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1 the seven transmembrane helices of the human C5a receptor.
2 he seven transmembrane segments of the human C5a receptor.
3 t couples in neutrophils is reported to be a C5a receptor.
4 kely G protein linked, but distinct from the C5a receptor.
5 ue to inhibition of C5a interaction with the C5a receptor.
6 er in mice treated with an antagonist of the C5a receptor.
7 icular, in ligand-mediated activation of the C5a receptor.
8 the order CXCR2 > CXCR1 > formyl peptide or C5a receptors.
9 onstitutively express functionally competent C5a receptors.
10 man and murine brains constitutively express C5a receptors.
11 human neuroblastoma cells express functional C5a receptors.
12 in CMs, which required availability of both C5a receptors.
13 e show that activation of complement C5a and C5a receptor 1 (C5aR1) controls GC accumulation and the
14 tracellular C5 activation and stimulation of C5a receptor 1 (C5aR1), which is negatively regulated by
15 , whereupon it interacts with the complement C5a receptor 1 expressed on tumor infiltrating myeloid-d
16 educing RPS19 in tumor cells or blocking the C5a receptor 1-RPS19 interaction decreases RPS19-mediate
17 t and third extracellular loops of the human C5a receptor, a GPCR that binds a 74-amino acid peptide
19 ttle energy transfer is observed between the C5a receptor and a co-expressed yeast pheromone receptor
21 with cDNAs encoding the complement component C5a receptor and PLC beta2 but not in cells transfected
23 L, signalling pathways downstream of C3a and C5a receptors and membrane C5b-9 assembly, and the preve
24 production of MIP-2 and KC by PTECs, whereas C5a receptor antagonism and prevention of membrane attac
25 d opsonization >2-fold, and compstatin and a C5a receptor antagonist (C5aRa) impaired granulocyte act
27 Here, oral delivery of a cyclic hexapeptide C5a receptor antagonist (PMX205) for 2-3 mo resulted in
32 -deficient mice and mice given injections of C5a-receptor antagonists developed significantly less pa
33 osition in mice deficient in C3a receptor or C5a receptor, as well as in wild-type mice depleted of h
37 TGF-beta), and whereas TGF-beta1 induced C3a/C5a receptor (C3aR/C5aR) expression, pharmacologic C3aR/
39 roid was assayed for the presence of C3a and C5a receptors (C3aR and C5aR) using RT-PCR and immunohis
42 autoantibody-induced arthritis requires the C5a receptor C5aR and FcgammaRs, but the simultaneous ne
43 the e2 loop with a smaller e2 loop from the C5a receptor (C5aR) abolished binding of 125I-C3a and C3
45 biting signaling of the complement component C5a receptor (C5aR) altered the composition and diversit
47 signals transmitted through T cell-expressed C5a receptor (C5aR) and C3a receptor (C3aR) to activatio
50 onocytic cell line U937 transfected with the C5a receptor (C5aR) and loaded with a fluorescent intrac
53 the terminal complement component C5 and the C5a receptor (C5aR) are upregulated in spinal microglia
56 ast cancer that the complement anaphylatoxin C5a receptor (C5aR) facilitates metastasis by suppressin
58 d the role of the active fragment complement C5a receptor (C5aR) in dental nerve regeneration in rega
59 prevented by the deficiency of either C3 or C5a receptor (C5aR) in the APC, demonstrating a link bet
60 We found that mice deficient in MCs or the C5a receptor (C5aR) injected with pathogenic anti-BP180
62 there are some suggestions that C5a and the C5a receptor (C5aR) might be directly linked to apoptosi
65 lacking the chemotactic or adhesion receptor C5a receptor (C5aR) or CD11a/lymphocyte function-associa
66 e show that pharmacological targeting of the C5a receptor (C5aR) or the bradykinin B2 receptor (B2R)
67 that local pharmacological targeting of the C5a receptor (C5aR) prior to initial allergen sensitizat
68 8(+) T cells lacking C3a receptor (C3aR) and C5a receptor (C5aR) proliferate weakly to allogeneic DCs
69 ells deficient in C3a receptor (C3aR) and/or C5a receptor (C5aR) responded weakly in allogeneic hosts
72 in untreated fibroblast cultures express the C5a receptor (C5aR), here we show that all dental pulp f
73 f a cyclic peptide antagonist (C5aRa) to the C5a receptor (C5aR), the binding of murine 125I-C5a to m
80 own that mice deficient either in complement C5a receptor (C5aR; CD88) or TLR2 are highly and similar
81 ibody raised against residues 9 to 29 of the C5a receptor (C5aR; CD88), we demonstrate that noncystei
83 ins C3a and C5a (ie, C3a receptor [C3aR] and C5a receptor [C5aR]), and C3a and C5a are generated duri
86 d the potential of peritoneal TLR2, TLR4 and C5a receptors, C5aR and C5L2, as therapeutic targets in
