ライフサイエンスコーパス: IL-6R

1 IL-6R mRNA and protein were not detected in controls, bu

2 IL-6R mRNA is weakly expressed in the biliary tree, and

3 IL-6R protein expression was observed in bronchoalveolar

4 IL-6R signaling activates the transcription factor STAT1

5 ) expression, IFN-alpha also reduced KAS-6/1 IL-6R expression.

6 This finding reveals a GATA3/miR-125a-5p/IL-6R and STAT3/FOXP3 regulatory pathway, which determin

7 Significant upregulation in IL-6, IL-6R, and gp130 occurred only at 24 hours of sustained

8 roles for CLCF1-CNTFR and interleukin (IL)-6-IL-6R signaling in promoting growth of NSCLCs.

9 ignaling, it acts as a spacer to ensure IL-6.IL-6R.gp130 signal complex formation.

10 eloma cell growth through modulation of IL-6/IL-6R autocrine/paracrine loop and the principle of achi

11 This suggests that anti-IL-6/IL-6R blockade could be effective in modifying T- and B-

12 Here, we explore the biology of IL-6/IL-6R interactions and the evidence for an important rol

13 autiously optimistic that targeting the IL-6/IL-6R pathway could offer a novel alternative for diffic

14 IL-6/IL-6R signaling pathway, in particular, has been propose

15 amples, some Th2 genes (IL-3, IL-5, and IL-6/IL-6R) were found to be up-regulated as well.

16 t]) and tocilizumab or siltuximab (anti-IL-6/IL-6R).

17 The mRNAs for LIF/LIFR, IL-6/IL-6R, and their common signal-transduction molecule, gp

18 noic acid, previously shown to modulate IL-6/IL-6R, on the in vitro growth of a human myeloma cell li

19 suppresses tumor progression by inhibiting a IL-6R/STAT3/miR-34a feedback loop.

20 An active IL-6R/STAT3/miR-34a loop was necessary for EMT, invasion

21 actor receptor (EGFR) and the high-affinity, IL-6R/gp130-derived pY-peptide, GpYLPQTV-NH(2).

22 mbrane-bound or soluble IL-6 receptor alpha (IL-6R, sIL-6R), which is referred to as classic and tran

23 ponsiveness to IL-6 via the activation of an IL-6R sheddase, resulting in an immediate production of

24 Therefore, we generated and analyzed IL-6R stalk region deletion variants for cleavability an

25 The similar actions of IL-10R and IL-6R on the induction of endogenous IL-6-responsive gen

26 Expression of IL-1R and IL-6R was enhanced by LPS and IFN-gamma.

27 -regulation of expression of LIFR, IL-6, and IL-6R in ensheathing cells by 3 days post-OBX.

28 CB1R and IL-6R co-stimulation enhanced the differentiation of rat

29 itself has no effect, we found that CB1R and IL-6R stimulation together induced synergistic neurite o

30 will allow discriminating between CNTFR- and IL-6R-mediated effects in vivo.

31 te direct binding of vIL-6 to both gp130 and IL-6R and vIL-6-induced gp130-IL-6R complex formation, a

32 , investigating the utilization of gp130 and IL-6R by vIL-6, and undertaking mutational analyses of v

33 mutational analyses of regions of gp130 and IL-6R potentially involved in interactions with ligand o

34 n, tumor cell-derived IL-6 induced gp130 and IL-6R-dependent activation of STAT3, leading to reduced

35 be involved directly in binding to gp130 and IL-6R.

36 Met protein expression is increased, and IL-6R(gp-80) protein is induced on the proliferating BEC

37 residues important for IL-6R-independent and IL-6R-dependent signaling through native gp130 and gp130

38 that are important for IL-6R-independent and IL-6R-mediated functional complex formation between vIL-

39 B expression but restored IL-2 secretion and IL-6R and TGFbRII expression and signaling, as illustrat

40 is weakly expressed in the biliary tree, and IL-6R protein is detectable on hepatocytes, with a perip

41 Anti-IL-6R, selective blockade of sIL-6R, or gammadelta T-cel

42 omplex was reversed by the inclusion of anti-IL-6R and gp130 Abs, demonstrating the specificity of th

43 mphasize caution for therapeutic use of anti-IL-6R antibody.

