| pubmed-article:9774102 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9774102 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
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| pubmed-article:9774102 | lifeskim:mentions | umls-concept:C1420017 | lld:lifeskim |
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| pubmed-article:9774102 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:9774102 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:9774102 | lifeskim:mentions | umls-concept:C1704222 | lld:lifeskim |
| pubmed-article:9774102 | lifeskim:mentions | umls-concept:C2700633 | lld:lifeskim |
| pubmed-article:9774102 | pubmed:issue | 6701 | lld:pubmed |
| pubmed-article:9774102 | pubmed:dateCreated | 1998-11-5 | lld:pubmed |
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| pubmed-article:9774102 | pubmed:abstractText | In addition to triggering the activation of B- or T-cell antigen receptors, the binding of a ligand to its receptor at the cell surface can sometimes determine the physiological outcome of interactions between antigen-presenting cells, T and B lymphocytes. The protein SLAM (also known as CDw150), which is present on the surface of B and T cells, forms such a receptor-ligand pair as it is a self-ligand. We now show that a T-cell-specific, SLAM-associated protein (SAP), which contains an SH2 domain and a short tall, acts as an inhibitor by blocking recruitment of the SH2-domain-containing signal-transduction molecule SHP-2 to a docking site in the SLAM cytoplasmic region. The gene encoding SAP maps to the same area of the X chromosome as the locus for X-linked lymphoproliferative disease (XLP) and we found mutations in the SAP gene in three XLP patients. Absence of the inhibitor SAP in XLP patients affects T/B-cell interactions induced by SLAM, leading to an inability to control B-cell proliferation caused by Epstein-Barr virus infections. | lld:pubmed |
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| pubmed-article:9774102 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9774102 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9774102 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9774102 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:9774102 | pubmed:issn | 0028-0836 | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:WuCC | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:GehaRR | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:TerhorstCC | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:WaniHH | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:AllenDD | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:De VriesJ EJE | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:OettgenHH | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:ZhangXX | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:RoncaroloM... | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:AversaGG | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:NotarangeloLL | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:MorraMM | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:SayosJJ | lld:pubmed |
| pubmed-article:9774102 | pubmed:author | pubmed-author:van SchaikSS | lld:pubmed |
| pubmed-article:9774102 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9774102 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:9774102 | pubmed:volume | 395 | lld:pubmed |
| pubmed-article:9774102 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9774102 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9774102 | pubmed:pagination | 462-9 | lld:pubmed |
| pubmed-article:9774102 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:9774102 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9774102 | pubmed:articleTitle | The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM. | lld:pubmed |
| pubmed-article:9774102 | pubmed:affiliation | Division of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. jortega@bidmc.harvard.edu | lld:pubmed |
| pubmed-article:9774102 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9774102 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9774102 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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