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1 mely, aminoacylation, and as a mimic of host CXC chemokine.
2 phoma 2 (Bcl-2), but reduced serum levels of CXC chemokines.
3 n the lung requires the production of ELR(+) CXC chemokines.
4 ighly potent inhibitors of a range of CC and CXC chemokines.
5 acid insertion (41VSRYR45) relative to other CXC chemokines.
6 growth factor 1 and 5 and of several CC and CXC chemokines.
7 d by a group of chemoattractants, especially CXC chemokines.
9 a CC chemokine, and interleukin-8 (IL-8), a CXC chemokine, along with their individual interactions
11 nfection was enhanced by administration of a CXC chemokine and abrogated by antibodies that blocked t
14 y susceptible to OPC, with reduced levels of CXC chemokines and concomitantly impaired neutrophil rec
17 actor-1alpha (SDF-1alpha) is a member of the CXC chemokines and interacts with the G protein, seven-t
18 nity binding to multiple inflammatory CC and CXC chemokines and is expressed by erythrocytes and endo
19 e objective of this study was to investigate CXC chemokines and its receptor in patients with Behcet'
20 D88/NF-kappaB/AP-1 pathway and production of CXC chemokines and neutrophil infiltration to infected t
21 eparan sulfate inhibited the accumulation of CXC chemokines and neutrophils in tissues and attenuated
22 acerbated disease by impeding the removal of CXC chemokines and neutrophils, whereas administration o
23 ted closely with the removal of tissue-bound CXC chemokines and resolution of accumulated neutrophils
24 a compromised ability to express both CC and CXC chemokines and that this defect is at least partiall
25 prosurvival and proangiogenic role of ELR(+)-CXC chemokines and their receptor CXCR2 during metanephr
28 ression of CXCL2/MIP-2 and CXCL5/LPS-induced CXC chemokine, and activation of NF-kappaB and MAPKs in
29 keratinocyte-derived chemokine, LPS-induced CXC chemokine, and G-CSF were augmented in Adipo(-/-) ve
32 hion, vGPCR binds a broad spectrum of CC and CXC chemokines, and the roles of chemokines in vGPCR tum
35 amic acid-leucine-arginine-positive (ELR(+)) CXC chemokines associated with bronchiolitis obliterans
36 we measured the levels of a panel of CC and CXC chemokines at baseline and following mycobacterial A
37 in scaffold segments necessary for different CXC-chemokine-binding activities, implying that differen
38 ay, we identified and characterized 27 novel CXC-chemokine-binding evasins homologous to EVA3 and def
39 structural and mechanistic insight into how CXC-chemokine-binding tick EVAs achieve class specificit
44 at PE results in increased expression of the CXC chemokines CINC-1 and CINC-2 between 6 and 18 h afte
45 tumor cells constitutively produced the ELC-CXC chemokine CXCL-8 (IL8), enabling them to recruit APR
46 M-1 and VCAM-1), and enhanced the release of CXC chemokine CXCL1 when incubated with primary cultures
49 ontrast, cathepsins specifically process ELR CXC chemokines CXCL1, -2, -3, -5, and -8 N-terminally to
52 , as was recently reported, for example, for CXC chemokines CXCL4/PF4 and CXCL8/IL8 that interact to
54 tractant 1/CXCL1, lipopolysaccharide-induced CXC chemokine/CXCL5) and up-regulation of the angiogenes
55 and CCL4 are inactive, and the dimer of the CXC chemokine CXCL8 (which is closely related to CXCL1)
56 e up-regulation of three NF-kappaB-regulated CXC-chemokines, CXCL8, CXCL1 and CXCL2, in the resistant
57 e role of non-glutamic acid-leucine-arginine CXC chemokine CXCL9 for T-cell recruitment to prevent re
59 he interferon-inducible Glu-Leu-Arg-negative CXC chemokines CXCL9, CXCL10, and CXCL11 exhibit antimic
61 vaccine that is highly effective in blocking CXC chemokine degradation and permits opsonic Abs to kil
65 demonstrate that early, local treatment with CXC chemokines enhances neutrophil recruitment and clear
67 n vitro analysis demonstrated that all three CXC chemokines exerted direct antimicrobial effects agai
68 ages and epithelial cells, which facilitates CXC chemokine expression and aids neutrophil recruitment
69 onfirmed the importance of IL-1 signaling in CXC chemokine expression and neutrophil recruitment in v
70 The mutation was linked to modestly impaired CXC chemokine expression and neutrophil recruitment to t
71 L-1beta signaling or IL-17 signaling reduced CXC chemokine expression but did not alter the overall s
72 We also found that MIF induced angiogenic CXC chemokine expression in an autocrine manner in vitro
73 ed with the angiogenic activity and level of CXC chemokine expression in human specimens of non-small
74 itro and in vivo models indicate that ELR(+) CXC chemokine expression is higher in microvascular endo
75 eloid expression of CXCR2 directly regulated CXC chemokine expression levels after hepatic I/R, such
76 on reduces RSV-induced neutrophilia, mucosal CXC chemokine expression, activation of the IRF7-RIG-I a
79 In this Review, we discuss the biology of CXC chemokine family members, specifically as it relates
80 mokine receptor that binds to members of the CXC chemokine family possessing angiogenic properties.
