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1 f the nonsignaling gp80 alpha-subunit of the IL-6 receptor.
2 only when it was in complex with the soluble IL-6 receptor.
3 gp130, the signal-transducing subunit of the IL-6 receptor.
4 ndothelial cells through a newly constituted IL-6 receptor.
5 on in hepatic cells is equivalent to that of IL-6 receptor.
6 ression of the plasma membrane high-affinity IL-6 receptor.
7 e formation of complexes of IL-6 and soluble IL-6 receptor.
8 pression of CD27, and high levels of IgM and IL-6 receptor.
9 ulation and IL-6-induced endocystosis of the IL-6 receptor.
10 increase in the expression of high-affinity IL-6 receptors.
11 ilizumab directed against the interleukin 6 (IL-6) receptor.
14 veral factors, including interleukin (IL)-1, IL-6, receptor activator of NF-kappaB (RANK) ligand, par
15 demonstration of increased expression of the IL-6 receptor after loss of sex steroids provides an exp
16 the non-signaling membrane-bound or soluble IL-6 receptor alpha (IL-6R, sIL-6R), which is referred t
17 ted mice with deletion of the membrane bound IL-6 receptor alpha (IL-6Ralpha) on neural cells, on per
19 nstrate that T cell-specific deletion of the IL-6 receptor alpha chain (IL-6Ralpha) results in impair
20 ignal transducer but is not dependent on the IL-6 receptor alpha subunit (IL-6R, gp80) that is requir
21 reduction in the amount of mRNA encoding the IL-6 receptor alpha subunit and IL-6 binding activity.
22 requirement for transcription is the soluble IL-6 receptor alpha, which translocates to endothelial c
24 n lower expression of the genes encoding the IL-6 receptor alpha-chain (Il6ra) and the IL-6 signal tr
25 nor O-linked glycosylation is necessary for IL-6 receptor alpha-dependent binding to gp130 or signal
26 ot an agonist for this, but we found soluble IL-6 receptor alpha-subunit (IL-6Ralpha), with their con
27 Diminished hepatitis in IL-6-deficient, anti-IL-6 receptor alpha-treated, ovariectomized, or male mic
28 nstruct a model of IL-6 interacting with the IL-6 receptor (alpha-chain) and gp130 (beta-chain) that
30 romal cells acted cooperatively with soluble IL-6 receptor-alpha and thermally induced gp130 to promo
31 r both lymphoid and myeloid fates, expressed IL-6 receptor-alpha chain and responded to IL-6 by phosp
32 scular adhesion were induced by IL-6/soluble IL-6 receptor-alpha fusion protein in mouse tumors and p
33 g pathway, including increased expression of IL-6 receptor-alpha/gp80, activation of the signal trans
34 edly induced mIndy transcription through the IL-6 receptor and activation of the transcription factor
35 F in the peritoneum, do not bear the cognate IL-6 receptor and are thus unable to respond to classic
36 ean winter, with increased levels of soluble IL-6 receptor and C-reactive protein, risk biomarkers fo
37 ction of IL-6 with concomitant expression of IL-6 receptor and gp130 suggest that these factors may p
38 could be rescued by the addition of soluble IL-6 receptor and IL-6 or by retroviral transduction of
39 toplasmic domain of the gp130 subunit of the IL-6 receptor and is different from the SH2 domain-conta
40 omatin, but did not affect the expression of IL-6 receptor and phosphorylation of JAK/STAT3, MAPK, an
41 lassic signaling using the membrane-anchored IL-6 receptor and trans-signaling using its soluble form
42 Here we demonstrate loss of interleukin 6 (IL-6) receptor and IL-6-responsive colony-forming units
43 blotting; however, lower production of both IL-6-receptor and Stat3 explains, in part, reduced activ
46 s of the gp130 subunit of the interleukin-6 (IL-6) receptor, and a seven amino acid STAT1 recruitment
50 specific antibodies, IL-12/23 antibodies, an IL-6 receptor antagonist, a sphingosine-1-phosphate agon
51 rmeabilized osteoclasts incubated with anti- IL-6 receptor antibodies revealed intense, strictly peri
52 d this toxicity was strongly inhibited by an IL-6 receptor antibody (tocilizumab) and less well by TN
53 is study did not reveal any evidence that an IL-6 receptor antibody affects behavioral outcomes in sc
54 Inhibition of IL-6 signaling with the anti-IL-6 receptor antibody tocilizumab has provided some cli
55 purpose of this trial was to test whether an IL-6 receptor antibody, tocilizumab, would improve resid
56 immunosuppression using tocilizumab, an anti-IL-6 receptor antibody, with or without corticosteroids,
57 nt humanized monoclonal antibody against the IL-6 receptor approved for treatment of rheumatoid arthr
58 monoclonal antibodies targeting IL-6 and the IL-6 receptor are also being studied for the management
59 , an anti-inflammatory cytokine, and soluble IL-6 receptor are associated with systemic juvenile rheu
63 RI), IL-1RII, TNF receptor II (TNFR II), and IL-6 receptor as well as the level of proinflammatory cy
65 was associated with a 2-4-fold reduction of IL-6 receptor at protein and mRNA levels in SGN-40-treat
67 e and immunoabsorption as well as subsequent IL-6 receptor blockade through tocilizumab, a complete a
68 sults from the recent clinical studies using IL-6 receptor blockade, and describe potential mechanism
71 but failed to affect the mRNA expression of IL-6 receptor chains or activation of JAK2 and STAT3.
