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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
6 to leukocytes from gamma-chain-deficient and Fc gamma RII-deficient mice was reduced compared with bi
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
11 c gamma RII with IV.3 Fab fragments (an anti-Fc gamma RII mAb), and stimulated the platelets by cross
15 of Fc receptors for IgG, Fc gamma RI (CD64), Fc gamma RII (CD32), and Fc gamma RIII (CD16), are expre
17 rast, cross-linking of endocytosis-competent Fc gamma RII isoforms did not inhibit endocytosis or pro
19 IgG complexes via CD32 (the type II IgG FcR, Fc gamma RII) enhances Ag presentation 100-fold over non
21 co-clustering with the Fc receptor for IgG (Fc gamma RII) rather than stimulation of the BCR alone.
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
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
32 es is involved in binding to all Fc gamma R; Fc gamma RII and Fc gamma RIII also utilize residues out
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
44 RIIA-mediated phagocytic signaling and that Fc gamma RII cross-linking leads to tyrosine phosphoryla
47 The mechanism reflects the ability of the Fc gamma RII cytoplasmic tail to recruit specific phosph
50 receptor off-signal." IL-4 or blocking Ab to Fc gamma RII, present with whole anti-Ig, restores cell
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