ライフサイエンスコーパス: RANTES

1 RANTES (CCL5) is a chemokine implicated in many human di

2 RANTES (CCL5) is a chemokine that recruits immune cells

3 RANTES (regulated on activation, normally T cell express

4 RANTES and eotaxin were also up-regulated in the substan

5 RANTES promoter analysis showed that cis elements proxim

6 RANTES, IL-6, and IL-1beta, but not TNF-alpha, were enha

7 RANTES-NIS-MSCs were injected intravenously, followed by

8 RANTES/CCL5 analogs are more potent inhibitors of infect

9 monocyte chemoattractant protein 1 (MCP-1), RANTES, and CXCL10; and other important innate immune mo

10 ivo studies identified the chemokines MCP-1, RANTES, and CXCL10 as MAP3K14 targets in tubular cells.

11 s, including secretion of IL-8, IL-6, MCP-1, RANTES, and MIP-1beta, but not TNF-alpha, whereas AMs se

12 tic diameter and cytokine production (MCP-1, RANTES, KC, TNF-alpha, MIP-1alpha, and IFN-gamma) was si

13 tion of cox-2(-/-) macrophages toward MCP-1, RANTES, MIP-1alpha, or MIP-1beta, as well as cell adhesi

14 tein-1alpha, monocyte chemotactic protein-1, RANTES, and tumor necrosis factor-alpha) peaked at 6 hou

15 Poly(I-C)-induced expression of IP-10, RANTES, and IFN-beta mRNA was decreased in MKK4- or MKK7

16 IL-6, IL-8, IFN-gamma-inducible protein-10, RANTES, and platelet-derived growth factor-BB.

17 12ac, enhancing the effect of EtOH on IL-15, RANTES, TGF-beta1, and TNF-alpha cytokines while restori

18 sed serum concentrations of IL-12p40, IL-18, RANTES, and monocyte chemotactic protein-1, and elevated

19 ge inflammatory protein 1alpha (MIP-1alpha), RANTES, and IP-10 were individually cloned into the geno

20 tory protein 1alpha [MIP-1alpha], MIP-1beta, RANTES) and CXC families (growth-related oncogene alpha

21 , such as those encoding CXCL-13, MIP-1beta, RANTES, and IL-8.

22 hemokine, macrophage inflammatory protein 2, RANTES, tumor necrosis factor alpha, gamma interferon, a

23 (1)-[l-thioprolyl(2), l-cyclohexylglycyl(3)]-RANTES(4-68)), which displays potent anti-HIV-1 activity

24 P-10/CXCL-10, MCP-1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interleukin 8) than SARS-CoV.

25 ly, therapy with the combination of 44AANA47-RANTES plus P8A-MCP-1 did not ameliorate AIA beyond the

26 ve inhibitor for endogenous RANTES (44AANA47-RANTES) nor the CCR1/CCR5 receptor antagonist, methionyl

27 estigated the interaction of RANTES and 5P12-RANTES with various commonly used detergents.

28 The RANTES derivative 5P12-RANTES is a highly potent HIV entry inhibitor that is be

29 kine (C-C motif) receptor 5 inhibitors, 5P12-RANTES (regulated on activation, normal T cell expressed

30 acterized the structure and dynamics of 5P12-RANTES by solution NMR.

31 the nine flexible N-terminal residues, 5P12-RANTES has the same structure as wild-type RANTES but un

32 T cell expressed and secreted) variant (5P12-RANTES or 5P14-RANTES linked to a gp41 fusion inhibitor,

33 d and secreted) variant (5P12-RANTES or 5P14-RANTES linked to a gp41 fusion inhibitor, C37.

