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• W2102267654 endingPage "1974" @default.
• W2102267654 startingPage "1965" @default.
• W2102267654 abstract "Natural killer (NK) cells are named based on their natural cytotoxic activity against a variety of target cells. However, the mechanisms by which sensitive targets activate killing have been difficult to study due to the lack of a prototypic NK cell triggering receptor. Pharmacologic evidence has implicated protein tyrosine kinases (PTKs) in natural killing; however, Lck-deficient, Fyn-deficient, and ZAP-70-deficient mice do not exhibit defects in natural killing despite demonstrable defects in T cell function. This discrepancy implies the involvement of other tyrosine kinases. Here, using combined biochemical, pharmacologic, and genetic approaches, we demonstrate a central role for the PTK Syk in natural cytotoxicity. Biochemical analyses indicate that Syk is tyrosine phosphorylated after stimulation with a panel of NK-sensitive target cells. Pharmacologic exposure to piceatannol, a known Syk family kinase inhibitor, inhibits natural cytotoxicity. In addition, gene transfer of dominant-negative forms of Syk to NK cells inhibits natural cytotoxicity. Furthermore, sensitive targets that are rendered NK-resistant by major histocompatibility complex (MHC) class I transfection no longer activate Syk. These data suggest that Syk activation is an early and requisite signaling event in the development of natural cytotoxicity directed against a variety of cellular targets." @default.
• W2102267654 created "2016-06-24" @default.
• W2102267654 creator A5009895370 @default.
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• W2102267654 creator A5078366360 @default.
• W2102267654 creator A5080426319 @default.
• W2102267654 creator A5088234677 @default.
• W2102267654 date "1997-12-15" @default.
• W2102267654 modified "2023-10-17" @default.
• W2102267654 title "Functional Role for Syk Tyrosine Kinase in Natural Killer Cell–mediated Natural Cytotoxicity" @default.
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• W2102267654 doi "https://doi.org/10.1084/jem.186.12.1965" @default.
• W2102267654 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2199178" @default.
• W2102267654 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9396765" @default.
• W2102267654 hasPublicationYear "1997" @default.
• W2102267654 type Work @default.

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