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1 ream of multiple Toll-like receptors and the interleukin-1 receptor.
2 ner dependent on signaling downstream of the interleukin-1 receptor.
3 s the key signaling adapter of Toll-like and interleukin-1 receptors.
5 In the amygdala significant up-regulation of interleukin-1 receptor 1 (IL1r1), interleukin-4 receptor
6 The 28-kDa form of IL-1beta cannot activate interleukin-1 receptor-1 (IL1R1) to signal inflammatory
7 terleukin-6) and alloimmune activation (CD3, interleukin-1 receptor 2, programmed cell death-1, and s
8 rferon-gamma, interleukin-6) and alloimmune (interleukin-1 receptor 2, programmed cell death-1, and s
9 013) describe a molecular system implicating interleukin-1 receptor-2 (IL-1R2) as a principal cytosol
10 to caspase proteolytic activity that cleaves interleukin-1 receptor-2, allowing IL-1alpha dissociatio
11 n assays show that IL-1alpha associates with interleukin-1 receptor-2, and this association is decrea
12 in 1 pathway, through either ablation of the interleukin 1 receptor 8 (IL-1R8, also known as SIGIRR o
14 elated (SIGIRR), which is also known as Toll/interleukin-1 receptor 8 (TIR-8), is a member of the TIR
15 rinsic to B cells and was independent of the interleukin-1 receptor, a cytokine receptor that also si
19 the X-linked intellectual disability protein interleukin-1 receptor accessory protein like 1 (IL1RAPL
20 E) epsilon4 status was identified in IL1RAP (interleukin-1 receptor accessory protein; rs12053868-G;
21 ude myeloid differentiation protein (MyD88), interleukin-1 receptor-activated kinase-1, and TNF recep
23 ndings broaden our understanding of how Toll/interleukin-1 receptor adaptor proteins may participate
25 EGF), basic fibroblast growth factor (bFGF), interleukin-1 receptor alpha (IL-1Ralpha), IL-6, IL-8, V
27 rotein 3) inflammasome signaling through the interleukin-1 receptor and its signaling protein myeloid
28 h rituximab alone, increased serum IL-12 and interleukin 1 receptor antagonist (IL-1RA) (P = .005 and
30 centrations of interleukin 1beta (IL-1beta), interleukin 1 receptor antagonist (IL-1Ra), and granuloc
31 lymorphisms of interleukin 1 beta (IL1B) and interleukin 1 receptor antagonist (IL1RA) genes for asso
32 rogation of the MSC transcriptome identified interleukin 1 receptor antagonist (IL1RN) as a potential
34 d P = .00005 for IMI, by the log-rank test), interleukin 1 receptor antagonist (IL1RN; rs419598; P =
36 nduced protein [IP-10]) and proinflammatory (interleukin 1 receptor antagonist [IL-1RA], IL-6) cytoki
37 sis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating
38 itric oxide synthase, interleukin-1beta, and interleukin 1 receptor antagonist but not transforming g
39 tory factor/glycosylation-inhibiting factor, interleukin 1 receptor antagonist, and serine protease i
42 the impact of an exogenous recombinant human interleukin-1 receptor antagonist (anakinra) in experime
43 multifocal osteomyelitis, deficiency of the interleukin-1 receptor antagonist (DIRA), Majeed syndrom
45 lute partial correlation coefficients >0.40: Interleukin-1 receptor antagonist (IL-1Ra) and IL-8.
