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1  enhanced renal expression of the macrophage chemokine CCL2.
2 quency and upregulates the expression of the chemokine CCL2.
3 nce of increased expression of the mast cell chemokine Ccl2.
4  manifest increased expression levels of the chemokine Ccl2.
5 learance, due to decreased production of the chemokine CCL2.
6 sion molecule E-selectin or secretion of the chemokine CCL2.
7 he islets is caused by overexpression of the chemokine CCL2.
8 ton and cell polarization in response to the chemokine CCL2.
9 -beta and the peripheral induction of the CC chemokine CCL2.
10 biological properties of the prototypical CC chemokine, CCL2.
11          The initial cellular sources of the chemokine CCL2, a ligand for CCR2, included perivascular
12 mutants also induced increased levels of the chemokine CCL2, a monocyte chemoattractant, in serum, an
13 udies in mice that implicated a role for the chemokine CCL2 (also known as MCP1) and macrophages.
14  usually characterized by high levels of the chemokine CCL2 and a prodigious monocyte/macrophage infi
15 omous manner by regulating production of the chemokine CCL2 and granulocyte-macrophage colony-stimula
16 e substantial amounts of the proinflammatory chemokine CCL2 and immunosuppressive cytokine IL-10, in
17                We show that the inflammatory chemokine CCL2 and its receptor CCR2 are necessary for t
18 (+) and CD8(+) T cells, upregulation of beta-chemokines (CCL2 and CCL22), basic fibroblast growth fac
19              Therefore, drugs targeting beta-chemokines (CCL2 and CCL22), FGF-basic, HGF, or MIF migh
20 the migration of macrophages directed by the chemokines CCL2 and CCL19, activation of the actin-remod
21 nd TNF-alpha, as well as the proinflammatory chemokines CCL2 and CCL3, and chemokine receptors CCR1 a
22 f the CXCL1 dimer is novel: dimers of the CC chemokines CCL2 and CCL4 are inactive, and the dimer of
23  expression of mRNAs for the proinflammatory chemokines CCL2 and CCL5 than mock- and E3 null virus-in
24 LTalpha1beta2 also induced production of the chemokines CCL2 and CCL5, which elicited transmigration
25 erred enhanced expression of proinflammatory chemokines CCL2 and CCL5.
26                                          The chemokines CCL2 and CCL7 are upregulated in the brain du
27 igand treatment, decreased expression of the chemokines CCL2 and CCL7 by astrocytes in EAE.
28 d TNF-alpha each stimulate production of the chemokines CCL2 and CCL7 in astrocytes in a concentratio
29 e relative contribution of the CCR2 ligands, chemokines CCL2 and CCL7, in directing monocyte mobiliza
30 ll as a reduction in the monocyte-recruiting chemokines CCL2 and CCL7.
31 at intercellular adhesion molecule-1 and the chemokines CCL2 and CX3CL1 probably are involved in leuk
32 a was associated with greater release of the chemokines CCL2 and CXCL12, the cytokines interleukin-6
33   Of interest, we found that expression of 2 chemokines, CCL2 and CXCL10, correlated with the median
34 hese observations by demonstrating that MPhi chemokine (CCL2) and receptor (CCR2) knockout mice displ
35 e resulting products by Nod2, release of the chemokine CCL2, and CCR2-dependent recruitment of the ad
36 ukin-1beta, tumor necrosis factor-alpha, the chemokine CCL2, and interferon regulatory factor-5 (IRF5
37 k in our laboratory has shown a role for the chemokine, CCL2, and its receptor in the induction of hi
38 and IL-13-treated fibroblasts; we identified chemokine CCL2 as a potential target.
39 ocytes, which express CCR2 (the receptor for chemokine CCL2), as well as the subsequent recruitment o
40 re model of the human BBB in response to the chemokine CCL2, as well as in disruption of the BBB, as
41 d Schu S4 did not stimulate secretion of the chemokine CCL2 by HUVECs, whereas material released from
42 A treatment also reduced the MDSC-attracting chemokine CCL2 (C-C motif ligand 2) in the TME along wit
43  New work showing that the T cell-attracting chemokine CCL2 can be posttranslationally modified in th
44                              A subset of six chemokines (CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL10) w
45 ably, cytokines IL-6, TNF, and IFN-gamma and chemokines CCL2, CCL3, and CCL4 have been associated wit
46 croglial activation marker Iba1 and CC motif chemokines CCL2, CCL3, and CCL5.
47 roduction in the lung of the proinflammatory chemokines CCL2, CCL3, CCL5, CXCL9, and CXCL10 with diff
48 ic subsets of cytokines (TNFalpha, IL-6) and chemokines (CCL2, CCL4, CXCL1, CXCL2, CXCL10) are critic
49 eta, interleukin 12, and interleukin 17; the chemokines CCL2, CCL4, and CXCL10; and the growth factor
50 L-1beta), interleukin 18, and interleukin 6; chemokines CCL2, CCL4, CCL11, CCL22, CXCL8, and CXCL10;
51 e that H. pylori increases production of the chemokines CCL2, CCL5, and granulocyte-macrophage colony
52                                    mRNAs for chemokines CCL2, CCL5, CCL17, IFN-gamma inducible chemok
53  fibroblast growth factor 2 (FGF-2), and the chemokines CCL2, CCL5, CCL7, CCL13, CXCL8, and CXCL10 we
54 kaged in ESTA-MSV efficiently suppressed the chemokines, CCL2, CCL5, CCL8, and CXCL9, and monocyte ad
55 and (CXCL) 1 chemokines and up-regulation of chemokine (Ccl2, Ccl7, Cxcl1, Cxcl2, and Cxcl10) and cel
56 IFN-I signaling stimulated the production of chemokines (CCL2, CCL7, and CCL12) that recruited Ly6C(h
57 tokines (TNF-alpha, IL-1beta, IFN-gamma) and chemokines (CCL2, CCL8, and CCL5) and an increase in adi