34 ry cytokines and chemokines, including IL-6, RANTES, IP-10, and MIP-3a, which were regulated by NFkap

35 ormal T cell expressed and secreted) and 6P4-RANTES, fully protect against infection in the rhesus va

36 ted IFN-gamma- and IL-6-induced MCP-1, IL-8, RANTES, and TNF-alpha production in monocytes, indicatin

37 SK-3beta activity mimicked HGF and abolished RANTES expression, whereas ectopic expression of GSK-3be

38 In vitro, HGF abolished RANTES induction in human kidney epithelial cells, which

39 /macrophage proliferation but did not affect RANTES-induced SMLC proliferation, consistent with a lar

40 tion, functional blocking antibodies against RANTES and eotaxin reduced the infiltration of CD4(+) an

41 TNF-alpha, IL-1alpha (Interleukin-1 alpha), RANTES (regulated on activation, normal T cell expressed

42 Although RANTES induction depended on NF-kappaB signaling, parica

43 Although RANTES infusion in vivo promoted inflammatory cell accum

44 Although RANTES/CCL5-NIS targeting has shown efficacy in the trea

45 and increased sensitivity to aminooxypentane-RANTES and the CCR5 monoclonal antibody HGS004.

46 e common with high sputum IL-4 (P = .02) and RANTES (P = .02) levels, whereas BDR was associated with

47 displays a synchronous increase in SDF-1 and RANTES expression and a higher capability of attracting

48 (CCR1), which are the receptors of SDF-1 and RANTES, respectively.

49 monocyte chemotactic protein 1 (MCP-1), and RANTES (regulated on activation, normal T cell expressed

50 MCP-1 (monocyte chemotactic protein-1); and RANTES.

51 leukin-6 (IL-6), TNF-alpha, IL-8, MCP-1, and RANTES (Regulated on Activation, Normal T Cell Expressed

52 Plasma leukocyte chemokines (KC, MCP-1, and RANTES) and myeloperoxidase activity were also significa

53 ficantly higher levels of IL-17A, IP-10, and RANTES in the lung.

54 elicited the production of IL-8, IP-10, and RANTES.

55 ranslocation, and interleukin-10 [IL-10] and RANTES release).

56 chemokine CXCL1 (KC), interleukin 12p40, and RANTES in response to influenza virus infection.

57 tory protein 1beta (MIP-1beta), CXCL-13, and RANTES.

58 ress the T cell chemoattractants, IL-16, and RANTES.

59 ed expression of CCR5 ligands MIP-1alpha and RANTES in the microvasculature, increased BBB leakage an

60 late the secretion of interleukin 1alpha and RANTES, whereas purified F (fusion) protein elicited the

61 , and decreased production of MIP-1alpha and RANTES.

62 macrophage inflammatory protein 1alpha, and RANTES were significantly increased in infected MyD88(-/

63 of CC chemokines (MIP-1beta, MIP-1alpha, and RANTES) but not IL-2.

64 eukin-2 [IL-2], IL-6, IL-10, MIP-1alpha, and RANTES) that together enhanced beta-cell proliferation.

65 cytokines IFN-gamma, TNF-alpha, IL-1beta and RANTES and activation of p38/Stat pathways in T-cells ex

66 e chemoattractant protein-1), MIP-1beta, and RANTES (regulated on activation normal T cell expressed

67 The CC chemokines MIP-1alpha, MIP-1beta, and RANTES and their receptors CCR1 and CCR5 were strongly u

68 The MIP-1alpha, MIP-1beta, and RANTES chemokines are natural ligands of CCR5 and are kn

69 FN-gamma, GM-CSF, MIP-1alpha, MIP-1beta, and RANTES.

70 alpha (TNF-alpha), interleukin-2 (IL-2), and RANTES was upregulated in splenocytes harvested from mic

71 ue inhibitor of metalloproteinases 1/2], and RANTES [regulated on activation normal T-cell expressed

72 innate to adaptive immunity (MIP-3alpha and RANTES (regulated on activation normal T cell expressed

73 nesis of severe disease in malaria (IL-5 and RANTES) were assessed by cytometric bead assay in April

74 subsequent malaria, in contrast to IL-5 and RANTES, which increased the odds of malaria.

