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1 A(3) is about equipotent to TxA(2) at the TP alpha receptor.
2 ownstream to the tumor necrosis factor (TNF) alpha receptor.
3 r trimerization of the tumor necrosis factor alpha receptor.
4 recruitment and activation by the human IFN-alpha receptor.
5 vation of the platelet-derived growth factor-alpha receptor.
6 quirement for pre-complexation to a specific alpha-receptor.
7 s is a consequence of the activation of PPAR-alpha receptors.
8 ically act on 5-HT3, cholecystokinin, or TNF-alpha receptors.
9 gnaling from the IL-12/IL-23, IL-22, and IFN-alpha receptors.
10 CD47 to macrophage signal regulatory protein alpha receptors.
11 eak inducer of apoptosis (TWEAK) but not TNF-alpha receptors.
12 -agonist that has full efficacy at all brain alpha-receptors.
13 on, we introduced a deficiency of interferon alpha receptor 1 (Ifnar1) into B6.Aec1Aec2 mice, which a
15 = 0.009), and soluble tumor necrosis factor alpha receptor 1 (P = 0.007) than did no weight-loss tre
16 uble A8 indicated specific cleavage of a TNF-alpha receptor 1 (p55 TNF-R1) but not a TNF-R2 peptide.
19 alizing antibodies against TNF-alpha and TNF-alpha receptor 1 (TNF-R1), suggesting that TNF-alpha pla
21 ransgenic AD mice (3xTg-AD) lacking both TNF-alpha receptor 1 (TNF-RI) and 2 (TNF-RII), 3xTg-ADxTNF-R
23 pared with the well-characterized type 1 IFN-alpha receptor 1 and 2 in mediating innate immune and au
25 ng cancer by enhancing tumor necrosis factor-alpha receptor 1 and nuclear factor-kappaB activation an
27 or necrosis factor alpha (TNF-alpha) and TNF-alpha receptor 1 block rSV5DeltaSH-induced apoptosis, su
28 Changes in soluble tumor necrosis factor alpha receptor 1 but not in C-reactive protein or interl
29 sTNF-alpha) promotes the shedding of the TNF-alpha receptor 1 ectodomain via increased mitochondrial
32 ing monoclonal antibody directed against TNF-alpha receptor 1 inhibited FHA-associated apoptosis by 4
33 een baseline VCAM-1 or tumor necrosis factor alpha receptor 1 levels and risk of any of the DR end po
34 is essential for tumor necrosis factor (TNF) alpha receptor 1 regulation of intestinal epithelial cel
36 nsaminase, and soluble tumor necrosis factor alpha receptor 1 were lower after treatment with UDCA th
37 osomal degradation of the IFNAR1 (interferon alpha receptor 1) subunit of the type I interferon (IFN)
39 tibodies to Fas, tumor necrosis factor (TNF)-alpha receptor 1, or TNF-related apoptosis-inducing liga
40 eria toxin receptor (DTR) transgenic and IFN-alpha receptor 1-deficient mice, as well as purified pri
43 control livers, expression of IFN-beta, IFN-alpha receptor 1/2, Jak1, and Tyk2 remained unchanged in
44 centrations of soluble tumor necrosis factor alpha receptors 1 and 2 (sTNF-R1, sTNF-R2), interleukin
45 Activated tumor necrosis factor alpha (TNF-alpha) receptor 1 (TNFR1) recruits TNFR1-associated deat
46 ctivator of tumor necrosis factor alpha (TNF-alpha) receptor 1 (TNFR1) signaling, inducing both chemo
48 asma levels of soluble tumor necrosis factor-alpha receptor-1 (sTNFR-1) and brain natriuretic peptide
49 tumor necrosis factor-alpha (TNF-alpha), TNF-alpha receptor-1 (TNF-alphaR1), TNF-alphaR2, and interle
50 comitantly, the proinflammatory receptor TNF-alpha receptor-1 (TNFR1) was shed from the endothelial s
52 electively down-regulated the functional IFN-alpha receptor-1 chain of type I, but not type II (IFN-g
53 of tumor necrosis factor (TNF)-alpha and TNF-alpha receptor-1 in the retina of normal and glaucomatou