72 Furthermore, cholangiocytes possessed the IL-6 receptor complex subunits and intact signaling mech
76 ies against IL-6 or the gp130 subunit of the IL-6 receptor did not attenuate ET-1-induced collagen ac
85 tentiation is likely due to the induction of IL-6-receptor expression as well as prolonged intensity
86 (vIL-6), which does not require the cellular IL-6 receptor for binding to the ubiquitously expressed
88 ion results in the induction of the IL-6 and IL-6 receptor genes and neutralizing antibodies directed
89 RNA of the signal-transducing subunit of the IL-6 receptor (gp130) in cells of the bone marrow stroma
90 ted by the signal-transducing subunit of the IL-6 receptor, gp130, or by co-transfected IL-3 receptor
92 data suggest tissue-specific differences in IL-6-receptor-gp130-coupled signaling, thereby limiting
94 Stem-like and progenitor cells expressed the IL-6 receptor gp80 with concomitant expression of pSTAT3
95 dence that the ligand-binding subunit of the IL-6 receptor (gp80) is a limiting factor for the action
98 s have been observed in association with the IL-6 receptor; however, inhibition of Src kinases by Csk
102 liminary results have been obtained with the IL-6 receptor (IL-6R) antagonist tocilizumab for the tre
103 L-6 can mediate proinflammatory effects, and IL-6 receptor (IL-6R) blockade as a treatment for inflam
104 The current study evaluated the effect of IL-6 receptor (IL-6R) blockade with an antiYIL-6R monocl
105 ly competes for binding to the cytokine with IL-6 receptor (IL-6R) by using side chains of two CDR re
106 FN-alpha growth-inhibited cell lines reduced IL-6 receptor (IL-6R) expression, IFN-alpha also reduced
108 d by membrane-bound and soluble forms of the IL-6 receptor (IL-6R) in processes called classic and tr
109 by way of antibody-mediated blockade of the IL-6 receptor (IL-6R) markedly reduces pathologic damage
110 ession in the normal liver, but both met and IL-6 receptor (IL-6R) mRNA are detectable; met mRNA is e
113 efined, nor has the behavior of the specific IL-6 receptor (IL-6R) or the signal transducer gp130.
114 a receptor complex consisting of the cognate IL-6 receptor (IL-6R) or the soluble IL-6 receptor (sIL-
117 wth factor (IGF)/IGF-1 receptor (IGF-1R) and IL-6 receptor (IL-6R) signaling cascades, antiapoptotic
118 : classical signaling via its membrane-bound IL-6 receptor (IL-6R), and trans-signaling via a natural
119 e clinical usage of monoclonal antibodies to IL-6 receptor (IL-6R), designed to block IL-6 pathways.
