Background: SH2D1A, also SH2 domain protein 1A, SAP and CD150/SLAM (signaling lymphocyte activation molecule)-associated protein, influences signaling pathways involving SLAM molecules at the interface between T and B cells. SH2D1A modulates SLAM by blocking the recruitment of tyrosine phosphatase SHP2 to the phosphorylated cytoplasmic domain of SLAM. The cytoplasmic protein encoded by the SH2D1A gene plays an essential role in controlling EBV infection. It is expressed in T and NK cells, but not in B cells or in granulocytes. SH2D1A is expressed at a high level in thymus and lung, with a lower level of expression in spleen and liver. Defects in SH2D1A are a cause of X-linked lymphoproliferative disease (XLPD) also known as Duncan disease. XLPD is characterized by an immunodeficiency following Epstein-Barr virus (EBV) infection. Symptoms include fatal mononucleosis, hypogammaglobulinemia, pancytopenia or malignant lymphoma.
Description: Rabbit polyclonal to SAP
Immunogen: KLH conjugated synthetic peptide derived from SAP
Specificity: ·Reacts with Human, Mouse and Rat.
·Isotype: IgG
Application: ·Western blotting: 1/100-500. Predicted Mol wt: 14 kDa;
·Immunohistochemistry (Paraffin/frozen tissue section): 1/50-200;
·Immunocytochemistry/Immunofluorescence: 1/100;
·Immunoprecipitation: 1/50;
