Associated Papers
CoDIAC: A comprehensive approach for interaction analysis reveals novel insights into SH2 domain function and regulation.
Kandoor A et al.
Biorxiv : the Preprint Server for Biology, 2025
39091881 (PubMed )
Supplement: media-5.xlsx › B.Mutation_classification
2B4 dysfunction in XLP1 NK cells: More than inability to control EBV infection.
Pende D et al.
Clinical Immunology (orlando, Fla.), 2019
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
Biochemical and genetic evidence for a SAP-PKC-theta interaction contributing to IL-4 regulation.
Cannons JL et al.
Journal of Immunology (baltimore, Md. : 1950), 2010
Genome wide analysis of pathogenic SH2 domain mutations.
Lappalainen I et al.
Proteins, 2008
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
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
Association of the X-linked lymphoproliferative disease gene product SAP/SH2D1A with 2B4, a natural killer cell-activating molecule, is dependent on phosphoinositide 3-kinase.
Aoukaty A et al.
The Journal of Biological Chemistry, 2002
Lymphocytic vasculitis in X-linked lymphoproliferative disease.
Dutz JP et al.
Blood, 2001
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