75 LPS-induced IL-6 and RANTES expression was decreased, and BLC expression was

76 TNF-alpha) or no change over time (IL-6 and RANTES).

77 evels of the inflammatory cytokines IL-6 and RANTES, and increased cognate CD4 T cell responses in yo

78 s of keratinocyte chemoattractant, IL-6, and RANTES were produced in transgenic lungs.

79 roinflammatory genes (COX-2, IL-8, IL-6, and RANTES), and this was associated with repression of the

80 pression of AKT1, MTOR, chemokines [IL-8 and RANTES (regulated upon activation, normal T-cell express

81 NF-alpha and IL-1beta), chemokines (IL-8 and RANTES), and matrix metalloproteinases (MMP-1, -3, and -

82 th serum concentrations of interleukin-8 and RANTES.

83 and reduced tumor necrosis factor-alpha and RANTES (regulated on activation, normal T cell expressed

84 RNAs such as tumor necrosis factor alpha and RANTES early after stimulation.

85 HIV-1 coreceptors CCR5 (MIP-1alpha/beta and RANTES) and CXCR4 (SDF-1).

86 tion of the antiviral cytokines IFN-beta and RANTES.

87 ines interleukin 1beta, interferon beta, and RANTES (regulated on activation of normal T cells expres

88 n of interleukin 1beta, interferon beta, and RANTES in ZIKV-infected podocytes at 72 hours, compared

89 chemokines (MCP-1/CCL2, MIP-1alpha/CCL3, and RANTES/CCL5), and chemotactic factor receptors (CCR1, CC

90 ophage inflammatory protein 1alpha/CCL3, and RANTES/CCL5.

91 n contrast, high levels of virus, CD40L, and RANTES were documented locally at the tumor.

92 hage colony-stimulating factor (GM-CSF), and RANTES, but not IL-1alpha and IL-1beta, were detected in

93 ma activity, leading to decreased CXCL10 and RANTES production by smooth muscle cells.

94 nscript levels of Th1 cytokines, CXCL10, and RANTES in sciatic nerves of mice that developed SAP.

95 Our data indicated that SDF-1/CXCR4 and RANTES/CCR1 signals are pivotal and function synergistic

96 ges positively regulated gene expression and RANTES production in macrophages and cocultured alveolar

97 , including gamma interferon (IFN-gamma) and RANTES, were increased in acute infection and also were

98 FN-gamma, monokine induced by IFN-gamma, and RANTES.

99 inhibits renal inflammatory infiltration and RANTES expression by promoting VDR-mediated sequestratio

100 d chemokines (in particular MCP-5, IP10, and RANTES) were upregulated following infection and remaine

101 nduced LPCs to release MCP-1, MIP1alpha, and RANTES into conditioned medium causing HSC chemotaxis, w

102 ing the expression of adhesion molecules and RANTES inside the plaques.

103 ly, these cells produced IFN-gamma, TNF, and RANTES after ex vivo stimulation.

104 tified the chemokine CCL5 (formerly known as RANTES) as a candidate-specific downstream target for aS

105 tein 1 (MCP-1), MCP-3, and MCP-5, as well as RANTES and growth-related oncogene alpha (GROalpha), whi

106 Blockade of CCR5 attenuated RANTES-induced T-cell and monocyte/macrophage proliferat

107 e final ligation step driven by PPIs between RANTES and PF4.

108 Both RANTES and TNF induce ADM through activation of nuclear

109 Both RANTES variants are stable in Cymal-5, DHPC, Anzergent-3

110 ne, and sodium dodecyl-sulfate denature both RANTES variants at low pH, whereas at neutral pH the sta

111 ls, whereas the intratumoral release of both RANTES and IL15 attracted CAR-T cells and promoted their

112 ggest that induction of adaptive immunity by RANTES and eotaxin could hold the key for driving persis

113 n-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26, RANTES/CCL5, and MEC/CCL28.