55 glial cells, whereas immunostaining for TNF-alpha receptor-1 was mainly positive in the retinal gang
56 Both protein and mRNA of TNF-alpha or TNF-alpha receptor-1 were predominantly localized to the inn
57 howed that mRNA signals for TNF-alpha or TNF-alpha receptor-1 were similarly more intense in glaucoma
58 ession and localization of TNF-alpha and TNF-alpha receptor-1 were studied in retina sections from 20
59 eutralizing Ab or to an inhibitor of the TNF-alpha receptor-1, increases proliferative potential, del
60 tile, 2.18; P = .005), tumor necrosis factor-alpha receptor 2 (odds ratio, 1.78; P = .04), and interl
61 ukin 6 (IL-6), soluble tumor necrosis factor alpha receptor 2 (sTNF-R2), E-selectin, soluble intercel
63 seline levels of tumor necrosis factor (TNF)-alpha receptor 2, interleukin (IL)-6, and C-reactive pro
64 ty C-reactive protein, tumor necrosis factor-alpha receptor 2, interleukin-6, and soluble vascular ce
65 ty C-reactive protein, tumor necrosis factor-alpha receptor 2, interleukin-6, and white blood cell co
66 P), interleukin 6, and tumor necrosis factor alpha receptor 2-and risk of invasive epithelial ovarian
67 tation of the RACK-1 binding site in the IFN-alpha receptor 2/beta subunit of the type I IFN receptor
68 a multiprotein complex that includes the IFN-alpha receptor 2/beta-chain of the receptor, STAT1, Janu
69 ers, including soluble tumor necrosis factor-alpha receptor-2 (P<0.001), interleukin-6 (P=0.04), and
70 type peroxisome proliferator-activated (PPAR-alpha) receptors; (2) shifted nicotine self-administrati
73 gh affinity interaction between IL-2 and its alpha receptor, a moderately entropically favorable low
74 TNFR2-/- epidermis, suggesting that the TNF-alpha receptors act independently via different AP-1 com
75 predict that when EGFR is activated with TGF-alpha, receptor activation is biased toward the cell sur
76 ll-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand,
77 .v. treatment prevented the elevation of TNF-alpha, receptor activator of NF-kappaB, and other inflam
78 autoubiquitination of tumor necrosis factor (alpha) receptor adaptor protein 6 (TRAF6), a protein inv
79 dy, the authors hypothesized that either the alpha-receptor agonist phenylephrine or the nitric oxide
80 o generate point mutations in the human PDGF alpha receptor (alphaPDGFR) cDNA, which resulted in sing
81 at the platelet-derived growth factor (PDGF)-alpha receptor (alphaPDGFR) is required for experimental
82 ndicated that platelet-derived growth factor alpha receptor (alphaPDGFR) plays an important role in a
84 e binds to the same site that binds the IL-2 alpha receptor and buries into a groove not seen in the
85 volved the recruitment of PKCbeta to the IFN-alpha receptor and interaction with protein tyrosine pho
86 ed IFN-alpha receptor expression, though IFN-alpha receptor and NKP30 expression was closely associat
87 his report we show, using mice lacking PGF(2)alpha receptor and pregnant rats, that PGF(2)alpha is re
88 ated following stimulation of the interferon-alpha receptor and the TCR in T cells by two different e
90 erleukins, leptin, and tumor necrosis factor-alpha receptors and their downstream molecular adaptors
91 ions of haematopoietic cells on MSCs via TNF-alpha receptors and then activating NF-kappaB signaling
92 ng antibodies, soluble tumor necrosis factor-alpha receptors, and hemin by abolishing both sEng and s
93 lated in response to LPS challenge in an IFN-alpha receptor- and IFN regulatory factor (Irf)9-depende
94 aracterizing pharmaceutical agents including alpha receptor antagonists as medical expulsive agents.