81 tivating peptide-78 (CXCL5), a member of the CXC chemokine family, has been shown to be involved in a
83 ment of CXCR2, the receptor for ELR-positive CXC chemokines, for RV-induced airway neutrophilia and h
84 revealed lower expression levels of several CXC chemokine genes (CXCL-1, -2, -3, -5, -6, -12) in CWF
87 virulence by facilitating the generation of CXC chemokine gradients and stimulating chemokine-induce
88 and demonstrated that it readily cleaved the CXC chemokines GRO-alpha, GRO-beta, GRO-gamma, neutrophi
89 lished the abilities of three representative CXC chemokines, GRO-gamma, NAP-2, and GCP-2, to attract
90 detected by Sytox green staining, levels of CXC chemokines, histones, and cytokines also were measur
91 equivalently binds four different ELR-devoid CXC chemokines (ie, PF4/CXCL4, IP-10/CXCL10, MIG/CXCL9,
92 higher levels of tumor-associated angiogenic CXC chemokines (ie, the ELR score) and greater vasculari
93 ses (MMP-9, ADAM-8), CC chemokines (CCL-20), CXC chemokines (IL-8, CXCL-10, CXCL-11), oligoadenylate
94 ression of CXCL2/MIP-2 and CXCL5/LPS-induced CXC chemokine in Klebsiella-infected lungs, and 2) CXCL1
96 re, we analyzed expression of genes encoding CXC chemokines in M. tuberculosis-infected murine lung t
98 not TLR2-deficient mesangial cells produced CXC chemokines in response to stimulation with Pam(3)Cys
102 he second class bound both ELR(+) and ELR(-) CXC-chemokines, in several cases including CXC-motif che
106 potentiation of neutrophil mobilization via CXC chemokine induction is a putative mechanism underlyi
109 s one of two high-affinity receptors for the CXC chemokine interleukin-8 (IL-8), a major mediator of
113 lumican and keratocan core proteins bind the CXC chemokine KC during a corneal inflammatory response,
114 e susceptibility of C3H-HeN mice lacking the CXC chemokine KC or its receptor CXC receptor 2 (CXCR2)
115 dentium-stimulated induction of iNOS and the CXC chemokines KC and MIP-2 to the same degree as the NF
118 oid A and IL-6, and the neutrophil-selective CXC chemokines, KC and macrophage inflammatory protein-2
121 ere were no differences in the levels of the CXC chemokines keratinocyte-derived chemokine and MIP-2
122 hrough increased pulmonary expression of the CXC chemokines (keratinocyte-derived chemokine and macro
123 rived cells in the corneal stroma to produce CXC chemokines, leading to neutrophil recruitment to the
125 hagocytosis, and decreased IL-6 and MIP-2 (a CXC chemokine) levels after CLP in outbred (ICR/CD-1) mi
127 (CXCR) 4 in response to its natural ligands CXC chemokine ligand (CXCL) 12 and macrophage migration
132 em cells (MSCs) and their progeny, including CXC chemokine ligand (CXCL)12-abundant reticular (CAR) c
133 rophages and mesenchymal progenitors such as CXC chemokine ligand (CXCL)12-abundant reticular (CAR) c
134 ide evidence supporting functional roles for CXC chemokine ligand (CXCL)13 and interleukin (IL)-10 in
135 ligand (CCL)2, CCL3, CCL5, CCL19, CCL20, and CXC chemokine ligand (CXCL)8 were measured in gingival t
137 rum levels of interleukin-6, interleukin-10, CXC chemokine ligand 1, and interferon-gamma were signif
138 ed into murine lung, leading to induction of CXC chemokine ligand 1/2 and a neutrophilic response tha
139 [MHV]) expressing the T-cell chemoattractant CXC chemokine ligand 10 (CXCL10) resulted in increased s
141 uch as interferon-gamma-inducible protein 10/CXC chemokine ligand 10, interleukin 8, and monocyte che
142 nformations compared with the CXCR3 agonists CXC chemokine ligand 11 (CXCL11), VUF11418 [1-((1R,5S)-6
143 onse correlates with enhanced sensitivity to CXC chemokine ligand 12 (CXCL12) but not CXCL13 or CC ch
144 receptor 4 (CXCR4) in Cajal-Retzius cells by CXC chemokine ligand 12 (CXCL12) is important for contro
145 emokine receptor 4 (CXCR4), is selective for CXC chemokine ligand 12 (CXCL12), is broadly expressed i
146 ling postnatal HSCs expressed high levels of CXC chemokine ligand 12 (CXCL12, also known as stromal c