114 okine (C-C motif) ligand 3], MIP-1beta/CCL4, RANTES (regulated on activation, normal T-cell expressed

115 secretion of CXCL1, CXCL2, CCL2, CCL3, CCL4, RANTES, and TNF-alpha, but not IL-1alpha, IL-1beta, IL-6

116 CCL5 (RANTES) is an inflammatory chemokine which binds to chem

117 obodies directed against CCL2 (MCP-1), CCL5 (RANTES), CXCL11 (I-TAC), and CXCL12 (SDF-1alpha) bind th

118 n a subset of 81 children, we analyzed CCL5 (RANTES) mRNA expression in upper airway epithelial cells

119 the CCR1 ligands CCL3 (MIP-1alpha) and CCL5 (RANTES) compared with injured kidneys from wild-type con

120 , CCL2 (MCP-1), CCL3 (MIP-1alpha), and CCL5 (RANTES) in the cerebrospinal fluid (CSF).

121 hemoattractant protein 1 [MCP-1]), and CCL5 (RANTES) were elicited in the urethra following primary i

122 nocyte chemoattractant protein 1), and CCL5 (RANTES).

123 uited to the tumor microenvironment by CCL5 (RANTES), where their differentiation into mature DCs is

124 The chemokine CCL5 (RANTES) activates its cognate receptor, CCR5, to initiat

125 oinflammatory chemokines and cytokines CCL5 (RANTES), CXCL10 (IP-10), IL-1alpha, IL-1beta, and PGE(2)

126 attenuation of the marked induction of CCL5 (RANTES) that occurred in this model, a chemokine recentl

127 reased expression of T cell-recruiting CCL5 (RANTES).

128 beta, IL-6, CCL2(MCP-1), CXCL12(SDF-1), CCL5(RANTES), CCR7, CXCR4, GM-CSF, CD40, CD40L, and VCAM-1.

129 nes, including the chemokine ligand 5 (CCL5, RANTES); after TRAP activation, platelets release over 2

130 CCL5/RANTES, and its receptor CCR5 are known to contribute to

131 te IFN-gamma, CXCL8/IL-8, CXCL10/IP-10, CCL5/RANTES, CCL11/eotaxin-1, CCL2/MCP-1, CCL4/MIP-1beta, CCL

132 of interferon gamma, interleukin 1beta, CCL5/RANTES, and interleukin 10 (IL-10) were elevated in RSV+

133 arly, induction of mRNA for CXCL8/IL-8, CCL5/RANTES, matrix metalloproteinase 1 (MMP-1), and MMP-3 af

134 tion of tumor necrosis factor (TNF) and CCL5/RANTES and more efficient uptake and killing of C. neofo

135 f CCL3/MIP-1alpha, CCL4/ MIP-1beta, and CCL5/RANTES but not of CXCL12/SDF-1.

136 n inhibited production of TNF-alpha and CCL5/RANTES cytokines and down-regulated the activity of NFka

137 kines (e.g., IL-5, CCL11/eotaxin-1, and CCL5/RANTES) and IL-17 ex vivo.

138 ting chemokines such as CXCL10/IP10 and CCL5/RANTES.

139 assic HIV-inhibitory chemokines such as CCL5/RANTES, XCL1 acts via direct interaction with the extern

140 xpression to induction of the chemokine CCL5/RANTES allows a more focused expression within primary t

141 n, including the CCR5-binding chemokine CCL5/RANTES and CCL4 and several members of the tripartite mo

142 Chemokine CCL5/RANTES is highly expressed in cancer where it contribute

143 etion of the proinflammatory chemokines CCL5/RANTES and CXCL10/interferon-inducible protein 10 in vit

144 rsely correlated with the expression of CCL5/RANTES and CXCL10/interferon-inducible protein 10 in viv

145 IRF3 phosphorylation, and production of CCL5/RANTES and IFN-beta, but not IL-8.

146 secreted elevated levels of IL-6, TNF, CCL5/RANTES, and CCL3/MIP1alpha, and these results were confi

147 or the elevated secretion of IL-6, TNF, CCL5/RANTES, and CCL3/MIP1alpha.