46 f the folded and unfolded ensembles of human interleukin-1 receptor antagonist (IL-1ra) are strongly
47 ty of the method was demonstrated with human interleukin-1 receptor antagonist (IL-1ra) as a protein
50 L-1beta and its regulation by the endogenous interleukin-1 receptor antagonist (IL-1ra) in glutamate
52 e investigated whether the anti-inflammatory interleukin-1 receptor antagonist (IL-1Ra) prevents muri
53 itors enhance the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1Ra) secretion in
54 production of the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1RA) that could be
55 and structural behavior of human recombinant interleukin-1 receptor antagonist (IL-1ra) was revealed
58 necrosis factor (TNF) receptor-2 (TNFR2) and interleukin-1 receptor antagonist (IL-1ra) were fused to
61 culating levels of C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra), and soluble
62 so occurred, with GVHD-specific secretion of interleukin-1 receptor antagonist (IL-1Ra), IL-18, and C
65 at a single intracisternal administration of interleukin-1 receptor antagonist (IL-1RA; 112 mug) at t
66 sma levels of neopterin (P<;0.0001), soluble interleukin-1 receptor antagonist (P<;0.0001), IL-8 (P=0
68 nd methionine oxidation in recombinant human interleukin-1 receptor antagonist (rhIL-1ra) was investi
69 interleukin-10 (IL-10), and increased plasma interleukin-1 receptor antagonist (sIL-1ra) and soluble
70 D and confirmed six proteins (leptin, renin, interleukin-1 receptor antagonist [IL-1ra], hepatocyte g
71 etanercept, infliximab, and adalimumab), the interleukin-1 receptor antagonist anakinra, and to a muc
72 that can be blocked by administration of an interleukin-1 receptor antagonist and a specific p38 MAP
74 3), and antiinflammatory markers (increased interleukin-1 receptor antagonist and lower monocyte and
75 py efficacy stemmed from the upregulation of interleukin-1 receptor antagonist and suppression of MDS
77 -alpha), interleukin-6 (IL-6), IL-1beta, and interleukin-1 receptor antagonist but not IL-12 and indu
78 rosis factor-alpha and interleukin-6 and the interleukin-1 receptor antagonist compared with control
80 ntagonist gene overexpression has shown that interleukin-1 receptor antagonist is cardioprotective du
81 l activation by minocycline or by transgenic interleukin-1 receptor antagonist overexpression rescued
82 in plasma interleukin-8, interleukin-10, and interleukin-1 receptor antagonist posttransfusion compar
85 akinra is a recombinant version of the human interleukin-1 receptor antagonist used to treat autoinfl
86 nd 2, C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist were measured in 233 i
87 or necrosis factor-alpha, interleukin-6, and interleukin-1 receptor antagonist), their mRNA expressio
89 associated with augmented concentrations of interleukin-1 receptor antagonist, a key anti-inflammato
90 of TNF-alpha, interleukin-6, interleukin-8, interleukin-1 receptor antagonist, and interleukin-10 in
91 alpha2beta1 integrin polyclonal antibodies, interleukin-1 receptor antagonist, and the chemical inhi
92 interleukin-1 antibody, or anakinra, a human interleukin-1 receptor antagonist, improved beta-cell fu
94 We investigated the effects of anakinra, an interleukin-1 receptor antagonist, on coronary and left
96 ed growth factor receptors, and anakinra, an interleukin-1 receptor antagonist, respectively, increas
103 We hypothesized that administration of IL-1 (interleukin-1) receptor antagonist (anakinra) could inhi
104 ble CIAS1 mutations) to receive anakinra, an interleukin-1-receptor antagonist (1 to 2 mg per kilogra
107 to empirical treatment with the recombinant interleukin-1-receptor antagonist anakinra in the first
109 sed by mutations of IL1RN, which encodes the interleukin-1-receptor antagonist, with prominent involv
110 regulation of 2 inhibitors of TLR signaling: Interleukin 1 Receptor Associated Kinase (IRAK) M, and S
111 gh tyrosine nitration-mediated impairment of interleukin-1 receptor associated kinase (IRAK)4, a sign
112 a series of pyrrolopyrimidine inhibitors of interleukin-1 receptor associated kinase 4 (IRAK4) using
113 s undertaken to test the candidacy of IRAK1 (interleukin-1 receptor associated kinase-1) as an X chro
114 canonical downstream signaling intermediates interleukin 1 receptor-associated kinase (IRAK) and Ikap
116 mammals and overlaps with the 5' UTR of the interleukin 1 receptor-associated kinase (IRAK1) gene.
117 of EGFR and the NF-kappaB regulatory kinase interleukin 1 receptor-associated kinase 1 (IRAK-1).
121 mber 6, and rhophilin 2) and three proteins (interleukin 1 receptor-associated kinase-like 2, glutama
124 pathway involving the MyD88 adapter and the interleukin-1 receptor-associated kinase (IRAK) complex.
126 nes encoding non-RD kinases belonging to the interleukin-1 receptor-associated kinase (IRAK) family.