44 xpected, based on reports of the use of anti-IL-6R in inflammatory bowel disease, dnTGFbetaRII IL-6(-

45 Administration of anti-IL-6 or anti-IL-6R to wild-type recipients prior to transfer of CD8(-

46 Initial data from our group suggest anti-IL-6R therapy is of value in desensitization and prevent

47 signaling; in this model treatment with anti-IL-6R did not suppress airway inflammation.

48 the best candidates for treatment with anti-IL-6R if they have accompanying autoimmune liver disease

49 Preemptive treatment of mice with anti-IL-6R or anti-IL-6 worsened NTN, whereas selective block

50 lone did not induce T cell survival, because IL-6R expression on T cells in AqH was too low to facili

51 se results document that vIL-6 does not bind IL-6R and suggest that conformational change may be crit

52 e ADAM17 cleavage site substantially blocked IL-6R proteolysis by ADAM17 but only slightly affected p

53 various diseases, the origin of blood-borne IL-6R is still poorly understood.

54 ved primary human osteoblasts expressed both IL-6R and gp130 as determined by flow cytometry and immu

55 acetate induced a dramatic increase of both IL-6R shedding (i.e. the production of sIL-6R) and IL-6

56 lassically orchestrated via a membrane-bound IL-6R (CD126) alpha subunit (classical IL-6R signaling)

57 IL-6R mAb that binds to both membrane-bound IL-6R and soluble IL-6R with the unique property of spec

58 ently, IL-6 signaling through membrane-bound IL-6R seems to be limited to naive or central memory T c

59 However, the membrane-bound IL-6R was nonfunctional, as significant tyrosine phospho

60 s mediated by shedding of the membrane-bound IL-6R, and this process correlates with the expression o

61 or 201-206 promoted a loss of membrane-bound IL-6R, suggesting release by proteolytic shedding.

62 IL-6 can signal through the membrane-bound IL-6R, which is expressed only on hepatocytes and certai

63 with similar affinity as the membrane-bound IL-6R.

64 ells' in vivo angiogenic capacity induced by IL-6R, which simultaneously activates Jak/STAT and PI3K/

65 LIF and OSM receptors differed from that by IL-6R by the prominent activation of STAT5 as shown in t

66 s, as well as increased expression of CD126 (IL-6R) and CD115 (M-CSFR), were detected in APC-defectiv

67 Cellular IL-6R density was altered correspondingly without change

68 Although circulating IL-6R levels are altered in various diseases, the origin

69 bound IL-6R (CD126) alpha subunit (classical IL-6R signaling) or through a soluble form of this cogna

70 Therefore, we concluded that classical IL-6R signaling in naive or central memory CD4(+) T cell

71 ng, the identity of the protease(s) cleaving IL-6R in more physiological settings, or even in vivo, r

72 Cognate IL-6R was detected in aortic smooth muscle, but its leve

73 iption-3 activation are mediated via cognate IL-6R.

74 atRA decreased IL-6R expression and signaling by nTregs.

75 , whereas constitutive release of endogenous IL-6R is largely mediated by ADAM10.

76 eficient mice we established that endogenous IL-6R of both human and murine origin is shed by ADAM17

77 y similar to that mediated by the endogenous IL-6R.

78 chemistry was used to qualitatively evaluate IL-6R protein expression in bronchoalveolar lavage cells

79 ion experiments in Hep3B cells (that express IL-6R and gp130) showed that most were able to function

80 subset of naive CD8(+) T cells that express IL-6R into a unique population of effector CD8(+) T cell

81 Mice with a mutation in T cell-expressed IL-6R were unable to expand Tfh populations after HDM se

82 r this unused vIL-6 surface is available for IL-6R binding.