88 C5a upregulation and was markedly reduced by C5a receptor (C5aR1) knock-out or treatment with the C5a
91 e have analyzed the expression of the second C5a receptor C5L2, the putative "default" or nonsignalin
94 Phis and in the second by treatment with the C5a receptor (CD88) agonist EP67, which invokes MPhi pro
96 ed with pertussis toxin, suggesting that the C5a receptor couples to both Galpha15 and Galphai in viv
99 cordingly, we found enhanced Th1 immunity in C5a receptor-deficient mice, something that conferred pr
103 gulator of cell polarity, with inhibition of C5a receptors during embryogenesis leading to abnormal b
104 sonance energy transfer experiments on human C5a receptors expressed in the lower eukaryote Saccharom
106 disulfide-trapping experiments to show that C5a receptors, expressed in mammalian cells, reside in m
109 Based on these observations, we propose that C5a receptors form higher order oligomers (i.e. tetramer
111 a (C5a) for the knockdown of seven proteins (C5a receptor; G-beta-2; G-alpha,i-2,3; regulator of G-pr
112 N-terminal segment with that from the human C5a receptor had minimal effect on C3a binding, substitu
114 co-transfected with both G alpha 16 and the C5a receptor, iC5b67 could neither activate phospholipas
116 lar levels of energy transfer between tagged C5a receptors in endoplasmic reticulum compared with pla
118 ct surfaces, we demonstrate cross-linking of C5a receptors in membranes prepared from both human neut
120 w that mice deficient in the chemoattractant C5a receptor, in comparison to their wild-type littermat
122 plement heat-inactivation, C5 depletion, and C5a receptor inhibition suppressed the priming effect of
124 (CCX168), an orally administered, selective C5a receptor inhibitor, could replace oral glucocorticoi
125 we show that Ab's or peptides that block C5a-C5a receptor interactions prevent pregnancy complication
127 rprisingly the carboxyl-terminal tail of the C5a receptor is the most important specificity determina
128 that is, complement receptor C5a (C5aR) and C5a receptor-like 2 (C5L2), in sepsis have been demonstr
131 neither activate phospholipase C nor inhibit C5a receptor-mediated activation of phospholipase C. iC5
132 n the premetastatic lungs through complement C5a receptor-mediated proliferation but not through recr
133 bit distinct inhibitory effects on fMLP (and C5a) receptor-mediated superoxide production, but have n
135 ression is almost completely absent, whereas C5a receptor mRNA and protein expression is maintained.
136 collection of 133 functional mutants of the C5a receptor obtained in a mutagenesis screen targeting
137 receptor (encoded by STE2), indicating that C5a receptor oligomerization is both receptor-specific a
139 ntine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear n
140 gineered near a proposed binding site in the C5a receptor on transmembrane helices III and VI can sel
142 shown that antibody-induced blockade of C5a, C5a receptors, or IL-17A greatly reduced the harmful out
143 ng of the C5a component of complement to the C5a receptor plays an important role in CD8(+) T cell re
144 histones appearing in septic plasma required C5a receptors, polymorphonuclear leukocytes (PMNs), and
145 lates the Gi proteins known to couple to the C5a receptor, produced minimal inhibition of C5a-induced
147 te that simultaneous blockade of the C3a and C5a receptors represents a promising neuroprotective str
148 conducted to address the functional role of C5a receptors revealed that C5a triggered rapid activati
153 f IL-6/TNFalpha induction and lack of C3 and C5a receptor stimulation attenuated nuclear factor-kappa
156 idues on the intracellular face of the human C5a receptor that are involved in G protein activation,
158 tructural model of the inactive state of the C5a receptor, the preserved residues reside on one half
160 trophils and U937 cells transfected with the C5a receptor (U937-C5aR cells) and comparing chemotaxis
163 , internalization of the FPR, as well as the C5a receptor, was demonstrated to be independent of the
164 We found that the complement effect required C5a receptor, was evident at physiologically relevant le
165 might be involved in the oligomerization of C5a receptors, we constructed receptors with individual
166 or B, C3 and properdin, and C3a receptor and C5a receptor were detected in grade 3 versus grade 0 or
167 erefore different from that reported for the C5a receptor, which is required for the initial inductio
169 opy to measure the kinetics of movement of a C5a receptor-yellow fluorescent protein fusion in living
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