127 pretreatment in vivo inhibited expression of interleukin-1 receptor-associated kinase (IRAK)-1 while
128 , antisense JNK and dominant negative MyD88, interleukin-1 receptor-associated kinase (IRAK)-1, IRAK4
130 receptor-4 (TLR4) and its signaling molecule interleukin-1 receptor-associated kinase (IRAK-1) play a
131 s study, we examined the contribution of the interleukin-1 receptor-associated kinase 1 (IRAK-1) to L
132 id differentiation primary response (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK-1), and
133 ion with NF-kappaB-inducing kinase (NIK) and interleukin-1 receptor-associated kinase 1 (IRAK-1), deg
136 use of TMP with Bruton's tyrosine kinase or interleukin-1 receptor-associated kinase 1 and 4 inhibit
137 74 x 10(-6)) and a C203S polymorphism in the interleukin-1 receptor-associated kinase 1 gene (IRAK1)
140 ed NFkappaB activation, via interaction with interleukin-1 receptor-associated kinase 2 (IRAK2).
141 B cells isolated from patients deficient for interleukin-1 receptor-associated kinase 4 (IRAK-4), mye
142 onse was reversed in the patient, but not in interleukin-1 receptor-associated kinase 4 (IRAK-4)-defi
144 ying very rare loss-of-function mutations in interleukin-1 receptor-associated kinase 4 (IRAK4), a cr
147 he Toll-like receptor (TLR) pathway, such as interleukin-1 receptor-associated kinase 4 deficiency, h
148 R4-mediated signaling pathway (reduced MyD88-interleukin-1 receptor-associated kinase [IRAK] interact
149 l as GD1a itself inhibited flagellin-induced interleukin-1 receptor-associated kinase activation as w
150 nitude of flagellin signaling as measured by interleukin-1 receptor-associated kinase activation or t
151 Abs induced activation of TLR4 and triggered interleukin-1 receptor-associated kinase phosphorylation
152 main containing adaptor protein)-MyD88-IRAK (interleukin-1 receptor-associated kinase)1/4-TRAF6 (TNF
153 had impaired S aureus-induced activation of interleukin-1 receptor-associated kinase, c-Jun NH2 term
154 o-1 actions were likely to be independent of interleukin-1 receptor-associated kinase-1 (IRAK-1) regu
155 miRNA-146a down-regulates expression of the interleukin-1 receptor-associated kinase-1 (IRAK-1), an
156 h diminished IL-1beta-induced degradation of interleukin-1 receptor-associated kinase-1 (IRAK-1).
157 pression, myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1, and nuclear
159 Within innate immune signaling pathways, interleukin-1 receptor-associated kinases (IRAKs) fulfil
160 its DD and TIR domain and interacts with the interleukin-1 receptor-associated kinases (IRAKs) to for
161 LR-signaling molecules MyD88, IRAK-1 (type I interleukin-1 receptor-associated protein kinase), and T
164 entricular assist device, treatment with the interleukin-1 receptor blocking agent anakinra 100 mg/d
166 ride, suggesting a specific role for TFF2 in interleukin 1 receptor but not Toll-like receptor 4 sign
169 le nucleotide polymorphism A471T in the Toll-interleukin 1 receptor domain (TIR) of the IL-1Rrp2 that
170 ed the hypothesis that polymorphisms in Toll-interleukin 1 receptor domain containing adaptor protein
171 ctivate downstream signaling via TIRAP (Toll-interleukin 1 receptor domain containing adaptor protein
172 ne spanning region and an intracellular Toll/Interleukin 1 receptor domain which invokes signal trans
173 d differentiation factor 88 (MyD88) and toll/interleukin 1 receptor domain-containing adapter inducin
174 d differentiation factor 88 (MyD88) and Toll-interleukin 1 receptor domain-containing adapter inducin
175 8-independent TLR signals by inhibiting Toll/interleukin 1 receptor domain-containing adaptor inducin
176 was myeloid differentiation factor 88-, Toll-interleukin 1 receptor domain-containing adaptor inducin
177 rimary response protein 88 (MyD88), and Toll interleukin 1 receptor domain-containing adaptor protein
178 ndicating that the Toll-6 receptor, the Toll/interleukin-1 receptor domain adaptor dSARM, and FoxO fu