83 Tissues were immunostained for IL-6R, gp130, CD15(+) (polymorphonuclear), and CD3(+) (T

84 variants to identify residues important for IL-6R-independent and IL-6R-dependent signaling through

85 ied residues in vIL-6 that are important for IL-6R-independent and IL-6R-mediated functional complex

86 e antibody to IL-6, as was also observed for IL-6R mutants of Phe(279) In the second antibody, the si

87 Dual immunohistochemical staining for IL-6R and CD31 revealed IL-6R expression on human endoth

88 pressing proteolytic cleavage of sIL-6R from IL-6R and downregulation of the SOCS3 autoinhibitory pat

89 both gp130 and IL-6R and vIL-6-induced gp130-IL-6R complex formation, and we have extended our functi

90 naling by endogenous IL-6 proteins; however, IL-6R can enhance vIL-6 activity and can enable signalin

91 agonistic cytokine via the murine and human IL-6R, indicating that p28 exhibits no species specifici

92 ed NI-1201, a mAb that targets, in the human IL-6R sequence, the epitope recognized by 25F10 for mice

93 from variation in IL-6 and more importantly IL-6R.

94 the metalloproteinases ADAM10 and ADAM17 in IL-6R shedding, the identity of the protease(s) cleaving

95 cells in vitro leads to a downregulation in IL-6R expression.

96 ly conserved, alpha-helical, and involved in IL-6R binding.

97 gest haplotype associations were observed in IL-6R with IL-6 cytokine concentration as outcome: Cauca

98 Their combination caused a net reduction in IL-6R mRNA.

99 Finally, we identified the region in IL-6R that binds to CANDIS.

100 rkers rs1800797, rs1800796 and rs1800795; in IL-6R markers rs4075015, rs4601580, rs4645618, rs6687726

101 diverse oncogenic growth stimuli, including IL-6R, c-Src, Her2/Neu, is attenuated in cells without S

102 histochemistry and RT-PCR revealed increased IL-6R and decreased gp130 expression in amniochorion of

103 we also observed suppression of interleukin (IL)6R, c-Myc, and reduced STAT3 phosphorylation.

104 we have reported the limitations of isolated IL-6R-alpha inhibition on dendritic cell-stimulated allo

105 ferring IL-6-responsiveness to cells lacking IL-6R such as synoviocytes.

106 oviding IL-6-responsiveness to cells lacking IL-6R.

107 Instead, we found full-length IL-6R on circulating microvesicles, establishing microve

108 chain of HCDR3 valine ties into site I like IL-6R Phe(279), whereas a LCDR1 tyrosine side chain occu

109 t the role of the 52-amino acid-residue-long IL-6R stalk region in shedding and signal transduction.

110 l and experimental peritonitis episodes lose IL-6R expression, and anti-CD3/CD28 Ab costimulation of

111 sians; however, in African-American maternal IL-6R marker rs4553185 associated with PTB (allele P = 4

112 d amino acids also abrogated ADAM10-mediated IL-6R shedding.

113 ite, also reduced ADAM10 and ADAM17-mediated IL-6R shedding, questioning the importance of cleavage s

114 t be regulating IL-6 signaling by modulating IL-6R stabilization and recycling.

115 25F10 is an anti-mouse IL-6R mAb that binds to both membrane-bound IL-6R and so

116 the interactions of Phe(229) and Phe(279) of IL-6R.

117 espect to vIL-6 signalling in the absence of IL-6R but that retains the ability to mediate vIL-6 and

118 e to induce signaling even in the absence of IL-6R or EBI3.

119 ious studies that demonstrated activation of IL-6R by p28 (IL-30), new findings further suggest a com

120 Analysis of IL-6R and JAK1 expression in HCV patients by quantitativ

121 Appraisal of IL-6R expression on human and mouse T cells emphasized t

122 These data explain why blockade of IL-6R only achieves protection against EAE if used at th

123 the resultant conformation/dynamic change of IL-6R.

124 ands in the cytokine-binding domain (DII) of IL-6R.

