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1                                              Fc gamma RI cross-linking of U937IF cells results in the
2 G and Crkl provide the first evidence that a Fc gamma RI gamma-Crkl-C3G complex may link ITAM recepto
3 ti-Fc gamma RI or anti-gamma-chain Abs after Fc gamma RI clustering suggests that, like other recepto
4 s of tyrosine kinases become activated after Fc gamma RI clustering.
5 amma-treated cultured human mast cells after Fc gamma RI or Fc epsilon RI aggregation.
6 ased and generated to a greater degree after Fc gamma RI aggregation, suggesting that selected biolog
7 with Cbl, Hef-1, and Fc gamma RI gamma after Fc gamma RI activation and the constitutive association
8 hosphorylation of the kinase increases after Fc gamma RI clustering.
9                  We further found that after Fc gamma RI clustering, tyrosine-phosphorylated Syk asso
10 effects were mediated by the gamma chain, an Fc gamma RI accessory protein.
11 ced association of Crkl with Cbl, Hef-1, and Fc gamma RI gamma after Fc gamma RI activation and the c
12 ed enhancement of Fc gamma RI expression and Fc gamma RI gamma-chain complexes, the regulation of Fc
13 oupled G protein G alpha i3, Src kinase, and Fc gamma RI within LRs.
14                     Although Fc alpha RI and Fc gamma RI share a common signaling pathway contingent
15 gocytosis of SKBR-3 cells by Fc alpha RI and Fc gamma RI; however, IFN-gamma-treated MDM phagocytosed
16 d phagocytosis mediated by Fc gamma RIIa and Fc gamma RI in PMN and amplified receptor-triggered tyro
17 RP on human leukocytes are Fc gamma RIIa and Fc gamma RI, respectively.
18 ing cytoplasmic domains of Fc gamma RIIa and Fc gamma RI-associated gamma-chain.
19 nce that Fc gamma RIIb1, Fc gamma RIIb2, and Fc gamma RI are the receptors for CRP on mouse leukocyte
20 ylated proteins that coprecipitate with anti-Fc gamma RI or anti-gamma-chain Abs after Fc gamma RI cl
21 witch in the accessory molecule recruited by Fc gamma RI, which lacks its own intrinsic signal transd
22 ht days later neointimal thickening in CRPtg/Fc gamma RI(-/-) and CRPtg/FcR gamma (-/-) was significa
23 to release 5 times more IL-8 than did either Fc gamma RI or Fc gamma RII clustering (p = 0.001) and s
24 c gamma RIIIb, and can be induced to express Fc gamma RI by IFN-gamma.
25 fferentially express two additional IgG FcR, Fc gamma RI (CD64) and Fc gamma RIII (CD16), which may a
26 Cbl-Crkl and Crkl-C3G interactions following Fc gamma RI aggregation in U937IF cells.
27 human mast cells exhibit minimal message for Fc gamma RI.
28 x beads or cross-linking of Abs specific for Fc gamma RI, Fc gamma RII, or Fc gamma RIII.
29  of the binding site on human IgG1 for human Fc gamma RI, Fc gamma RIIA, Fc gamma RIIB, Fc gamma RIII
30  activities of the type I receptors for IgG (Fc gamma RI) and the IgA FcR (Fc alpha RI) on monocyte-d
31 mplex of the high affinity receptor for IgG (Fc gamma RI), we have undertaken the identification of t
32          The high affinity receptor for IgG (Fc gamma RI, CD64) is expressed on human mast cells, whe
33 y for the high-affinity Fc receptor for IgG (Fc gamma RI/CD64) and the B-cell differentiation antigen
34       Three classes of Fc receptors for IgG, Fc gamma RI (CD64), Fc gamma RII (CD32), and Fc gamma RI
35 sses of FcR that bind the Fc portion of IgG, Fc gamma RI, and Fc gamma RIIIa associate with a subunit
36  tyrosine kinases (PTKs), Syk and ZAP-70, in Fc gamma RI-mediated signaling.
37 inflammation, whereas no defect was found in Fc gamma RI(-/-) mice.
38                                The switch in Fc gamma RI signalling pathways upon monocyte differenti
39 e expression; they enhance IFN-gamma-induced Fc gamma RI mRNA and protein expression, yet inhibit IFN
40 ition, stem-loop Syk antisense ODN inhibited Fc gamma RI and Fc gamma RIIIA-mediated phagocytosis.
41 amined: gamma-chain-deficient mice that lack Fc gamma RI and Fc gamma RIII, Fc gamma RII-deficient mi
42            OVX NTG, CRPtg, and CRPtg lacking Fc gamma RI, Fc gamma RIIb, Fc gamma RIII, or the common
43 little or none was observed in those lacking Fc gamma RI or FcR gamma.
44 from the parent molecule or by cross-linking Fc gamma RI.