147 stromal cell-derived factor-1 (SDF-1alpha or CXC chemokine ligand 12) are involved in the trafficking
150 GR) recruitment to the neutrophil chemokine, CXC chemokine ligand 5 (CXCL5), providing a candidate me
151 lowered rolling velocity further and induced CXC chemokine ligand-1 (CXCL1) and CXC chemokine recepto
154 vels of chemokines CC chemokine ligand 5 and CXC-chemokine ligand 4 were increased in the trJAM-A(-/-
156 ysaccharide-stimulated human MPhi identified CXC chemokine ligands (CXCLs), such as IP-10 (interferon
158 TOF MS identified two differential proteins: CXC chemokine ligands 4 (CXCL4) and 7 (CXCL7), both of w
160 We found no effects of MMP-8 on LPS-induced CXC chemokine (LIX, or CXCL5)-induced neutrophil recruit
161 is associated with the local release of the CXC chemokines macrophage inflammatory protein 2 and KC.
166 oblasts and our previous studies showed that CXC chemokines mediate neutrophil recruitment, we examin
167 strating that IL-13 stimulates select CC and CXC chemokines (MIP-1alpha/CCL-3, MIP-1beta/CCL-4, MIP-2
168 matory cytokines (lipopolysaccharide-induced CXC chemokine, monocyte chemotactic protein-1, macrophag
171 s in the production of MIP-2 and LPS-induced CXC chemokine or activation of NF-kappaB and MAPKs in th
172 ly induced in the colon by infection encoded CXC chemokines, particularly CXCL1/2/5 and CXCL9/10, whi
174 cine-arginine (ELR) tripeptide motif (ELR(+) CXC chemokines) play an important role in leukocyte traf
175 lphabetaTCR+ cells and functions to regulate CXC chemokine production and neutrophil recruitment in v
176 ings indicate that IL-1R1 and MyD88 regulate CXC chemokine production and neutrophil recruitment to t
177 rTNF-alpha, rIL-1alpha, or rIL-1beta induced CXC chemokine production by corneal fibroblasts but not
180 Eritoran tetrasodium significantly inhibited CXC chemokine production in the cornea and development o
183 alization, patterns of neutrophil influx and CXC chemokine production were assessed in C57Bl/6 mice a
184 The immunomodulatory effects of PEP35 on CXC chemokine production were TLR2 and NF-kappaB depende
185 naling in alveolar macrophages, resulting in CXC chemokine production, and C5a appears to play a pivo
186 in S. aureus infections in controlling local CXC chemokine production, neutrophil recruitment to the
187 s CCL5, they exhibit significantly increased CXC chemokine production, neutrophil recruitment to the
191 a, IL-6, and LIX (lipopolysaccharide-induced CXC chemokine) production were attenuated in the lungs o
192 n transcript levels of genes encoding CC and CXC chemokines, proinflammatory cytokines, and TNF super
193 of the type IV collagen, thrombospondin, and CXC chemokine protein families, as well as somatotropin
194 eceptors, only CC chemokine receptor (CCR5), CXC chemokine receptor (CXCR) 3, and CXCR6 correlated wi
195 ein modifier inside the cell, functions as a CXC chemokine receptor (CXCR) 4 agonist outside the cell
199 G(+) plasma cells accompanied by defects in CXC chemokine receptor (CXCR) 4 expression, interleukin
200 activation and early signaling steps of the CXC chemokine receptor (CXCR) 4 in response to its natur
204 de neutrophils to sites of liver necrosis by CXC chemokine receptor 2 (CXCR2) and formyl peptide rece
205 flammation through activation of endothelial CXC Chemokine Receptor 2 (CXCR2) and production of endot
207 Our aim was to discover the role of IL-17, CXC chemokine receptor 2 (CXCR2) ligands, and cancer-ass
210 ound lymphotoxin-beta receptor (LTbetaR) and CXC chemokine receptor 2 (CXCR2), is involved in type B
214 gamma is required for efficient induction of CXC chemokine receptor 3 (CXCR3) on T cells upon activat
219 mulated MPhi of chemoattractant activity for CXC chemokine receptor 3-transfected (receptor for IP-10
220 ow that extracellular ubiquitin is a natural CXC chemokine receptor 4 (CXCR4 and CD184) agonist.