125 amining the signaling pathways downstream of IL-6R in primary human T cells.

126 iRNA-449a and miRNA-107 target expression of IL-6R and JAK1, respectively, in vitro and also inhibit

127 duced by GATA-3 to inhibit the expression of IL-6R and STAT3.

128 (sIL-6R), but the cell surface expression of IL-6R and the mechanism of sIL-6R production are largely

129 n was enhanced in mice lacking expression of IL-6R by CD4(+) T cells and by treatment of wild-type mi

130 ted a possible role of tumoral expression of IL-6R in ovarian cancer.

131 two groups and found that high-expression of IL-6R mRNA in tumor tissues was a positive prognostic fa

132 acts in part by modulating the expression of IL-6R on T cells.

133 The expression of IL-6R was detected in 52.6% of hepatic CD3(+) T cells an

134 n in several models that the soluble form of IL-6R (sIL-6R) is involved in the recruitment of mononuc

135 otential clinical and biological function of IL-6R mRNA expression in ovarian cancer.

136 revealed that 25F10 interacts at site IIb of IL-6R but allows the binding of IL-6 to the IL-6R and th

137 ecall responses and to examine the impact of IL-6R blockade on Th17, Treg, follicular T helper (Tfh)

138 can function in human cells independently of IL-6R.

139 within site I and mimics the interactions of IL-6R Phe(229).

140 Simultaneously, high expression level of IL-6R mRNA correlates with better survival of patients w

141 sion, our results showed that mRNA levels of IL-6R in ovarian cancer was positively associated with b

142 al fibroblasts also express higher levels of IL-6R than do skin-derived cells.

143 Loss of IL-6R expression by activated T cells further suggests t

144 This reflected the loss of IL-6R expression by T cells over time.

145 Finally, systemic neutralization of IL-6R did not reduce arteriosclerotic thickening but red

146 les of putative cytokine-binding residues of IL-6R in ligand-induced functional complex formation are

147 acetate-induced and spontaneous shedding of IL-6R resulting in the absence of sIL-6R in the culture

148 model, it is not ADAM17-mediated shedding of IL-6R within the pouch that orchestrates this inflammato

149 antibody reactive with the gp130 subunit of IL-6R abrogated signaling of both responses.

150 Blocking the IL-1R or IL-6R reversed cytokine impairment.

151 that could be reversed by blocking IL-1R or IL-6R.

152 ncomitant therapy with COX inhibitors and/or IL-6R antibodies might increase the clinical effect of p

153 a novel molecular switch induced by EBI3 or IL-6R, respectively.

154 complexes consisting of CNTFR.gp130.LIFR or IL-6R.gp130.LIFR, respectively.

155 experiments using ectopically overexpressed IL-6R and candidate proteases revealed major roles for t

156 he beta-receptor chains gp130 and Wsx-1, p28/IL-6R specifically recruits two gp130 beta-receptor chai

157 However, as we have shown previously, IL-6R can enhance vIL-6 signal transduction and can enab

158 ng mediated by IL-6 and its soluble receptor IL-6R (sIL-6R); by an antibody to the IL-6 receptor; or

159 onal amino acid change in the IL-6 receptor (IL-6R Asp358Ala; rs2228145) was significantly associated

160 An antibody to the IL-6 receptor (IL-6R) alpha subunit effectively neutralized the respons

161 Signaling by the interleukin 6 receptor (IL-6R) also activates STAT3 through Jak kinase.

162 substrates of ADAM17 are the IL-6 receptor (IL-6R) and TNF-alpha.

163 s have been obtained with the IL-6 receptor (IL-6R) antagonist tocilizumab for the treatment of large

164 proinflammatory effects, and IL-6 receptor (IL-6R) blockade as a treatment for inflammatory diseases

165 study evaluated the effect of IL-6 receptor (IL-6R) blockade with an antiYIL-6R monoclonal (mMR16-1)

166 binding to the cytokine with IL-6 receptor (IL-6R) by using side chains of two CDR residues filling

167 ng components of the interleukin-6 receptor (IL-6R) complex.

