2012
DOI: 10.1371/journal.pone.0029672
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Kinome Analysis of Receptor-Induced Phosphorylation in Human Natural Killer Cells

Abstract: BackgroundNatural killer (NK) cells contribute to the defense against infected and transformed cells through the engagement of multiple germline-encoded activation receptors. Stimulation of the Fc receptor CD16 alone is sufficient for NK cell activation, whereas other receptors, such as 2B4 (CD244) and DNAM-1 (CD226), act synergistically. After receptor engagement, protein kinases play a major role in signaling networks controlling NK cell effector functions. However, it has not been characterized systematical… Show more

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Cited by 18 publications
(18 citation statements)
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“…We speculated that PKCη might be responsible for DNAM-1-dependent PKC signaling. This possibility is based on prior studies where phosphorylation of the cytoplasmic motifs of DNAM-1 was assessed in the presence and absence of PKC (Shibuya et al, 1998; Shirakawa et al, 2005), kinome analysis after cross-linking of DNAM-1 (Konig et al, 2012), transcriptional profiling of PKC isozymes in mouse and human NK cells (http://www.immgen.org/), and analysis of PKCθ-deficient ( Prkcq −/− ) mice after MCMV infection (Tassi et al, 2008). To address whether Fyn and PKC are directly involved in downstream signaling of DNAM-1, Cd226 −/− hematopoietic progenitor cells (HPCs) were transduced with retroviral vectors encoding WT DNAM-1, a S326F mutant in a PKC-binding motif, a Y319F mutant in a Fyn-binding site, or a SFYF mutant with both mutations.…”
Section: Resultsmentioning
confidence: 99%
“…We speculated that PKCη might be responsible for DNAM-1-dependent PKC signaling. This possibility is based on prior studies where phosphorylation of the cytoplasmic motifs of DNAM-1 was assessed in the presence and absence of PKC (Shibuya et al, 1998; Shirakawa et al, 2005), kinome analysis after cross-linking of DNAM-1 (Konig et al, 2012), transcriptional profiling of PKC isozymes in mouse and human NK cells (http://www.immgen.org/), and analysis of PKCθ-deficient ( Prkcq −/− ) mice after MCMV infection (Tassi et al, 2008). To address whether Fyn and PKC are directly involved in downstream signaling of DNAM-1, Cd226 −/− hematopoietic progenitor cells (HPCs) were transduced with retroviral vectors encoding WT DNAM-1, a S326F mutant in a PKC-binding motif, a Y319F mutant in a Fyn-binding site, or a SFYF mutant with both mutations.…”
Section: Resultsmentioning
confidence: 99%
“…Cytotoxicity, but not development, was studied in NK-92 and YTS NK cells by 2D-PAGE and peptide sequencing approaches pending on activating signals (28 -32). At least one proteome study investigates ex vivo expanded primary human NK cells, and focuses on the characterization of kinases, involved in NK cell activation (33). Attempts to unravel the basics of NK cell development in mice were successful (34) but not completely transferable to the human NK cell system because of a different set of surface receptors.…”
mentioning
confidence: 99%
“…NK cells do express other candidate IP 4 effectors, including the PIP 3 -binding TFKs Itk and Tec. 48 They also express IP 4 /PIP 3 nonbinding Rlk. Although TFKs activate PLC␥1-dependent signals important for IFN␥ and granule secretion, 4,18 no NK cell defects were reported for Itk Ϫ/Ϫ or Itk Ϫ/Ϫ Rlk Ϫ/Ϫ mice, possibly because of TFK redundancy.…”
Section: Soluble Ip4 Limits Nk Cell Effector Functions 295mentioning
confidence: 99%