58 L-1A, IL-1B, IL-23A, IL-17C, and IL-32), and chemokines (CCL2, CCL8, and CXCL5).
59                                          The chemokines CCL2, CCL8, CXCL1, and CXCL2 ranked highest a
60 or alpha [TNFalpha], interleukin [IL]-6) and chemokines (CCL2, CXCL2) were also significantly lower i
61 ptionally high levels of IFN-gamma-inducible chemokines, CCL2, CXCL9, and CXCL10; and this pronounced
62 ovascular endothelial cells (BMECs) with the chemokine CCL2 (formerly called MCP-1).
63                                          The chemokine, CCL2, has been shown to play a major role in
64 vels of pro- and anti-inflammatory cytokines/chemokines (CCL2, IL-6, CXCL2, KC, TNF-alpha, and IL-10)
65 tween RNS-modified tyrosine residues and the chemokine CCL2 in diseased kidneys.
66 ntified a microRNA-regulated pathway for the chemokine CCL2 in HCV-induced hepatitis.
67 ociated with increased concentrations of the chemokine CCL2 in lung lavage.
68 dependent) upregulation of expression of the chemokine CCL2 in mast cells.
69                  Increased expression of the chemokine CCL2 in the CNS has been demonstrated to be im
70   The present study examined the role of the chemokine CCL2 in the control of Salmonella infection.
71 ent study dissects the mechanisms by which a chemokine, CCL2, induces TJ disassembly.
72                                          The chemokine CCL2 is one of the most elevated inflammatory
73                                 However, the chemokine CCL2 is significantly expressed in the DRG of
74 though recent studies have suggested that CC chemokine CCL2 may directly affect the angiogenesis, the
75 ation-induced increases in mRNA encoding the chemokine CCL2 (MCP-1) and release of the protein.
76 IFN-gamma) and tumor necrosis factor and the chemokine CCL2 (MCP-1) were seen after infection of susc
77 ly decreases expression and secretion of the chemokine CCL2 (MCP-1).
78 s B4 and C4, the cytokines IL-6 and TNF, and chemokines CCL2 (MCP-1) and CCL4 (MIP-1beta).
79  dramatic reduction in the production of the chemokines CCL2 (MCP-1) and CXLC2 (MIP-2) in TNFR1-defic
80 lation, such as heightened expression of the chemokines CCL2 (MCP-1), CCL3 (MIP-1alpha), CCL4 (MIP-1b
81                      Moreover, expression of chemokine CCL2, MCP-1 and its receptor CCR2, which play
82            Cytokine array indicated that the chemokine CCL2/MCP-1 (monocyte chemoattractant protein-1
83                                              Chemokine CCL2/MCP-1 is known to attract CCR2(+) monocyt
84 in a marked increase in SMC secretion of the chemokine CCL2/MCP-1, which has been previously shown to
85 d IL-6, and markedly enhanced secretion of a chemokine, CCL2/MCP-1, important modulators of inflammat
86  this study, we identified four inflammatory chemokines (Ccl2/Mcp-1, Ccl7, Cxcl16, and Cx3cl1) of ove
87  necrosis factor-alpha, IL-6, and IL-1beta), chemokines (CCL2/MCP-1, CXCL1/GROalpha, CXCL3/GROgamma,
88 ular mechanism by which the pro-inflammatory chemokine CCL2 mediates brain endothelial barrier disrup
89 kines (IL-1 beta, TNF-alpha, and S100B), the chemokine CCL2, microglial activation, seizure susceptib
90 timulated HUVEC, and the endothelium-derived chemokine CCL2 (monocyte chemoattractant protein 1) was
91 a recombinant coronavirus that expressed the chemokine CCL2/monocyte chemoattractant protein-1.
92 ) were found to be the most abundant, but CC chemokines (CCL2/monocyte chemotactic protein 1 and CCL3
93                The neuroinflammatory markers chemokine CCL2, NF-kappaB and nitrotyrosine were localiz
94 ired the chemokine receptor CCR2 but not the chemokine CCL2 or receptor CCR7.
95 cible skin signature wherein the profibrotic chemokine CCL2 plays a key role.
96 n, leukotriene C(4) (LTC(4)) generation, and chemokine CCL2 production.
97 F-induced LTC(4) generation, is required for chemokine CCL2 production.
98                                          The chemokine CCL2 promotes kidney disease in two models of
99           We also show that the inflammatory chemokine, CCL2, protects against tat toxicity and inhib
100 wth factor, transforming growth factor beta, chemokine CCL2, SDF-1, and complements C3, C4, and facto
101 ecrosis factor-alpha, interleukin-6, and the chemokine CCL2, than CD11b(+)Gr-1(+) cells isolated from
102  430, and the effects on serum levels of the chemokine CCL2 were measured 4 h later.
103  macrophages, inducing the production of the chemokine CCL2, which in turn recruited circulating CCR2
104 ted that macrophages and the inflammatory CC-chemokine CCL2, which is scavenged by ACKR2, are associa
105 e I IFN response inhibited production of the chemokine CCL2, which promotes the recruitment of macrop
106 loss of Mir155 reduced the expression of the chemokine CCL2, which promotes the recruitment of monocy
107 cells leads to an increased secretion of the chemokine CCL2, which recruits IBA1-expressing myeloid c
108 mice exhibited increased serum levels of the chemokine CCL2, which resulted in the recruitment of bot

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