179 -protein ligase that interacts with the Toll/interleukin-1 receptor domain of TLRs and promotes their
180 Pharmacologic and genetic disruption of Toll/interleukin-1 receptor domain-containing adapter inducin
183 d differentiating factor 88 (MyD88) and Toll/interleukin-1 receptor domain-containing adapter-inducin
184 , such as Cardif/MAVS/IPS-1/VISA, TRIF (Toll-interleukin-1 receptor domain-containing adaptor inducin
185 g RNA knockdown of TLR3 or its adaptor, Toll-interleukin-1 receptor domain-containing adaptor inducin
186 cell line Mono Mac 6, induction of the Toll-interleukin-1 receptor domain-containing adaptor-inducin
187 duced autophagy was regulated through a Toll-interleukin-1 receptor domain-containing adaptor-inducin
188 production of ETs by S cells requires a Toll/Interleukin-1 receptor domain-containing protein TirA an
190 ring RNA, and macrophages isolated from Toll/interleukin-1 receptor-domain-containing adaptor inducin
191 e deficient in the TLR adaptor proteins Toll/interleukin-1 receptor-domain-containing adaptor protein
192 r the SAM (sterile alpha motif) or TIR (Toll-interleukin-1 receptor) domains abolishes the ability of
193 the patient-specific characteristics of the interleukin-1 receptor family member ST2 in patients wit
194 s to examine the value of measurement of the interleukin-1 receptor family member ST2 in patients wit
196 Four biomarkers, soluble form of ST2 (an interleukin-1 receptor family member), galectin-3, matri
199 chemoattractant protein-1, resistin, soluble interleukin-1 receptor I, soluble interleukin-2 receptor
201 activation is mediated through TRAF6 in the interleukin 1 receptor (IL-1R) and toll-like receptor (T
202 h their role in Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) mediated signaling pathwa
203 LLIP) regulates Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) signaling against mycobac
204 rotein is critical in Toll-like receptor and interleukin 1 receptor (IL-1R) signaling, but has not be
205 ive influenza A virus, signaling through the interleukin 1 receptor (IL-1R) was required for producti
206 DA-5), as well as cytokine receptors such as interleukin 1 receptor (IL-1R), have been implicated in
208 ated innate signaling pathway, as well as in interleukin-1 receptor (IL-1R) and IL-18R signaling.
210 d was first characterized as an inhibitor of interleukin-1 receptor (IL-1R) and Toll-like receptor (T
212 members of the Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signal
213 ta (IkappaBzeta), a Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) inducible transcription f
214 ), a negative regulator of the Toll-like and interleukin-1 receptor (IL-1R) signaling pathways, contr
216 e expression of the Toll-like receptor (TLR)/interleukin-1 receptor (IL-1R) superfamily, IL-1beta pro
218 ting microglia expressed high amounts of the interleukin-1 receptor (IL-1R), and treatment with an IL
219 a signaling adaptor shared by most TLRs and interleukin-1 receptor (IL-1R), in an in vitro model of
220 c expression of toll-like receptor 4 (TLR4), interleukin-1 receptor (IL-1R), or interferon-gamma rece
224 fied nearly two decades ago as a mediator of interleukin-1 receptor (IL-1R)-mediated activation of NF
225 ponses are controlled through members of the interleukin-1 receptor (IL-1R)/Toll-like receptor superf
228 in that links toll-like receptors (TLRs) and Interleukin-1 receptors (IL-1Rs) with downstream signali
230 D88(-/-), MyD88/TLR adaptor molecule 1(-/-), interleukin-1 receptor [IL-1R1](-/-), and interleukin (I
232 -/-)), caspase-1 knockout (Casp-1(-/-)), and interleukin-1 receptor knockout (IL-1R(-/-)) mice treate
234 ivates many immune cell types expressing the interleukin 1 receptor-like 1 (IL1RL1) receptor ST2, inc
236 dipocyte differentiation, whereas Got2, Cpq, interleukin-1 receptor-like 1/ST2-IL-33, Sparc, and Lgal
