| pubmed-article:9625766 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0597032 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C1515881 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C1171362 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0019627 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0024348 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C1416942 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C1515670 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0205148 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:9625766 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:9625766 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:9625766 | pubmed:dateCreated | 1998-7-7 | lld:pubmed |
| pubmed-article:9625766 | pubmed:abstractText | After culture in interleukin (IL)-2, natural killer (NK) cells acquire an increased capability of mediating non-major histocompatibility complex (MHC)-restricted tumor cell lysis. This may reflect, at least in part, the de novo expression by NK cells of triggering receptors involved in cytolysis. In this study we identified a novel 44-kD surface molecule (NKp44) that is absent in freshly isolated peripheral blood lymphocytes but is progressively expressed by all NK cells in vitro after culture in IL-2. Different from other markers of cell activation such as CD69 or VLA.2, NKp44 is absent in activated T lymphocytes or T cell clones. Since NKp44 was not detected in any of the other cell lineages analyzed, it appears as the first marker specific for activated human NK cells. Monoclonal antibody (mAb)-mediated cross-linking of NKp44 in cloned NK cells resulted in strong activation of target cell lysis in a redirected killing assay. This data indicated that NKp44 can mediate triggering of NK cell cytotoxicity. mAb-mediated masking of NKp44 resulted in partial inhibition of cytolytic activity against certain (FcgammaR-negative) NK-susceptible target cells. This inhibition was greatly increased by the simultaneous masking of p46, another recently identified NK-specific triggering surface molecule. These data strongly suggest that NKp44 functions as a triggering receptor selectively expressed by activated NK cells that, together with p46, may be involved in the process of non-MHC-restricted lysis. Finally, we show that p46 and NKp44 are coupled to the intracytoplasmic transduction machinery via the association with CD3zeta or KARAP/DAP12, respectively; these associated molecules are tyrosine phosphorylated upon NK cell stimulation. | lld:pubmed |
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| pubmed-article:9625766 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9625766 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9625766 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9625766 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9625766 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:9625766 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:MorettaLL | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:MorettaAA | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:VitaleMM | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:SanseverinoLL | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:BottinoCC | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:AugugliaroRR | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:SivoriSS | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:MarcenaroEE | lld:pubmed |
| pubmed-article:9625766 | pubmed:author | pubmed-author:CastriconiRR | lld:pubmed |
| pubmed-article:9625766 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9625766 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:9625766 | pubmed:volume | 187 | lld:pubmed |
| pubmed-article:9625766 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9625766 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9625766 | pubmed:pagination | 2065-72 | lld:pubmed |
| pubmed-article:9625766 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9625766 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9625766 | pubmed:articleTitle | NKp44, a novel triggering surface molecule specifically expressed by activated natural killer cells, is involved in non-major histocompatibility complex-restricted tumor cell lysis. | lld:pubmed |
| pubmed-article:9625766 | pubmed:affiliation | Istituto Nazionale per la Ricerca sul Cancro and Centro Biotecnologie Avanzate, 16132 Genova, Italy. | lld:pubmed |
| pubmed-article:9625766 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9625766 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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