148 ype was further enhanced by exposure to CCL5/RANTES, a US28 ligand, associated with poor patient outc

149 system and a possible disruption of the CCR5-RANTES axis.

150 Role of chemokine RANTES in the regulation of perivascular inflammation, T

151 ic activity of the proinflammatory chemokine RANTES with potency similar to that of heparin, without

152 f SK1 potentiates induction of the chemokine RANTES (regulated on activation, normal T cell expressed

153 r adipose tissue expression of the chemokine RANTES (relative quantification, 1.2 +/- 0.2 vs. 3.5 +/-

154 tively regulates expression of the chemokine RANTES 3-5 d after activation of T cells.

155 an oncolytic virus armed with the chemokine RANTES and the cytokine IL15, reasoning that the modifie

156 Thus, chemokine RANTES is important in the regulation of vascular dysfun

157 , matrix metalloproteinase 9, and chemokine (RANTES).

158 transcription of a potent T cell chemokine, RANTES, which selectively recruits T cells into the vess

159 ipts for the keratinocyte-derived chemokine, RANTES, macrophage inflammatory protein 2, tumor necrosi

160 TNFalpha, and the Th1-associated chemokines RANTES, MIG, and IP-10 were each elevated significantly

161 eated mice was observed, certain chemokines (RANTES, monocyte chemoattractant protein 1[MCP-1], and I

162 correlation was observed between circulating RANTES levels as a biomarker and vascular function measu

163 Neutralization of circulating RANTES decreased liver neutrophilic infiltration and att

164 led to HIF-1alpha activation and concomitant RANTES expression.

165 Moreover, type I IFNs controlled RANTES production during pneumococcal pneumonia in vivo.

166 issue, we report the synthesis of a covalent RANTES-PF4 heterodimer (termed OPRAH) by total chemical

167 st abundant of these were GRO-alpha (CXCL1), RANTES (CCL5), IL-6 and MCP-1 (CCL2).

168 exposure to seven biomarkers (CXCL9, CXCL10, RANTES, IL1-RA, IL-17, MCP1 and IL-13) by calculating th

169 icant reductions in TNFalpha, MCP-1 (CXCL2), RANTES (CCL5) and KC (CCL5).

170 cluded IP-10/CXCL10, MCP-1/CCL2, IL-8/CXCL8, RANTES/CCL5, and Groalpha/CXCL1.

171 e macrophage-secreted inflammatory cytokines RANTES and tumor necrosis factor alpha (TNF) as mediator

172 HeLa cells stimulated with TNF-alpha despite RANTES induction being highly dependent on the NF-kappaB

173 e dominant-negative inhibitor for endogenous RANTES (44AANA47-RANTES) nor the CCR1/CCR5 receptor anta

174 f RANTES, we propose a model in which excess RANTES in combination with low CCR5 favors recovery from

175 parent rHEP and recombinant RABVs expressing RANTES (CCL5) or IP-10 (CXCL10).

176 and], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed

177 - to 7-fold), CXCL9/10/11 (45- to 338-fold), RANTES (724-fold), and interleukin-7 (IL-7; 128-fold).

178 IL-8, -56.6% (-30.7, -72.9 [P = 0.0011]) for RANTES, and -24.9% (2, -44.8 [P = 0.0656]) for monocyte

179 ceptor (CCR) 1, CCR3, and CCR5 receptors for RANTES chemokine was increased by Ang II (CCR1, 15.6 +/-

180 induction of the T(H)1 cytokines IFN-gamma, RANTES, and TNF-alpha.

