of Biological Chemistry, 2001
X-linked lymphoproliferative disease is caused by deficiency of a novel SH2 domain-containing signal transduction adaptor protein.
Schuster V et al.
Immunological Reviews, 2000
Crystal structures of the XLP protein SAP reveal a class of SH2 domains with extended, phosphotyrosine-independent sequence recognition.
Poy F et al.
Molecular Cell, 1999