168 taneous reduction of interleukin-6 receptor (IL-6R) expression on myeloid progenitor cells by Delta-1

169 -inhibited cell lines reduced IL-6 receptor (IL-6R) expression, IFN-alpha also reduced KAS-6/1 IL-6R

170 the epitope of human interleukin-6 receptor (IL-6R) for two adnectins with distinct affinities (Kd, A

171 58Ala variant in the interleukin-6 receptor (IL-6R) gene has been implicated in asthma, autoimmune an

172 A variant in the IL-6 receptor (IL-6R) gene increases asthma risk and is predicted to de

173 ound and soluble forms of the IL-6 receptor (IL-6R) in processes called classic and trans-signaling,

174 body-mediated blockade of the IL-6 receptor (IL-6R) markedly reduces pathologic damage attributable t

175 ormal liver, but both met and IL-6 receptor (IL-6R) mRNA are detectable; met mRNA is expressed strong

176 wn-regulation of the interleukin 6 receptor (IL-6R) on naive CD4(+) T cells on the mRNA as well as on

177 Mice lacking IL-6 receptor (IL-6R) or IL-1 receptor 1 (IL-1R1) specifically on B cel

178 r, antibodies specific to the IL-6 receptor (IL-6R) or the gp130 subunit were capable of blocking the

179 the behavior of the specific IL-6 receptor (IL-6R) or the signal transducer gp130.

180 lex consisting of the cognate IL-6 receptor (IL-6R) or the soluble IL-6 receptor (sIL-6R) and glycopr

181 Interleukin-6 (IL-6)/IL-6 receptor (IL-6R) plays a major role in autocrine/paracrine growth

182 IL6R coding change increases IL-6 receptor (IL-6R) shedding and promotes IL-6 transsignaling.

183 eceptor (IGF-1R) and interleukin-6 receptor (IL-6R) signaling (eg, IKK/NF-kappaB, PI-3K/Akt, and Raf/

184 )/IGF-1 receptor (IGF-1R) and IL-6 receptor (IL-6R) signaling cascades, antiapoptotic molecules (e.g.

185 naling via its membrane-bound IL-6 receptor (IL-6R), and trans-signaling via a naturally occurring so

186 e of monoclonal antibodies to IL-6 receptor (IL-6R), designed to block IL-6 pathways.

187 with the specific alpha-chain IL-6 receptor (IL-6R), is accessible and not occupied by gp130.

188 Expression of IL-6, IL-6 receptor (IL-6R), or glycoprotein 130, as well as IL-6 secretion,

189 nal antibody against interleukin-6 receptor (IL-6R), tocilizumab, prevented M2-differentiation.

190 urthermore, we identified the IL-6 receptor (IL-6R), which mediates IL-6-dependent STAT3 activation,

191 DES using a novel drug (anti-IL-6 receptor (IL-6R),Tocilizumab [TCZ]) + intravenous Ig (IVIg) to ass

192 not show activation of other IL-6 receptor (IL-6R)-mediated Janus kinase substrates, gp130, SHP-2, a

193 y the association of two IL-6.IL-6 receptor (IL-6R).gp130 trimers, with gp130 being the signal transd

194 s: by directly binding to the IL-6 receptor (IL-6R; CD126) or via trans-signaling, in which soluble I

195 t on the structurally related IL-6 receptor (IL-6R; gp80) subunit of the receptor-signal transducer c

196 ignaling membrane-bound IL-6 alpha-receptor (IL-6R) as an agonistic cytokine but also as a gp130 beta

197 ) and interleukin 6 (IL-6) and its receptor (IL-6R) in intercellular signaling pathways in the olfact

198 on that includes the gene for this receptor (IL-6R).

199 s conditioned by the transmembrane receptor (IL-6R) and homodimerization of gp130.