223 ll-derived factor-1 (SDF-1) and its receptor CXC chemokine receptor 4 (CXCR4) are important regulator
226 romal cell-derived factor 1 and its receptor CXC chemokine receptor 4 (CXCR4) critically mediate the
230 38+ cells in the blood, higher leukemic cell CXC chemokine receptor 4 (CXCR4) levels, and increased r
232 The stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) signaling axis appears
235 gous to the V3 loop of HIV-1, which binds to CXC chemokine receptor 4 (CXCR4), we hypothesized that B
236 ations covering all 352 residues of the GPCR CXC chemokine receptor 4 (CXCR4), we identified 41 amino
241 imerization among known GPCR homodimers: the CXC chemokine receptor 4 and sphingosine-1-phosphate rec
243 a promising protein therapeutic and implies CXC chemokine receptor 4 as a drug target after polytrau
247 vels and corresponding surface expression of CXC chemokine receptor 4 on clonal PCs, suggesting that
248 The HIV envelope glycoprotein interacts with CXC chemokine receptor 4 to activate the lysosomal degra
249 stem cell mobilizer or its receptor, CXCR4 (CXC chemokine receptor 4), would attenuate and reverse h
250 s, such as protease-activated receptor 1 and CXC chemokine receptor 4, RGS4 disrupted Rac1-dependent
252 bone marrow; in particular, the role of the CXC chemokine receptor 4/stromal-derived factor 1 axis,
253 ided in the T cell areas, expressed CCR7 and CXC chemokine receptor 5 (CXCR5), and like follicular he
254 y modified unselected CD8 T cells to express CXC chemokine receptor 5 (CXCR5), the chemokine receptor
255 ssion of B-cell leukemia/lymphoma 6 (Bcl-6), CXC chemokine receptor 5, programmed death-1, and other
260 derstanding of the pathways involved in both CXC chemokine receptor signaling in other cell types, mo
261 e evaluated their inhibitory activity on the CXC chemokine receptor type 4 (CXCR4), toxicity properti
264 ed the significance of signaling through the CXC chemokine receptor-2 (CXCR2) receptor in the process
267 d induced CXC chemokine ligand-1 (CXCL1) and CXC chemokine receptor-2 (CXCR2)-dependent leukocyte arr
268 tic parental cells (686LN-Ps), we found that CXC chemokine receptor-4 (CXCR4) mRNA levels were signif
269 ral differentiation, we observed that CXCR4 (CXC chemokine receptor-4) expressing central nervous sys
270 ce markers of neutrophils (Ly6G, L-selectin, CXC chemokines receptor 2, and 7/4) and DCs (CD11c, MHC
271 ection within the liver was not dependent on CXC-chemokine receptor 2 (CXCR2) signaling as anti-CXCR2
276 iae lacking FimCDE fail to interact with the CXC-chemokine receptor 4 (CXCR4), and bacteria expressin
277 Recent crystal and NMR structures of the CXC chemokine receptors (CXCR) CXCR4 and CXCR1, combined
279 "minor pocket," previously characterized in CXC chemokine receptors-1 and -2, is functionally conser
280 he nucleus, transcription of CXCL1 and other CXC chemokines, recruitment of neutrophils to the cornea
281 hereas T(H)17 transfer resulted in increased CXC chemokine secretion and neutrophil influx that was n
282 ne-cytokine receptor interaction (especially CXC-chemokine) signaling as well as cancer-related pathw
283 XC chemokines in the augmented inflammation, CXC chemokine-specific antibodies were delivered to the
284 ports indicate that interactions between the CXC chemokine stromal cell-derived factor 1 and its rece
285 protein 2) and CXCR4 (specific receptor for CXC chemokine stromal cell-derived factor-1) in CLL cell
289 related with the strain's ability to degrade CXC chemokines, thereby preventing neutrophil chemotaxis
292 erferon-inducible Glu-Leu-Arg (ELR)-negative CXC chemokines was not affected by the BaPGN-induced ant
294 neutrophil influx (along with expression of CXC chemokines) was significantly enhanced in infected t
296 ents, plasma levels of CXCL5, another ELR(+) CXC chemokine, were elevated during acute lesion formati
297 hich included EVA3, exclusively bound ELR(+) CXC-chemokines, whereas the second class bound both ELR(