181 d inhibited NK cell production of IFN-gamma, RANTES, MIP1-alpha, and MIG in response to IFN-alpha sti

182 Production of interferon-gamma, RANTES, and matrix metalloproteinase 3 (MMP-3) by NK cel

183 Spleen cell production of interferon-gamma, RANTES, and monocyte chemotactic protein-1 was elevated

184 se patients have increased levels of hepatic RANTES/CCL5.

185 and p50 binding to the kappaB site in human RANTES promoter as revealed by chromatin immunoprecipita

186 luding increased expression of MDA-5, RIG-I, RANTES, MCP-1, ISG-15, ISG-54, ISG-56, ISG-60, STAT1, IR

187 HIF-1 activation in male mice and identifies RANTES as a novel therapeutic target for NASH and NASH-d

188 (IL)-1 alpha (IL1A), IL-1 beta (IL1B), IL8, RANTES, colony stimulating factor 3 (CSF3), and superoxi

189 +/- 5% in wild type Ang II vs. 15 +/- 4% in RANTES(-/-)), which was associated with protection from

190 Therapeutic application of (131)I in RANTES-NIS-MSC-treated mice resulted in a significant de

191 Accordingly, we found a rapid increase in RANTES (regulated on activation normal T cell expressed

192 s (E-rLSECs) showed severalfold increases in RANTES and hypoxia-inducible factor 1alpha (HIF-1alpha)

193 eraction between functional polymorphisms in RANTES (a CCR5 ligand) and CCR5 impacts recovery.

194 , IL-6, and IL-10) and chemokines, including RANTES (regulated on activation normal T cell expressed

195 Chemokines, including RANTES/CCL5 and MCP-1/CCL2, are highly expressed in the

196 vels of proinflammatory cytokines, including RANTES, granulocyte colony-stimulating factor, IL-6, IL-

197 tinocytes in vitro and in vivo and increased RANTES production.

198 F-beta1 inhibited TNF-alpha- or IL-1-induced RANTES expression in human kidney tubular epithelial cel

199 Furthermore, treatment with IL-15 induced RANTES production by Rag2(-/-)gamma(c)(-/-) bone marrow

200 on of HIF-1alpha and AP-1 in ethanol-induced RANTES expression provides new strategies to ameliorate

201 porting the role of c-Jun in ethanol-induced RANTES expression.

202 Ethanol-induced RANTES mRNA expression required ethanol metabolism, p38

203 the molecular mechanisms for ethanol-induced RANTES up-regulation.

204 f GSK-3beta mimicked TGF-beta1 and inhibited RANTES induction, whereas overexpression of GSK-3beta ab

205 SCH-C inhibited RANTES (regulated on activation, normal T cell expressed

206 ar cell line (HKC-8), paricalcitol inhibited RANTES mRNA and protein expression and abolished the abi

207 thetic PPARgamma agonists potently inhibited RANTES (regulated upon activation, normal T cell express

208 te the mechanism by which TGF-beta1 inhibits RANTES expression, we examined the potential signal path

209 high plasma levels of CXCL13, sCD40L, IP10, RANTES, and TNFalpha, was observed in HIV controllers wh

210 er activity as well as IFN-beta, IRF5, IRF7, RANTES, IFN-inducible protein-10, MCP-1, and MIP1alpha g

211 s in chemokine receptor CCR5, and its ligand RANTES, which influence the migration of effector T cell

212 eases the seminal levels of the CCR5 ligands RANTES and eotaxin, and of the CXCR3 ligand monokine ind

213 Mechanistically, RANTES(-/-) knockout protected against vascular leukocyt

214 This IL-15-mediated RANTES production by Rag2(-/-)gamma(c)(-/-) bone marrow

215 ction by NK cells but reduces IL-15-mediated RANTES production by Rag2(-/-)gamma(c)(-/-) myeloid bone

216 e 14-3-3 proteins inhibit poly(I:C)-mediated RANTES production, 14-3-3 proteins augment Pam(3)CSK(4),

217 to -244) were required for ethanol-mediated RANTES expression.