96 ressin antagonists and tumor necrosis factor-alpha receptor antibody are in phase II and III clinical
97 CV replicon expression, whereas the anti-IFN-alpha receptor antibody could partially block IRF-7-medi
98 e blockade of IFN-alpha receptor by anti-IFN-alpha receptor antibody on the replicon cells increased
100 deficiency of NO synthesis and (2) both TNF-alpha receptors are necessary for TNF-alpha's prothrombo
102 s work identifies PDGF signaling through the alpha receptor as an important event downstream of Sry i
103 ghts the role of Netrin-1 and a specific TNF-alpha receptor as candidate targets to prevent or treat
104 e p55 (p55 TNFR-/-) or p75 (p75 TNFR-/-) TNF-alpha receptors as donors in well-defined bone marrow tr
105 wn to act both as a ligand by binding to TNF-alpha receptors, as well as a receptor that transmits ou
106 he abundance of tyrosine-phosphorylated PDGF alpha receptors; as a result, STAT5 does not become acti
107 nt-negative mutants of tumor necrosis factor-alpha receptor-associated factor (TRAF) 6, TRAF2, and NF
108 tion-dependent manner: tumor necrosis factor-alpha receptor-associated factor 2 (TRAF2) and C-termina
112 or the MyD88-dependent ubiquitination of TNF-alpha receptor-associated factor 6; activation of TGF-be
114 tors, including beta-alpha-gamma/delta-alpha-alpha receptors at lower levels of gamma2/delta expressi
115 otein kinase A with KT5720, but not with the alpha receptor blockers prazosin (alpha1) and/or yohimbi
117 Inhibition of the stromal cell-derived 1 alpha receptor (C-X-C receptor type 4 or CXCR4) using AM
125 have found that TAK1 is recruited to the TNF-alpha receptor complex in a RIP-dependent manner followi
126 as the forced recruitment of NEMO to the TNF-alpha receptor complex is insufficient for TNF-alpha-ind
127 can activate STAT4 by recruitment to the IFN-alpha receptor complex specifically via the carboxy-term
128 is to specifically recruit MEKK3 to the TNF-alpha receptor complex, whereas the forced recruitment o
130 NF-alpha monoclonal antibody (MAb) and a TNF-alpha receptor construct (p75-Fc) were compared with tha
131 ody to platelet-derived growth factor (PDGF) alpha receptors coprecipitated STAT5 from extracts of un
132 d to interact with the tumor necrosis factor alpha receptor [corrected].We have identified a locus co
133 es, opioid-mediated down-regulation of MIP-1 alpha receptors could be blocked by the general PKC inhi
134 ly affect FE, nor does FE depend on Fas, TNF-alpha receptor, cytotoxic T-lymphocyte antigen-4, IL-2,
141 ed progesterone, glucocorticoid, or estrogen alpha receptors did not translocate FLAG-beta-catenin to
143 erved in mice also lacking both types of TNF-alpha receptors, excluding excess TNF-alpha production a
144 cells lacking the p55 (but not the p75) TNF-alpha receptor exhibited decreased proliferation and pro
147 pendency of DCs and Ly6C(+) monocytes on IFN-alpha receptor expression for EmGFP/IL-15 upregulation a
148 efect was not attributable to diminished IFN-alpha receptor expression, though IFN-alpha receptor and
151 the effects of etanercept, a soluble p75 TNF alpha receptor-Fc fusion protein, in 2 patients with HID
152 r a soluble tumor necrosis factor alpha (TNF-alpha) receptor/Fc construct (TNFR-Fc, etanercept).
153 ls that express the NG2 proteoglycan and the alpha receptor for PDGF (NG2 cells, polydendrocytes) mak
154 such as the use of a nonstandard sushi-type alpha receptors for IL-2 and IL-15 in assembling quatern
155 tingly, prostate cancer cells expressing the alpha-receptor for platelet-derived growth factor (PDGFR
156 t, and that these events are mediated by the alpha-receptor for platelet-derived growth factor (PDGFR
158 llebrand factor nor platelet glycoprotein Ib-alpha receptor (GPIb-alpha) is required for RBCs to adhe
159 inflammation (soluble tumor necrosis factor alpha receptor I [sTNF-RI], interleukin 6 [IL-6], and hi
161 interleukin (IL)-8 and tumor necrosis factor-alpha receptor I, were significantly elevated in the cas
162 or-necrosis factor (TNF)-alpha; soluble TNF- alpha receptor I; and C-reactive protein (CRP) were meas
163 sis factor alpha (TNF-alpha) and soluble TNF-alpha receptors I and II; interleukin 1 beta (IL-1 beta)
164 ds to 2 distinct cell-surface receptors: TNF-alpha receptor-I (TNFR-I: p55) and TNF-alpha receptor-II
165 cytes deficient in the interferon-alpha (IFN-alpha) receptor IFN-alphaR showed reduced expression of
166 (NK) cells from mice lacking the type I IFN-alpha receptor (Ifnar(-/-)) or STAT1 (which signals down
167 er, in both CD4 competent, wild-type and IFN-alpha receptor (IFNAR) KO mice, Pneumocystis infection l
169 ties through an evolutionarily conserved IFN-alpha receptor (IFNAR), consisting of IFNAR1 and IFNAR2.
