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1 ynthesis of two soluble peptides: peptide A [Fc gamma RII-(108-119), RCHSWRNKLLNRamide] and peptide B
2 ytoplasmic regions of the mouse low-affinity Fc gamma RII isoforms, Fc gamma RIIb1 and Fc gamma RIIb2
3  Fc gamma RII tyrosine phosphorylation after Fc gamma RII cross-linking did not change in the absence
4           Since co-clustering of the BCR and Fc gamma RII also down-regulates proliferation induced b
5 , and mice deficient in both gamma-chain and Fc gamma RII that lack all Fc gamma R.
6 to leukocytes from gamma-chain-deficient and Fc gamma RII-deficient mice was reduced compared with bi
7 Ns did not change beta-actin mRNA levels and Fc gamma RII cell-surface expression.
8 s indicate that occupancy of Fc gamma RI and Fc gamma RII on the monocytic cell line THP-I and on pol
9 o form complexes with both Fc epsilon RI and Fc gamma RII, and inhibit mast-cell and basophil functio
10 psilon bound to both human Fc epsilon RI and Fc gamma RII.
11 c gamma RII with IV.3 Fab fragments (an anti-Fc gamma RII mAb), and stimulated the platelets by cross
12 MA, dextran sulfate, and the monoclonal anti-Fc gamma RII 2.4G2).
13 (108-119), RCHSWRNKLLNRamide] and peptide B [Fc gamma RII-(153-165), CKGSLGRTLHQSKamide].
14 atidylserine receptor, but not CD36 or CD32 (Fc gamma RII).
15 of Fc receptors for IgG, Fc gamma RI (CD64), Fc gamma RII (CD32), and Fc gamma RIII (CD16), are expre
16  RII isoform typically expressed by B cells (Fc gamma RII-B1) is incompetent for endocytosis.
17 rast, cross-linking of endocytosis-competent Fc gamma RII isoforms did not inhibit endocytosis or pro
18             By linking surface Ig to the FcR Fc gamma RII on the mouse B lymphocyte surface, whole an
19 IgG complexes via CD32 (the type II IgG FcR, Fc gamma RII) enhances Ag presentation 100-fold over non
20 gage with FcgammaRIIIA, as well as the human Fc gamma RII subset.
21  co-clustering with the Fc receptor for IgG (Fc gamma RII) rather than stimulation of the BCR alone.
22                           When cross-linked, Fc gamma RII-B1 acts as a dominant negative inhibitor of
23 sine phosphorylation, we found that such non-Fc gamma RII-mediated cross-linking of CD9, CD42 and gly
24 can be analysed provided that the effects of Fc gamma RII engagement can either be reduced or elimina
25  Trapping of IC in spleen and lymph nodes of Fc gamma RII-/- mice was significantly reduced compared
26 linking leads to tyrosine phosphorylation of Fc gamma RII independent of Syk kinase.
27 o detected upon aggregation of Fc alpha R or Fc gamma RII, which induced the phosphorylation of nonag
28 mes more IL-8 than did either Fc gamma RI or Fc gamma RII clustering (p = 0.001) and stimulated 77% m
29                                  Several pan-Fc gamma RII Abs that label the placental endothelium di
30           We have therefore blocked platelet Fc gamma RII with IV.3 Fab fragments (an anti-Fc gamma R
31 he Fc portion of these mAb with the platelet Fc gamma RII.
32 es is involved in binding to all Fc gamma R; Fc gamma RII and Fc gamma RIII also utilize residues out
33 ma-chains and low affinity IgG Fc receptors (Fc gamma RII).
34                          Fc gamma receptors (Fc gamma RII) on B lymphocytes negatively regulate B cel
35 ked by antibodies to the other Fc receptors, Fc gamma RII and Fc gamma RIII.
36                               Fc epsilon RI, Fc gamma RII, and Fc gamma RIII expression was not affec
37 elative to typical Fc gamma Rs: Fc gamma RI, Fc gamma RII, and Fc gamma RIII.
38 oss-linking of Abs specific for Fc gamma RI, Fc gamma RII, or Fc gamma RIII.
39 ted cytotoxicity (ADCC) through Fc gamma RI, Fc gamma RII, or Fc gamma RIII.
40 ever, because IgG receptors (Fc-gamma RIIb2, Fc-gamma RII) were present on eosinophils purified from
41 ice that lack Fc gamma RI and Fc gamma RIII, Fc gamma RII-deficient mice, and mice deficient in both
42 for IgG than the lower affinity Fc gamma Rs, Fc gamma RII and Fc gamma RIIIb.
43 mmune-complex binding to immobilized soluble Fc gamma RII.
44  RIIA-mediated phagocytic signaling and that Fc gamma RII cross-linking leads to tyrosine phosphoryla
45       Immunoblotting assay demonstrated that Fc gamma RII tyrosine phosphorylation after Fc gamma RII
46                      This occurs because the Fc gamma RII isoform typically expressed by B cells (Fc
47    The mechanism reflects the ability of the Fc gamma RII cytoplasmic tail to recruit specific phosph
48            These experiments showed that the Fc gamma RII expressed in villus endothelium was the b2
49                                        Thus, Fc gamma RII-B1 acts not only to prevent B cell activati
50 receptor off-signal." IL-4 or blocking Ab to Fc gamma RII, present with whole anti-Ig, restores cell

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