200 line, B9, and that the gp80 (IL-6 receptor [IL-6R]) component of the IL-6 receptor-signal transducer

201 ng these is tocilizumab (anti-IL-6 receptor [IL-6R]) which holds promise for modulating multiple immu

202 inally, although IFN-alpha treatment reduced IL-6R numbers on each cell line, analysis of Stat protei

203 ased, while all-trans retinoic acid reduced, IL-6R but not gp130 mRNA expression.

204 The resulting IL-6R/STAT3/miR-34a feedback loop was present in primary

205 hemical staining for IL-6R and CD31 revealed IL-6R expression on human endothelial cells within norma

206 nsive to requiring both IL-6 and soluble (s) IL-6R for activation.

207 otein and mRNA expression of sIL-6R, sgp130, IL-6R, and gp130.

208 sgp130) receptor to capture the IL-6/soluble IL-6R complex has shown promise for the treatment of rhe

209 hy results showed EGCG inhibits IL-6/soluble IL-6R-induced matrix metalloproteinase-2 activity in RA

210 High levels of both IL-6 and soluble IL-6R were found in AqH.

211 However, combinations of IL-6 and soluble IL-6R were highly effective inhibitors of T cell apoptos

212 nds to both membrane-bound IL-6R and soluble IL-6R with the unique property of specifically inhibitin

213 g ligand-occupied anti-IL-6 and anti-soluble IL-6R IgG.

214 ells responded to trans-signaling by soluble IL-6R/IL-6 complexes, whereas no response was evident in

215 450- and 200-kDa complexes included soluble IL-6R, with the 200-kDa complexes additionally containin

216 -signaling via a naturally occurring soluble IL-6R.

217 358Ala had increased serum levels of soluble IL-6R (P = 4 x 10(-14)), with homozygote carriers showin

218 ristics, whereas local regulation of soluble IL-6R activity might serve to maintain the cytokine prof

219 1 treatment combined with removal of soluble IL-6R using a dynamically fed culture system, reduces ma

220 acterized by excessive production of soluble IL-6R.

221 both with leukocyte numbers and i.p. soluble IL-6R (sIL-6R) levels.

222 APP gene induction with recombinant-soluble IL-6R linked to IL-6 cytokine (Hyper-IL-6) or with anoth

223 Elevated serum soluble IL-6R levels were associated with lower percent predicte

224 Serum soluble IL-6R levels were measured in subjects from SARP.

225 Moreover, we demonstrate that soluble IL-6R levels were higher in patients with AD than in con

226 amily members, OSM and IL-6 plus the soluble IL-6R (IL-6/R), prevent NMDA and glutamate-induced neuro

227 IL-6 trans-signaling via the soluble IL-6R (sIL-6R) plays an important role in the progressio

228 o induce p28-trans-signaling via the soluble IL-6R (sIL-6R), a characteristic property that was initi

229 The soluble IL-6R (slL-6R alpha)/IL-6 complex and oncostatin M (OM),

230 The soluble IL-6R is mainly generated by ADAM10- and ADAM17-mediated

231 leukocytes (classic), or through the soluble IL-6R, which binds the ubiquitously expressed gp130 (alt

232 cytokines, such as oncostatin M, the soluble IL-6R-IL-6 complex, TNF-alpha, and IL-1beta.

233 uring trans-signaling, IL-6 binds to soluble IL-6R (sIL-6R), enabling activation of cells expressing

234 to soluble gp130 (sgp130) but not to soluble IL-6R (sIL-6R).

235 d unaffected by a neutralizing Ab to soluble IL-6R.

236 the classical membrane-bound versus soluble IL-6R signaling pathways.

237 26) or via trans-signaling, in which soluble IL-6R/IL-6 complexes bind to the signaling component CD1

238 al tumors displayed upregulation of p-STAT3, IL-6R, and SNAIL and progressed to invasive carcinomas,

239 ependent on the IL-6 receptor alpha subunit (IL-6R, gp80) that is required for signaling by endogenou

240 ased 80-fold, and the IL-6 receptor subunits IL-6R alpha and gp130 were present in the adrenal cells.