218 Our studies showed that ethanol-mediated RANTES/CCL5 expression occurs via HIF-1alpha activation

219 Met-RANTES was used to block CCR5 in vivo.

220 WT mice treated with the CCR5 inhibitor Met-RANTES, exacerbated arthritis developed late in the dise

221 CCR1/CCR5 receptor antagonist, methionylated-RANTES, had an effect on clinical signs of arthritis whe

222 n demonstrated that tumor microenvironmental RANTES and MCP-1 secreted by tumor cells and tumor-deriv

223 Moreover, RANTES induced SMLC proliferation in vitro but did not p

224 ated p65 binding to kappaB sites and negated RANTES induction, suggesting that unliganded PPARgamma i

225 A and protein levels of MCP-1 (CCL2) but not RANTES (CCL5) were significantly reduced in GCH/ApoE-KO

226 was accompanied by a decreased expression of RANTES and TNF-alpha.

227 te (3-5 days after activation) expression of RANTES in T lymphocytes and that KLF13 itself is transla

228 s KLF13 protein, resulting in an increase of RANTES mRNA and protein.

229 ponse, associated with impaired induction of RANTES (Regulated upon Activation, Normal T-cell Express

230 Induction of RANTES was localized primarily to the tubular epithelium

231 monstrated that Bryo-1-mediated induction of RANTES was regulated by NF-kappaB and the interferon reg

232 ucted to determine whether the inhibition of RANTES and MCP-1 therapeutically was capable of ameliora

233 we have also investigated the interaction of RANTES and 5P12-RANTES with various commonly used deterg

234 x)-Mx-1-Cre mice showed attenuated levels of RANTES compared with ethanol-fed control mice, supportin

235 of -403A is reported to be higher levels of RANTES, we propose a model in which excess RANTES in com

236 e, we investigated whether neutralization of RANTES and eotaxin could protect against nigrostriatal d

237 In contrast, overexpression of RANTES or IP-10 increased RABV pathogenicity by causing

238 the IL-10 modulation/and or potentiation of RANTES/CCL5, macrophage inflammatory protein 2 (MIP-2)/C

239 ), LPS, R848, and CpG-mediated production of RANTES (regulated on activation normal T cell expressed

240 CpG-A IC induced enhanced production of RANTES and markedly reduced levels of IL-6 when compared

241 98059, significantly decreased production of RANTES, indicating that this effect of TWEAK is mediated

242 The role of RANTES and SDF-1 in the therapeutic effect of exogenous

243 12 keratinocytes stimulated the secretion of RANTES via Fn14 and promoted apoptosis.

244 Supplementation of RANTES and eotaxin was also associated with the inductio

245 terestingly, twice-weekly supplementation of RANTES and eotaxin, chemokines that are involved in T ce

246 SAA proteins stimulated the transcription of RANTES (regulated upon activation normal T-cell expresse

247 Finally, we detected marked upregulation of RANTES, CCR1, and CCR5 in patients with hepatic cirrhosi

248 However, only RANTES, IL-6, and IFN-gamma increased significantly with

249 neous production of chemokines, particularly RANTES, in vitro and in vivo.

250 8 MAPK, like SK1 knockdown, also potentiates RANTES induction.

251 that TGF-beta1 inhibition of proinflammatory RANTES expression is mediated by beta-catenin-triggered

252 S under control of the RANTES/CCL5 promoter (RANTES-NIS-MSC) in a colon cancer liver metastasis mouse

253 This rhesus CCR5-specific/PSC- RANTES resistance selection is particularly alarming giv

254 PSC-RANTES binds to CCR5, inhibits human immunodeficiency vi

255 characteristics of the chemokine analog PSC-RANTES (N-alpha-(n-nonanoyl)-des-Ser(1)-[l-thioprolyl(2)

256 icate that a pool of spare CCR5 may bind PSC-RANTES but not native chemokines.