173 tion factor signaling through the interferon-alpha receptor (Ifnar1), resulting in the antigen-indepe
174 n (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular
175 d decreased HLA-DR and Tumor necrosis factor-alpha receptor II (CD120b) expression compared with cont
176 s included solubilized tumor necrosis factor-alpha receptor II (sTNF-alphaRII), vascular cell adhesio
177 erleukin-6 (IL-6), and tumor necrosis factor-alpha receptor II (TNF-alpha RII) in the atorvastatin gr
179 10 [IL-10]), placental (TNF-alpha, IL-6, TNF-alpha receptor II [RII], and IL-1beta), and cord (IL-1be
181 C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellul
182 n the AHEI and soluble tumor necrosis factor-alpha receptor II, interleukin-6, soluble intercellular
183 rotein, interleukin-6, tumor necrosis factor-alpha receptor II, pro-brain natriuretic peptide (pro-BN
184 V and caspase 8, and >80% expressed the TNF-alpha receptor II, while Fas, TNFR-I, and CD27 expressio
185 e precursor, as well as sequestration of TNF-alpha receptors II and I, is performed by the zinc-depen
187 of the unliganded form of the interleukin-7 alpha receptor (IL-7Ralpha) extracellular domain (ECD) a
188 ct via the non-signaling membrane-bound IL-6 alpha-receptor (IL-6R) as an agonistic cytokine but also
189 lex, the viral cytokine can engage the human alpha-receptor (IL-6Ralpha) to form a hexameric vIL-6/IL
190 ignaling assembly composed of IL-6, the IL-6 alpha-receptor (IL-6Ralpha), and the shared signaling re
191 ical studies of interleukin-7 (IL-7) and its alpha-receptor (IL-7Ralpha) and comparisons with other g
192 raction between interleukin-7 (IL-7) and its alpha-receptor, IL-7Ralpha, plays fundamental roles in t
193 ransduction pathways generating from the TNF-alpha receptor in cardiomyocytes and leading preferentia
195 To evaluate the role played by each TNF-alpha receptor in the pathogenesis of this syndrome, mic
196 ions, estradiol up-regulates the level of ER-alpha receptors in keratinocytes and induces keratinocyt
198 ion to canonical beta-alpha-gamma/delta-beta-alpha receptors, including beta-alpha-gamma/delta-alpha-
199 rotective, whereas signaling through the TNF-alpha receptor increases the severity of 1918 virus infe
201 jected into lean mice lacking individual TNF-alpha receptors indicated that TNF-alpha autoamplificati
202 exercise with microspheres before and after alpha-receptor inhibition (phentolamine) and then NPY Y1
204 pathways, such as hypoxia-inducing factor-1-alpha, receptor-interacting protein 1, and apoptosis-ind
205 ibitory effects of roscovitine on STAT5/PDGF alpha receptor interaction, STAT5 activity, and cell sur
206 necrosis factor-alpha, tumor necrosis factor-alpha receptor, interleukin-6 receptor, or L-selectin.
207 licit a calcium flux, failed to induce MIP-1 alpha receptors internalization, and mediated a less pot
208 examined the paradoxical hypothesis that the alpha-receptor inverse agonist doxazosin might produce b
209 e studies thus provide insights into the TNF-alpha receptors involved in mediating and modulating the
216 uggest that inhibition of the T cell p55 TNF-alpha receptor may provide an additional useful therapeu
217 f NO synthesis and selective blockade of TNF-alpha receptors may provide unique therapeutic approache
219 showed that tumor necrosis factor-alpha (TNF-alpha) receptors mediated cytoprotective signaling again
221 uced NK cell activity and not to altered IFN-alpha receptor, NKP30, NKP44, NKP46, or NKG2D expression
223 receptor, Stat4 activation by the human IFN-alpha receptor occurs through indirect recruitment by in
224 s infection, but the broad expression of IFN-alpha receptors often leads to adverse reactions in many
225 e, a process that required expression of IFN-alpha receptor on the T cells and IL-15 in the host.
227 of TNF-alpha, which, acting through the TNF-alpha receptor p55, augments macrophage colony-stimulati
228 ng a probe to platelet-derived growth factor-alpha receptor (PDGF alpha R), an OPC-expressed mRNA.
