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1 icular, in ligand-mediated activation of the C5a receptor.
2 the seven transmembrane helices of the human C5a receptor.
3 he seven transmembrane segments of the human C5a receptor.
4 t couples in neutrophils is reported to be a C5a receptor.
5 kely G protein linked, but distinct from the C5a receptor.
6 ue to inhibition of C5a interaction with the C5a receptor.
7 er in mice treated with an antagonist 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 activation is implicated in AKI, the role of C5a receptor 1 (C5aR1) in kidney tubular cells is unclea
15 ent anaphylatoxin C5a-mediated activation of C5a receptor 1 (C5aR1) on platelets as a negative regula
17 gnals through the G-protein-coupled receptor C5a receptor 1 (C5aR1) to induce the chemotaxis of prima
18 tracellular C5 activation and stimulation of C5a receptor 1 (C5aR1), which is negatively regulated by
19 receptor [C3aR] and complement anaphylatoxin C5a receptor 1 [C5aR1]) on human umbilical vascular endo
20 , whereupon it interacts with the complement C5a receptor 1 expressed on tumor infiltrating myeloid-d
21 rmostable mutations of the complement factor C5a receptor 1 retrieved 36% of the thermostable mutants
24 educing RPS19 in tumor cells or blocking the C5a receptor 1-RPS19 interaction decreases RPS19-mediate
25 ent, as did impaired AM phagocytosis through C5a receptor 1/Fc-gamma receptor I inhibition or by stea
28 t and third extracellular loops of the human C5a receptor, a GPCR that binds a 74-amino acid peptide
30 ttle energy transfer is observed between the C5a receptor and a co-expressed yeast pheromone receptor
32 with cDNAs encoding the complement component C5a receptor and PLC beta2 but not in cells transfected
34 L, signalling pathways downstream of C3a and C5a receptors and membrane C5b-9 assembly, and the preve
35 production of MIP-2 and KC by PTECs, whereas C5a receptor antagonism and prevention of membrane attac
36 d opsonization >2-fold, and compstatin and a C5a receptor antagonist (C5aRa) impaired granulocyte act
38 Here, oral delivery of a cyclic hexapeptide C5a receptor antagonist (PMX205) for 2-3 mo resulted in
44 -deficient mice and mice given injections of C5a-receptor antagonists developed significantly less pa
45 osition in mice deficient in C3a receptor or C5a receptor, as well as in wild-type mice depleted of h
46 nd synaptic loss, elevation of anaphylatoxin C5a receptor, astrocytic-C3, and microglial-TLR4 express
51 TGF-beta), and whereas TGF-beta1 induced C3a/C5a receptor (C3aR/C5aR) expression, pharmacologic C3aR/
53 roid was assayed for the presence of C3a and C5a receptors (C3aR and C5aR) using RT-PCR and immunohis
54 nt studies, we showed that autocrine C3a and C5a receptor (C3ar1 and C5ar1) G protein-coupled recepto
56 his article, we show that suppressed C3a and C5a receptor (C3ar1/C5ar1) signaling in murine Tregs pla
58 activation and neutrophil-expressed C3a and C5a receptors (C3aR1/C5aR1) that promote BAFF-dependent
60 autoantibody-induced arthritis requires the C5a receptor C5aR and FcgammaRs, but the simultaneous ne
61 the e2 loop with a smaller e2 loop from the C5a receptor (C5aR) abolished binding of 125I-C3a and C3
63 biting signaling of the complement component C5a receptor (C5aR) altered the composition and diversit
65 signals transmitted through T cell-expressed C5a receptor (C5aR) and C3a receptor (C3aR) to activatio
68 onocytic cell line U937 transfected with the C5a receptor (C5aR) and loaded with a fluorescent intrac
72 the terminal complement component C5 and the C5a receptor (C5aR) are upregulated in spinal microglia
75 ast cancer that the complement anaphylatoxin C5a receptor (C5aR) facilitates metastasis by suppressin
78 d the role of the active fragment complement C5a receptor (C5aR) in dental nerve regeneration in rega
79 prevented by the deficiency of either C3 or C5a receptor (C5aR) in the APC, demonstrating a link bet
80 We found that mice deficient in MCs or the C5a receptor (C5aR) injected with pathogenic anti-BP180
82 there are some suggestions that C5a and the C5a receptor (C5aR) might be directly linked to apoptosi
85 lacking the chemotactic or adhesion receptor C5a receptor (C5aR) or CD11a/lymphocyte function-associa
86 e show that pharmacological targeting of the C5a receptor (C5aR) or the bradykinin B2 receptor (B2R)
87 that local pharmacological targeting of the C5a receptor (C5aR) prior to initial allergen sensitizat
88 8(+) T cells lacking C3a receptor (C3aR) and C5a receptor (C5aR) proliferate weakly to allogeneic DCs
89 ostaining data demonstrate that blocking the C5a receptor (C5aR) reduced BDNF production in DPSCs, wh
90 ells deficient in C3a receptor (C3aR) and/or C5a receptor (C5aR) responded weakly in allogeneic hosts
93 in untreated fibroblast cultures express the C5a receptor (C5aR), here we show that all dental pulp f
94 f a cyclic peptide antagonist (C5aRa) to the C5a receptor (C5aR), the binding of murine 125I-C5a to m
101 own that mice deficient either in complement C5a receptor (C5aR; CD88) or TLR2 are highly and similar
102 ibody raised against residues 9 to 29 of the C5a receptor (C5aR; CD88), we demonstrate that noncystei
104 ins C3a and C5a (ie, C3a receptor [C3aR] and C5a receptor [C5aR]), and C3a and C5a are generated duri
107 d the potential of peritoneal TLR2, TLR4 and C5a receptors, C5aR and C5L2, as therapeutic targets in
112 C5a upregulation and was markedly reduced by C5a receptor (C5aR1) knock-out or treatment with the C5a
118 ulatory actions through interacting with its C5a receptors, C5aR1 and C5aR2, modulating multiple sign