45 induced the phosphorylation of nonaggregated Fc gamma RI gamma-chains.
46 ced by human mast cells after aggregation of Fc gamma RI are incompletely described, and it is unknow
47 ignificantly up-regulated via aggregation of Fc gamma RI compared with Fc epsilon RI.
48                  In contrast, aggregation of Fc gamma RI in the presence of vanadate induced the sust
49                               Aggregation of Fc gamma RI on human mast cells, and only after IFN-gamm
50                         Thus, aggregation of Fc gamma RI on mast cells led to up-regulation and/or re
51                               Aggregation of Fc gamma RI resulted in histamine release and PGD(2) and
52 ed to a more macrophage type, aggregation of Fc gamma RI resulted in the Fc gamma RIIa-mediated activ
53 ception of IFN-gamma-mediated enhancement of Fc gamma RI expression and Fc gamma RI gamma-chain compl
54 fects on the IFN-gamma-induced expression of Fc gamma RI and Ia mRNA and cell surface expression; the
55 hat IFN-gamma up-regulated the expression of Fc gamma RI.
56 so inhibited IFN-gamma-induced expression of Fc gamma RI.
57 DEX) treatment on the IFN-gamma induction of Fc gamma RI and Ia mRNA in murine primary peritoneal mac
58 nduced enhancement of IFN-gamma induction of Fc gamma RI, suggesting a common GR-mediated mechanism.
59       Our results indicate that occupancy of Fc gamma RI and Fc gamma RII on the monocytic cell line
60 in the transient tyrosine phosphorylation of Fc gamma RI gamma-chain but not the phosphorylation of g
61 ed the sustained tyrosine phosphorylation of Fc gamma RI gamma-chains and the rapid and extensive pho
62  RI gamma-chain complexes, the regulation of Fc gamma RI- or Fc alpha RI-mediated activity occurred w
63  Fc gamma RIIa or the gamma-chain subunit of Fc gamma RI and Fc gamma RIIIa.
64 te that the ITAM-containing gamma subunit of Fc gamma RI is induced to form a complex with the Crkl p
65 jury provoked by CRP in OVX CRPtg depends on Fc gamma RI and probably requires its expression by F4/8
66                            In contrast, only Fc gamma RI cross-linking significantly induced monocyte
67              Aggregation of Fc epsilon RI or Fc gamma RI led to an induction or accumulation of 22 cy
68 rcinoma cell line, SKBR-3, to Fc alpha RI or Fc gamma RI on MDM.
69 d that clustering of either Fc gamma RIIa or Fc gamma RI is effective in inducing SHIP phosphorylatio
70 s, aggregation of the high-affinity receptor Fc gamma RI resulted in the activation of phospholipase
71 might express the high-affinity IgG receptor Fc gamma RI and in turn be activated through aggregation
72 gement of the high-affinity IgG Fc receptor (Fc gamma RI) activates a signal transduction pathway inv
73  of U937 cell high affinity IgG Fc receptor (Fc gamma RI) results in the transient tyrosine phosphory
74 n of ITP by CRP-treated splenocytes required Fc gamma RI on the donor cell and Fc gamma RIIb in the r
75  cell types relative to typical Fc gamma Rs: Fc gamma RI, Fc gamma RII, and Fc gamma RIII.
76 nt lysis of tumor cells via Fc alpha RI than Fc gamma RI, while M-CSF-cultured MDM were relatively le
77                Our findings demonstrate that Fc gamma RI requires gamma -chain association to attain
78 ent, the gamma response region (GRR), of the Fc gamma RI gene, substantially less tyrosine phosphoryl
79                         Cross-linking of the Fc gamma RI multimeric receptor in monocytic cells resul
80 dy constructs bind to an epitope outside the Fc gamma RI ligand binding site, we show that autologous
81 d MDM phagocytosed tumor cells only with the Fc gamma RI-directed bispecific Abs.
82 nt cell-mediated cytotoxicity (ADCC) through Fc gamma RI, Fc gamma RII, or Fc gamma RIII.
83 monocyte IL-8 is stimulated directly through Fc gamma RI cross-linking and indirectly through an Fc g
84 ells may be preferentially generated through Fc gamma RI in an IFN-gamma-rich environment.
85 RP generates suppressive macrophages through Fc gamma RI, which then act through an Fc gamma RIIb-dep
86 dependent phagocytosis was triggered through Fc gamma RI and could be blocked only by using F(ab')2 f
87  due to the avid binding of monomeric IgG to Fc gamma RI.
88 d MDM lysed tumor cells more efficiently via Fc gamma RI then by Fc alpha RI as measured in Ab-depend
89  This was confirmed by flow cytometry, where Fc gamma RI expression on human mast cells was increased
90 I were expressed in the CRPtg arteries, with Fc gamma RI expression increasing by threefold after lig
91 ly with the gamma-chain subunit and not with Fc gamma RI itself.

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