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 and eotaxin were also up-regulated in the substan

4 RANTES promoter analysis showed that cis elements proxim

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

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

7 RANTES/CCL5 analogs are more potent inhibitors of infect

8 nocyte chemoattractant protein 1 (P = .028), RANTES (P = .005), IL-2 (P = .002), and IL-17 (P = .007)

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

10 However, chemokine release (e.g. MCP-1, RANTES and TARC) was significantly reduced in inhibitor-

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

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

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

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

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

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 beta, IL-6, IL-17, MCP-1, MIP-1alpha, MIP-2, RANTES, and TNF-alpha), inflammatory cell infiltration (

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

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

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

26 PO)-DNA complexes (NETs), platelet factor 4, RANTES, and selected cytokines.

27 5P12-RANTES does not elicit receptor phosphorylation or arres

28 binding affinities for the two analogs 5P12-RANTES and 5P14-RANTES and about 20-fold reduced affinit

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

30 se of the protein microbicide candidate 5P12-RANTES, an experimental chemokine analogue that potently

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

32 For 5P12-RANTES, sustained release was obtained for 31 days using

33 er, we show that the released inhibitor 5P12-RANTES was functional both in vitro and in ex vivo color

34 ibody (IgG) or the potent HIV inhibitor 5P12-RANTES.

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

36 mer cores - each containing lyophilised 5P12-RANTES and exposed to the external environment by two la

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

38 - provided sustained concentrations of 5P12-RANTES in vaginal fluid and vaginal tissue between 10 an

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

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

41 5P14-RANTES induces comparable levels of receptor phosphoryla

42 ies for the two analogs 5P12-RANTES and 5P14-RANTES and about 20-fold reduced affinities for PSC-RANT

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

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

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

46 ld reduced affinities for PSC-RANTES and 6P4-RANTES.

47 ponse (elevated IL-1beta, IL-6, IL-10, IL-8, RANTES, and TNFalpha) while the response to the parent s

48 interleukin 1alpha (IL-1alpha), IL-6, IL-9, RANTES, tumor necrosis factor alpha (TNF-alpha), CXCL1,

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

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

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

52 chemokines (IL-1beta, IL-5, IL-6, TNF-alpha, RANTES, MIP-1beta, MCP-1, KC and IL-10).

53 Although RANTES infusion in vivo promoted inflammatory cell accum

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

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

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

57 f eosinophil chemoatttractants eotaxin-1 and RANTES in the muscle tissue of all three dystrophin-defi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 TNF-alpha but not MIP-1alpha, MIP-1beta, and RANTES.

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

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

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

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

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

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

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

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

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

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

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

90 th serum concentrations of interleukin-8 and RANTES.

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

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

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

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

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

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

97 effects of BVR-A deletion on chemotaxis and RANTES expression were blocked in the presence of a C5aR

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

99 T-cell chemoattractants CXCL10, CXCL11, and RANTES.

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

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

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

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

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

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

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

107 e secretion of the stored-chemokines PF4 and RANTES, but not newly synthesized IL-1beta, when culture

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

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

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

111 Because RANTES and eotaxin share a common receptor, CCR5, we exa

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

113 Both RANTES and TNF induce ADM through activation of nuclear

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

133 CCL2/MCP-1, CCL3/MIP-1a, CXCL10/IP-10, CCL5/RANTES, and CCL20/MIP-3a.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 ment of macrophages via the chemoattractants RANTES, MIF, CCL2, and CXCL12 and activation of their tu

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

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

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

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

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

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

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

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

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

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

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

164 ma levels of the platelet-derived chemokines RANTES/CCL5 and PF4/CXCL4 were lower in coinfection.

165 vated levels of C5aR1 as well as chemokines (RANTES, IP10) but not proinflammatory markers, such as i

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

167 ke macrophage markers, including chemokines (RANTES, IP-10), as well as chemotaxis in response to LPS

168 binding site, whereas the native chemokines (RANTES and MIP-1alpha) fail to displace bound fluorescen

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

170 Neutralization of circulating RANTES decreased liver neutrophilic infiltration and att

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

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

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

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

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

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

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

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

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

180 e of inflammation, including IL-12, eotaxin, RANTES, IL-10 and interferon-gamma (p < 0.05).

181 Numerous cytokines such as I-TAC, Eotaxin, RANTES, MCP-1, IFNgamma and MIG demonstrated a biphasic

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

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

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

185 lony-stimulating factor (GM-CSF) (6.6-fold), RANTES (14.8-fold), and interferon gamma inducible prote

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

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

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

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

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

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

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

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

194 +/- 5% in wild type Ang II vs. 15 +/- 4% in RANTES(-/-)), which was associated with protection from

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

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

197 ingly, we have reported a marked increase in RANTES and eotaxin, chemokines that are involved in T ce

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

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

200 markers and chemokines by PDLSCs, including RANTES, eotaxin, interferon (IFN)-gamma- inducible prote

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 98059, significantly decreased production of RANTES, indicating that this effect of TWEAK is mediated

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

239 12 keratinocytes stimulated the secretion of RANTES via Fn14 and promoted apoptosis.

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

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

242 However, this observed suppression of RANTES is not mediated by CPAF.

243 four orders of magnitude higher than that of RANTES itself.

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

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

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

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

248 8 MAPK, like SK1 knockdown, also potentiates RANTES induction.

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

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

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

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

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

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

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

256 In contrast, PSC-RANTES induces CCR5 hyperphosphorylation, driving enhanc

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

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

259 and about 20-fold reduced affinities for PSC-RANTES and 6P4-RANTES.

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 effect of TGF-beta1 and completely restored RANTES expression.

271 tion, normal T-cell-expressed, and secreted (RANTES) (CCL5) that have anti-HIV potencies of around 25

272 ation, normal T cell expressed and secreted (RANTES) at week 4 and week 8; macrophage inflammatory pr

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

274 ation, normal T cell expressed and secreted (RANTES) values in PS group were lower in PS group compar

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

276 ation, Normal T Cell Expressed and Secreted (RANTES) was higher in transplant SAB vs nontransplant SA

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

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

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

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

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

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

283 tion, normal T-cell-expressed and -secreted (RANTES; P = .002) than NOP children during viral URIs.

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

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

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

287 se to C. trachomatis and found evidence that RANTES, another T-cell chemoattractant, is actively supp

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

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

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

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

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

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

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

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

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

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

298 2-RANTES has the same structure as wild-type RANTES but unlike the wild-type, does not dimerize via i

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

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