120 e have analyzed the expression of the second C5a receptor C5L2, the putative "default" or nonsignalin
123 ively investigated how C5a signaling through C5a receptors can modulate diverse PRR-mediated cytokine
124 Phis and in the second by treatment with the C5a receptor (CD88) agonist EP67, which invokes MPhi pro
125 ated the regulated expression of the C3a and C5a receptors (complement anaphylatoxin C3a receptor [C3
127 ed with pertussis toxin, suggesting that the C5a receptor couples to both Galpha15 and Galphai in viv
130 cordingly, we found enhanced Th1 immunity in C5a receptor-deficient mice, something that conferred pr
134 eptor, endothelin 1 type A receptor, C3a and C5a receptors, did not show significant associations wit
135 gulator of cell polarity, with inhibition of C5a receptors during embryogenesis leading to abnormal b
136 sonance energy transfer experiments on human C5a receptors expressed in the lower eukaryote Saccharom
138 disulfide-trapping experiments to show that C5a receptors, expressed in mammalian cells, reside in m
141 Based on these observations, we propose that C5a receptors form higher order oligomers (i.e. tetramer
143 nists have been developed to interrogate the C5a receptor function but none show selectivity for C5aR
144 a (C5a) for the knockdown of seven proteins (C5a receptor; G-beta-2; G-alpha,i-2,3; regulator of G-pr
145 N-terminal segment with that from the human C5a receptor had minimal effect on C3a binding, substitu
147 is a pore-forming toxin targeting the human C5a receptor (hC5aR), enabling this pathogen to battle t
148 co-transfected with both G alpha 16 and the C5a receptor, iC5b67 could neither activate phospholipas
149 the anaphylotoxin receptors C3a receptor and C5a receptor in nonimmune respiratory cells can prevent
151 lar levels of energy transfer between tagged C5a receptors in endoplasmic reticulum compared with pla
153 ct surfaces, we demonstrate cross-linking of C5a receptors in membranes prepared from both human neut
155 w that mice deficient in the chemoattractant C5a receptor, in comparison to their wild-type littermat
156 d macrophages to produce IL-6 and IL-10 in a C5a receptor-independent manner, which was driven throug
157 d macrophages to produce IL-6 and IL-10 in a C5a receptor-independent manner, which was driven throug
159 plement heat-inactivation, C5 depletion, and C5a receptor inhibition suppressed the priming effect of
162 (CCX168), an orally administered, selective C5a receptor inhibitor, could replace oral glucocorticoi
163 we show that Ab's or peptides that block C5a-C5a receptor interactions prevent pregnancy complication
165 rprisingly the carboxyl-terminal tail of the C5a receptor is the most important specificity determina
167 that is, complement receptor C5a (C5aR) and C5a receptor-like 2 (C5L2), in sepsis have been demonstr
170 ic DAF overexpression or deletion of C3a and C5a receptors limited the activation of mechanistic targ
171 neither activate phospholipase C nor inhibit C5a receptor-mediated activation of phospholipase C. iC5
173 n the premetastatic lungs through complement C5a receptor-mediated proliferation but not through recr
174 bit distinct inhibitory effects on fMLP (and C5a) receptor-mediated superoxide production, but have n
176 ression is almost completely absent, whereas C5a receptor mRNA and protein expression is maintained.
177 collection of 133 functional mutants of the C5a receptor obtained in a mutagenesis screen targeting
178 receptor (encoded by STE2), indicating that C5a receptor oligomerization is both receptor-specific a
180 ntine receptor that is co-expressed with the C5a receptor on many cells including polymorphonuclear n
181 gineered near a proposed binding site in the C5a receptor on transmembrane helices III and VI can sel
183 shown that antibody-induced blockade of C5a, C5a receptors, or IL-17A greatly reduced the harmful out
184 ng of the C5a component of complement to the C5a receptor plays an important role in CD8(+) T cell re
185 histones appearing in septic plasma required C5a receptors, polymorphonuclear leukocytes (PMNs), and
186 lates the Gi proteins known to couple to the C5a receptor, produced minimal inhibition of C5a-induced
188 te that simultaneous blockade of the C3a and C5a receptors represents a promising neuroprotective str
189 conducted to address the functional role of C5a receptors revealed that C5a triggered rapid activati
190 Africans and linked to a polymorphism of the C5a receptor (rs11880097 T/G), the cellular target of th
194 mbrane attack complex and activated C3a- and C5a-receptor signals required for positive selection.
196 f IL-6/TNFalpha induction and lack of C3 and C5a receptor stimulation attenuated nuclear factor-kappa
199 idues on the intracellular face of the human C5a receptor that are involved in G protein activation,
201 tructural model of the inactive state of the C5a receptor, the preserved residues reside on one half
203 trophils and U937 cells transfected with the C5a receptor (U937-C5aR cells) and comparing chemotaxis
206 , internalization of the FPR, as well as the C5a receptor, was demonstrated to be independent of the
207 We found that the complement effect required C5a receptor, was evident at physiologically relevant le
208 might be involved in the oligomerization of C5a receptors, we constructed receptors with individual
209 or B, C3 and properdin, and C3a receptor and C5a receptor were detected in grade 3 versus grade 0 or
210 erefore different from that reported for the C5a receptor, which is required for the initial inductio
212 opy to measure the kinetics of movement of a C5a receptor-yellow fluorescent protein fusion in living