241 sion, human osteoblasts express cell surface IL-6R, which is unable to transmit IL-6-induced signals

242 -alpha-mediated growth inhibition other than IL-6R downregulation must exist in myeloma.

243 more promiscuous than that of hIL-6 but that IL-6R may play a role in vIL-6 signaling in vivo.

244 n on human and mouse T cells emphasized that IL-6R expression is closely linked with that of CCR7 and

245 e to support vIL-6 activity, indicating that IL-6R can form part of the signaling complex.

246 t population-based birth cohorts showed that IL-6R 358Ala specifically predisposes to the persistent

247 or cross-talk between the BCR, TLR4, and the IL-6R or CD40.

248 nrelated 55-kDa, type I TNF receptor and the IL-6R, we propose that ARTS-1 may play an important role

249 Additionally, genes encoding the IL-6R and TGFbRII subunits were stably repressed, result

250 Both endothelial cell lines expressed the IL-6R and their stimulation with the exogenous ligand si

251 IL-6, the soluble form of the IL-6R (sIL-6R), or both IL-6 plus sIL-6R, had no effect

252 recruitment by IL-6 requires shedding of the IL-6R from infiltrating neutrophils.

253 re, we ruled out alternative splicing of the IL-6R mRNA as a potential source of circulating sIL-6R i

254 es demonstrate that antibody blockade of the IL-6R serves to recalibrate the effector and regulatory

255 ponse increase in the mRNA expression of the IL-6R signaling inhibitor protein suppressors of cytokin

256 Our findings underline a dual role of the IL-6R stalk region in IL-6 signaling.

257 Downstream of the IL-6R, HDAC inhibition was followed by a decrease in STA

258 set of NK cells expressed both chains of the IL-6R, IL-6 upregulated expression of the Th17-associate

259 via a membrane-bound or soluble form of the IL-6R, respectively.

260 st to the type I transmembrane proteins, the IL-6R, and IL-1RII, CANDIS does not bind the type II tra

261 IL-6R but allows the binding of IL-6 to the IL-6R and the recruitment of gp130, forming a trimer com

262 y on the low-affinity binding of CNTF to the IL-6R.

263 ons and disrupts the binding of Stat3 to the IL-6R/gp130 peptide, GpYLPQTV-NH(2).

264 IL-6 can signal via the IL-6R complex composed of membrane-bound IL-6Ralpha (mIL

265 Here, we investigated the role of these IL-6R components in hypertension and vascular hypertroph

266 We show that acute signaling through IL-6R or CD40 integrates with chronic BCR-mediated ERK a

267 Binding of 25F10 to IL-6R prevented the formation of the hexameric complex o

268 d CV-5, however, lost the ability to bind to IL-6R.

269 n in hIL-6 participates in site I binding to IL-6R.

270 ypothesized that Arg(28) might contribute to IL-6R/CNTFR plasticity of CNTF.

271 he IL-10R has signaling functions similar to IL-6R in cells normally expressing these receptors, leuk

272 that the IL-11R can serve as a substitute to IL-6R in activating gene expression in target cells that

273 t3 mutated at serine 727 and using truncated IL-6Rs suggested that the target of inhibition is contai

274 Using IL-6R-deficient mice and recombinant tools that modulate

275 only CV-3 induced STAT3 phosphorylation via IL-6R.gp130.LIFR.

276 When IL-6R was blocked, LPS-responsive IkappaBepsilon(-/-) B

277 human IL-6 (hIL-6) signal transduction when IL-6R is coexpressed.

278 ly translated to experimental colitis, where IL-6R expression was suppressed in naive T cells, parall

279 s, we did not observe myoferlin binding with IL-6R.

280 t vIL-6, like hIL-6, can form complexes with IL-6R and gp130 but that the roles of putative cytokine-

281 te (HDM) or cockroach at day 0, treated with IL-6R inhibitors at day 13, and challenged with the same

282 the airways is attenuated by treatment with IL-6R inhibitors.