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1 ion by chemoattractants, such as the peptide N-formyl-methionyl-leucyl-phenylalanine.
2 nules in the cremaster muscle in response to N-formyl- methionyl-leucyl-phenylalanine.
4 chemotactic responses upon stimulation with N-formyl methionyl leucyl phenylalanine and CC chemokine
5 g when cells are simultaneously treated with N-formyl-methionyl-leucyl-phenylalanine and IgE plus pol
6 of PMN to two biologically relevant agents, N-formyl-methionyl-leucyl-phenylalanine and leukotriene
7 to the chemoattractants interleukin 8, C5a, N-formyl-methionyl-leucyl-phenylalanine, and interleukin
8 however, P. stomatis significantly increased N-formyl-methionyl-leucyl phenylalanine (fMLF)-stimulate
9 Pak translocates to the plasma membrane upon N-formyl-methionyl-leucyl-phenylalanine (fMLF) stimulati
12 horbol 12-beta-myristate 13-alpha-acetate or N-formyl methionyl-leucyl-phenylalanine (fMLP) for stimu
13 ound that the chemotactic bacterial peptide, N-formyl- methionyl-leucyl-phenylalanine (fMLP), was abl
14 by lung isolation and ex vivo perfusion with n-formyl-methionyl-leucyl-phenylalanine (fMLP) (10(-)(7)
15 (oxidative species and elastase) exposed to N-formyl-methionyl-leucyl-phenylalanine (fMLP) and/or mu
17 porally decreasing chemoattractant signal of N-formyl-methionyl-leucyl-phenylalanine (FMLP) in the ab
19 pendent decreases in secondary activation by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbo
20 ha (TNF-alpha)-primed human neutrophils with N-formyl-methionyl-leucyl-phenylalanine (fMLP) results i
21 kinases (MAPK)] were assessed in response to N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulati
22 Secondary stimulation of PMNs with 1 muM N-formyl-methionyl-leucyl-phenylalanine (fMLP) triggered
23 , interleukin-8 (IL-8), formylpeptides (e.g. N-formyl-methionyl-leucyl-phenylalanine (fMLP)), and pla
24 h was stimulated using N-formylated peptide (N-formyl-methionyl-leucyl-phenylalanine (fMLP)), platele
25 n by HT29-Cl.19A cells permits absorption of N-formyl-methionyl-leucyl-phenylalanine (fMLP), as occur
26 ating factor (G-CSF) and then activated with N-formyl-methionyl-leucyl-phenylalanine (FMLP), C(2)-cer
28 AA receptor in the CNS, and also reduces the N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced n
29 2alpha, was used to examine the mechanism of N-formyl-methionyl-leucyl-phenylalanine (fMLP)-mediated
34 ol myristate acetate, opsonized zymosan, and N-formyl-methionyl-leucyl-phenylalanine) induce p22(phox
35 3580, was able to abolish the TNF-alpha- and N-formyl-methionyl-leucyl-phenylalanine-induced activati
36 ing was examined by quantitative analysis of N-formyl-methionyl-leucyl-phenylalanine-induced increase
37 eutrophils were deficient in spontaneous and N-formyl-methionyl-leucyl-phenylalanine-induced polariza
38 migration in response to multiple agonists (N-formyl-methionyl-leucyl-phenylalanine, interleukin-8,
39 abeled chemotactic peptide receptor agonist (N-formyl-methionyl-leucyl-phenylalanine-lysine; N-For-ML
40 sPLA(2)-X to eosinophils under conditions of N-formyl-methionyl-leucyl-phenylalanine-mediated cPLA(2)
41 oth activities when cells were stimulated by N-formyl-methionyl-leucyl-phenylalanine or opsonized zym
42 in perforated-patch configuration with PMA, N-formyl-methionyl-leucyl-phenylalanine, or anti-IgE gre
43 L-13, in basophils stimulated with anti-IgE, N-formyl-methionyl-leucyl-phenylalanine, or phorbol 12-m
44 ly suppressed basophil activation induced by N-formyl-methionyl-leucyl-phenylalanine, phorbol 12-myri
45 the rate of pseudopod extension induced with N-formyl-methionyl-leucyl-phenylalanine, platelet activa
47 d (CD11b/CD18, the mannose receptor, and the N-formyl-methionyl-leucyl-phenylalanine receptor) did no
48 lly, it inhibited arachidonate production in N-formyl-methionyl-leucyl-phenylalanine-stimulated U937
49 g activity of alphaMbeta2 integrin following N-formyl-methionyl-leucyl phenylalanine stimulation.
50 necrosis factor-alpha (TNF-alpha) as well as N-formyl-methionyl-leucyl-phenylalanine treatment leads
51 ization method that retains coupling between N-formyl-methionyl-leucyl-phenylalanine tripeptide (FMLP
52 otaxis defects were also seen in response to N-formyl-methionyl-leucyl-phenylalanine, zymosan-activat
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