229 of the mouse platelet-derived growth factor alpha receptor (PDGFalphaR) is fused to the cytosolic do
230 we show that platelet-derived growth factor-alpha receptor (PDGFR-alpha) is specifically phosphoryla
231 ects are mediated through activation of PDGF-alpha receptors (PDGFR-alpha) on perivascular astrocytes
233 brain express platelet-derived growth factor alpha-receptors (PDGFRA), as they do in more caudal regi
234 utside of the PDGF family activated the PDGF alpha receptor (PDGFRalpha) and promoted disease progres
235 disease, the platelet-derived growth factor alpha receptor (PDGFRalpha) is dramatically more capable
240 alpha (TNF-alpha), acting via the type 1 TNF-alpha receptor, promotes fibrin deposition, while gamma
241 eukin-6 must first complex with its specific alpha-receptor (Ralpha) in order to bind and activate gp
242 s contain one of five chimeric retinoic acid alpha-receptor (RAR alpha) genes (X-RAR alpha) created b
243 ption factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisom
244 olabeling for androgen (AR) and estrogen (ER alpha) receptors revealed no colocalization of hcrt/orx
245 a converting enzyme (TACE) prevented the TNF-alpha receptor shedding response, which suggests that ex
246 Ob/ob male but not female mice lacking TNF-alpha receptors showed significantly lower levels of adi
248 cytosis activity, indicating that intact TNF-alpha receptor signaling is critical for microglial-medi
252 body response requires B cell-autonomous IFN-alpha receptor signaling, it is independent of B cell-in
254 RY produced "classic" inverse agonism at all alpha receptor subtypes; thus, a neutral efficacy was no
256 to construct IL-2 mutants that bind the IL-2 alpha receptor subunit (IL-2Ralpha, CD25) with affinitie
257 indicate that reduced expression of the RXR-alpha receptor subunit may represent a mechanism for res
258 of the cytokine subunit p19 and the soluble alpha receptor subunit p40, binds to a receptor complex
259 in that it does not require the nonsignaling alpha-receptor subunit for the formation of gp130-based
266 Cs with the antibody against the type II TNF-alpha receptor (TNF-RII), but not by the antibody agains
267 are primarily mediated through the major TNF-alpha receptor, TNF-R1, which is constitutively expresse
268 lacking either of the tumor necrosis factor-alpha receptor (TNFR) genes were also studied; the induc
269 in a subset of peripheral glia, and the TNF-alpha receptor (TNFR), Wengen, is expressed in motoneuro
270 mpared delivery of the tumor necrosis factor alpha receptor (TNFR)-immunoglobulin G1 (IgG1) Fc fusion
271 cluding the tumor necrosis factor alpha (TNF-alpha) receptor (TNFR), Fas, and death domain receptors
276 b/ob mice, p55 and p75 tumor necrosis factor-alpha receptors (TNFRs) act cooperatively to induce PAI-
277 seases; however, the precise role of the TNF-alpha receptors (TNFRs) has not been well defined using
278 t in TTP and either or both of the known TNF-alpha receptors (TNFRs), type 1 (TNFR1) and type 2 (TNFR
279 ce deficient in TNFR-I, TNFR-II, or both TNF-alpha receptors (TNFRs), we determined that AQARSAASKVKV
281 s, including the redistribution of the SDF-1 alpha receptor, to the basal surface and leading edge of
282 ceptor complex composed of an IL-15-specific alpha receptor, together with beta and gammac receptors
283 s of type 1 tumor necrosis factor alpha (TNF-alpha) receptor transcription in gastrointestinal cells
284 hain of the tumor necrosis factor alpha (TNF-alpha) receptor transcripts with IFN-gamma activation.
285 ptosis, because macrophages deficient in IFN-alpha receptor type I (IFNAR1) are highly resistant to n
286 ith adenoviral vector expressing soluble TNF-alpha receptor type I attenuated both MMP-2 and MMP-9 ac
287 , resistin and soluble tumor necrosis factor alpha receptor type II) in peripheral blood were measure
288 of soluble tumor necrosis factor alpha (TNF-alpha) receptors types 1 and 2 (sTNF-R1 and sTNF-R2), C-
290 studies demonstrate that activation of PPAR-alpha receptors using a selective PPAR-alpha ligand resu
291 th factor, soluble p75 tumor necrosis factor alpha receptor, vascular cell adhesion molecule 1, and m
292 Consistent with this observation, the IFN-alpha receptor was essential for the ability of MNV to c
295 rotoxin (CIRL or latrophilin) and neurexin 1 alpha receptors were found to be functionally present.
298 genetically deficient in the p55 and p75 TNF-alpha receptors were used to study the roles of these re
299 ssues was mediated primarily via the p55 TNF-alpha receptor whereas the p75 TNF-alpha receptor appear
300 of the cytokine growth factor, IL-6, and its alpha receptor, would elicit growth of injured spinal co
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