257 Improved recognition of CCR5 by PSC-RANTES may explain why the analog promotes higher amount

258 icate even at the highest tissue culture PSC-RANTES concentrations (100 nM).

259 s in sensitivity to inhibition by either PSC-RANTES or the small-molecule allosteric inhibitor TAK-77

260 to macromolecular CCR5 inhibitors (e.g., PSC-RANTES) that act by both CCR5 internalization and recept

261 ace of a protective vaginal microbicide, PSC-RANTES.

262 fail to prevent high-affinity binding of PSC-RANTES, analog-mediated calcium release (in desensitizat

263 84) pretreated with a 100 microM dose of PSC-RANTES.

264 ed replicative fitness and resistance to PSC-RANTES was therefore surprising.

265 ases in 50% inhibitory concentrations to PSC-RANTES with env(m584) were modest (sevenfold) and most p

266 3)-infected rhesus macaques treated with PSC-RANTES were analyzed for possible drug escape variants.

267 ing to the cis-acting kappaB elements in rat RANTES promoter, whereas disruption of PPARgamma.p65 by

268 riggers type I IFN production, and regulates RANTES production.

269 type I IFN response and positively regulates RANTES production.

270 eas ectopic expression of GSK-3beta restored RANTES induction.

271 effect of TGF-beta1 and completely restored RANTES expression.

272 ation, normal T-cell expressed and secreted (RANTES) in this effect.

273 vation normal T-cell expressed and secreted (RANTES) was assessed.

274 ation, normal T-cell expressed and secreted (RANTES), compared to wild type.

275 vation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor

276 vation normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, a

277 vation normal T cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, M

278 ted on normal T-cell expressed and secreted (RANTES), mediates monocyte trafficking to sites of infla

279 ation, normal T cell expressed and secreted (RANTES).

280 tion, normal T cell expressed, and secreted (RANTES)] after CCl(4) treatment versus wild-type (WT) mi

281 NA expression of ICAM-1, VCAM-1, E-selectin, RANTES, IL-17, IL-33, thymic stromal lymphopoietin, indu

282 e TGF-beta1 effect and completely suppressed RANTES expression induced by TNF-alpha.

283 ry inhibitors composed of one CCR5-targeting RANTES (regulated on activation normal T cell expressed

284 The RANTES derivative 5P12-RANTES is a highly potent HIV ent

285 In contrast, the RANTES treatment induces a recovery of the receptor on t

286 p65 to its cognate cis-acting element in the RANTES promoter.

287 ing to its cognate cis-acting element in the RANTES promoter.

288 but not JunB, bound to the AP-1 site of the RANTES promoter.

289 Cs transfected with NIS under control of the RANTES/CCL5 promoter (RANTES-NIS-MSC) in a colon cancer

290 ndent and was up to 100-fold better than the RANTES variant alone or in combination with unlinked C37

291 ory factors (IRF)-1, IRF-3, and IRF-7 to the RANTES independently of myeloid differentiation primary

292 nse elements (HREs; -31 to -9 bp) within the RANTES promoter in response to ethanol.

293 g., platelet factor 4, beta-thromboglobulin, RANTES, thromboxane, or serotonin) in the pathogenesis o

294 Finally, in addition to RANTES, loss of SK1 also potentiated the induction of mu

295 C chemokine receptor-1 (CCR1) and respond to RANTES by increased migration and proliferation.

296 Moreover, the ability of Bryo-1 to trigger RANTES and MIP1-alpha suggests that Bryo-1 could potenti

297 2-RANTES has the same structure as wild-type RANTES but unlike the wild-type, does not dimerize via i

298 extract or LPS - secretory responses (VEGF, RANTES, MCP-1, IL-17A, IFN-gamma, GM-CSF, eotaxin, MIP1-

299 ated with recovery from an HBV infection was RANTES -403A with CCR5Delta32 (odds ratio 0.36, p = 0.02

300 Results show robust MSC recruitment with RANTES/CCL5-promoter activation within the stroma of liv