238 because deletion of Nlrp3, caspase-1 and the interleukin-1 receptor markedly protects against rheumat
239 uide cleavage of transcripts of the Toll and Interleukin-1 receptor-NB-LRR immune receptor N from tob
240 r-triggered immunity conditioned by the Toll Interleukin-1 Receptor-nucleotide binding (NB)-Leu-rich
241 gered immunity specifically mediated by Toll-interleukin-1 receptor-nucleotide binding-leucine-rich r
243 all genes predicted to contain either a Toll/interleukin-1 receptor or nucleotide-binding site domain
245 rphan receptor SIGIRR (single immunoglobulin interleukin-1 receptor-related protein) acts as a negati
248 mmune responses that was independent of Toll-Interleukin 1 Receptor signaling and directed toward det
250 mon adaptor for toll-like receptor (TLR) and Interleukin-1 receptor signaling, are critical for radio
254 ignaling by the toll-like receptor (TLR) and interleukin-1 receptor superfamily requires the adapter
255 ch signal through adaptors containing a Toll-interleukin 1 receptor (TIR) domain, such as MyD88 and T
257 n primary response gene 88 (MyD88)- and Toll-interleukin 1 receptor (TIR) domain-containing adaptor i
259 SENSITIVE 3 (CHS3) encodes an atypical Toll/Interleukin 1 Receptor (TIR)-type NLR protein with an ad
261 abase for proteins with homology to the Toll/interleukin-1 receptor (TIR) domain of the mammalian Tol
265 rly Leu265Pro (L265P), within the MyD88 Toll/interleukin-1 receptor (TIR) domain sustain lymphoma cel
266 e-rich repeat (NLR) protein with a Toll-like interleukin-1 receptor (TIR) domain, which mediates XopQ
268 lipopolysaccharide, this is a delayed, Toll/interleukin-1 receptor (TIR) domain-containing adapter-i
269 esponses by targeted degradation of the Toll/interleukin-1 receptor (TIR) domain-containing adaptor p
270 ckouts including TLR2, TLR4, MyD88, and Toll-interleukin-1 receptor (TIR) domain-containing adaptor p
275 ults in dimerization of their cytosolic Toll/interleukin-1 receptor (TIR) domains and recruitment of
276 Toll-like receptors (TLRs), cytoplasmic Toll/interleukin-1 receptor (TIR) domains of the receptors un
277 The heterotypic interaction between the Toll/interleukin-1 receptor (TIR) domains of TLRs and adaptor
278 aling adapter protein interactions with Toll/Interleukin-1 Receptor (TIR) domains present in sensory
279 effectors through adaptors that contain Toll/interleukin-1 receptor (TIR) domains, but the mechanisms
282 illo motif (SARM) is a highly conserved Toll/interleukin-1 receptor (TIR)-containing adaptor protein
283 structures of MAL revealed a nontypical Toll/interleukin-1 receptor (TIR)-domain fold stabilized by t
284 equires the P loops of each protein and Toll/interleukin-1 receptor (TIR)-domain-mediated heteromeric
287 lays an essential role in Toll-like receptor/interleukin-1 receptor (TLR/IL-1R) -associated NF-kappaB
288 can activate signaling by the Toll-like and interleukin-1 receptors (TLR and IL-1R) to mediate patho
289 signalling (tumour necrosis factor receptor/interleukin-1 receptor, TNFR/IL-1R in mammals) is indisp
290 ch are adaptor molecules that couple TNF and interleukin-1 receptor/Toll-like receptor family members
291 mediating signals from both TNF receptor and interleukin-1 receptor/Toll-like receptor superfamilies.
292 am of many receptors in the TNF receptor and interleukin-1 receptor/Toll-like receptor superfamilies.
293 he negative regulation of Toll-like receptor/interleukin-1 receptor-triggered inflammatory cascades a
294 was developed to analyze recombinant soluble Interleukin 1 receptor type II (sIL-1R type II) drug sub
295 d the role of toll-like receptors (TLRs) and interleukin-1 receptor type 1 (IL-1R1) in S. marcescens-
296 nization, we show that mice deficient in the interleukin-1 receptor type 1 (Il1r1(-/-)) have reduced
297 y protein (IL1RAP; IL1R3) is a coreceptor of interleukin-1 receptor type 1 and has been found upregul
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