120 would interact with the specific alpha-chain IL-6 receptor (IL-6R), is accessible and not occupied by
123 pilot study of DES using a novel drug (anti-IL-6 receptor (IL-6R),Tocilizumab [TCZ]) + intravenous I
124 tocytes also do not show activation of other IL-6 receptor (IL-6R)-mediated Janus kinase substrates,
125 xamer, formed by the association of two IL-6.IL-6 receptor (IL-6R).gp130 trimers, with gp130 being th
126 nction in 2 ways: by directly binding to the IL-6 receptor (IL-6R; CD126) or via trans-signaling, in
127 is not dependent on the structurally related IL-6 receptor (IL-6R; gp80) subunit of the receptor-sign
128 hybridoma cell line, B9, and that the gp80 (IL-6 receptor [IL-6R]) component of the IL-6 receptor-si
130 a role in cytokine signaling, including the IL-6 receptor, IL-1 receptor type I, and IL-1 receptor t
131 an ability of interferon-alpha and a soluble IL-6 receptor/IL-6 (sIL-6R alpha/IL-6) trans-signaling c
132 elated common variants in the interleukin-6 (Il-6) receptor (IL6R) gene to plasma C-reactive protein
133 We demonstrate a higher ratio of SOCS3 to IL-6 receptor in adult monocytes than in fetal monocytes
135 ially due to increased expression of soluble IL-6 receptor in the brain relative to the spinal cord t
136 Neutralizing autocrine IL-6 and/or blocking IL-6 receptors in IL-6(+)/gp80(+) MCL cells inhibited ce
137 ther oncostatin M (OSM) or IL-6 plus soluble IL-6 receptor increased the levels of p21 mRNA and prote
138 found that these cells synthesized IL-6 and IL-6 receptors; interruption of this pathway by IL-6 ant
142 lobal IL-1 receptor gene knockout or central IL-6 receptor knockdown showed attenuated decrease in fo
143 ncrease: 2.3, 1.4-3.8, P = .001) and soluble IL-6 receptor level was associated within 6 years after
144 ptin binding and responded to leptin with an IL-6 receptor-like signaling that includes the activatio
145 these studies suggest that blocking IL-1 or IL-6 receptors may improve the regenerative capacity of
149 se transcriptase-PCR analysis indicated that IL-6 receptor mRNA was present in all carcinoma cell lin
150 6 showed a significant reduction in IL-6 and IL-6 receptor mRNA, together with significant decreases
151 sed to study the effects of dexamethasone on IL-6 receptor number in the well-differentiated human he
153 Activated T cells expressed lower levels of IL-6 receptors on their surfaces, yet there were suffici
154 clast formation stimulated by IL-6 + soluble IL-6 receptor, oncostatin M, or IL-1 but not by parathyr
158 y receptor-mediated (i.e., TNFalpha, NGF, or IL-6 receptor) or direct activation of protein kinase Ce
159 ceptor IL-6R (sIL-6R); by an antibody to the IL-6 receptor; or by minocycline, which inhibits the mic
161 DL1-mediated reduction in membrane (m)-bound IL-6 receptor (R) expression, converting progenitor cell
162 hich blocks leukocyte TNF, TNF receptor, and IL-6 receptor release, also inhibits L-selectin shedding
163 dependently of the gp80 alpha-subunit of the IL-6 receptor, required for hIL-6 signal transduction.
166 aft proteins caveolin-1 and flotillin-1, the IL-6-receptor signal transducing chain gp130, the interf
167 p80 (IL-6 receptor [IL-6R]) component of the IL-6 receptor-signal transducer (gp180) complex plays a
168 al protein S6 kinase, respectively) and IL-6/IL-6 receptor signaling (i.e., IL-6 production and signa
172 dentify TRAF5 as a negative regulator of the IL-6 receptor signaling pathway that limits the inductio
176 o investigate the role of the interleukin 6 (IL-6) receptor signaling in the pathogenesis of MCD and
178 though treatment with either IL-6 or soluble IL-6 receptor (sIL-6R) alone had no effect on VEGF produ
179 cognate IL-6 receptor (IL-6R) or the soluble IL-6 receptor (sIL-6R) and glycoprotein 130 (gp130).
181 tagonist of the interleukin-6 (IL-6)/soluble IL-6 receptor (sIL-6R) complex and selectively inhibits
184 s to evaluate the effect of IL-6 and soluble IL-6 receptor (sIL-6R) on hematopoietic and skeletal act
186 al fibroblasts treated with IL-6 and soluble IL-6 receptor (sIL-6R) was used to probe a cytokine micr
187 hanced through transsignaling by the soluble IL-6 receptor (sIL-6r), allowing for the pleiotropic cyt
188 liver enzymes, interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and soluble tumor necrosis facto
189 d respond to IL-6 in the presence of soluble IL-6 receptor (sIL-6R), but the cell surface expression
190 Expression of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), IL-10, and IL-13 was detected by
191 production of interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), IL-10, and tumor necrosis factor
196 dium of cytokine (TNF-alpha and IL-6/soluble IL-6 receptor)-stimulated human cartilage explants.
197 athecal treatment with antisense directed to IL-6 receptor subunit gp130 (gp130), but not to tumor ne
198 with colitis was increased 80-fold, and the IL-6 receptor subunits IL-6R alpha and gp130 were presen
199 Moreover, addition of soluble interleukin-6 (IL-6) receptor to the medium endowed IL-6 with the abili
201 pression of IL-6 in combination with soluble IL-6 receptor was a reliable predictor of ALI in SAP.
203 SHV-positive plasmablasts, whereas the human IL-6 receptor was expressed in most KSHV-positive cells.
205 s phosphorylated after IL-6 binding to gp80 (IL-6 receptor), we hypothesized that gp130 could be invo
206 1 and 2), as well as interleukin (IL)-6 and IL-6 receptor were measured on a daily, weekly and month
208 well as signaled by increased pSTAT3 via the IL-6 receptor, which inhibits IRS 1/2 phosphorylation.
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