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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 quirement for pre-complexation to a specific alpha-receptor.
4 or necrosis factor alpha (TNF-alpha), or TNF-alpha receptors.
5 s is a consequence of the activation of PPAR-alpha receptors.
6 CD47 to macrophage signal regulatory protein alpha receptors.
7 ically act on 5-HT3, cholecystokinin, or TNF-alpha receptors.
8 gnaling from the IL-12/IL-23, IL-22, and IFN-alpha receptors.
9 eak inducer of apoptosis (TWEAK) but not TNF-alpha receptors.
10 -agonist that has full efficacy at all brain alpha-receptors.
11 CI, 1.13-1.42]), TNF (tumor necrosis factor)-alpha receptor 1 (hazard ratio, 1.09 [95% CI, 1.08-1.11]
12 on, we introduced a deficiency of interferon alpha receptor 1 (Ifnar1) into B6.Aec1Aec2 mice, which a
14 = 0.009), and soluble tumor necrosis factor alpha receptor 1 (P = 0.007) than did no weight-loss tre
15 uble A8 indicated specific cleavage of a TNF-alpha receptor 1 (p55 TNF-R1) but not a TNF-R2 peptide.
18 alizing antibodies against TNF-alpha and TNF-alpha receptor 1 (TNF-R1), suggesting that TNF-alpha pla
20 ransgenic AD mice (3xTg-AD) lacking both TNF-alpha receptor 1 (TNF-RI) and 2 (TNF-RII), 3xTg-ADxTNF-R
24 pared with the well-characterized type 1 IFN-alpha receptor 1 and 2 in mediating innate immune and au
26 ng cancer by enhancing tumor necrosis factor-alpha receptor 1 and nuclear factor-kappaB activation an
28 or necrosis factor alpha (TNF-alpha) and TNF-alpha receptor 1 block rSV5DeltaSH-induced apoptosis, su
29 Changes in soluble tumor necrosis factor alpha receptor 1 but not in C-reactive protein or interl
30 sTNF-alpha) promotes the shedding of the TNF-alpha receptor 1 ectodomain via increased mitochondrial
33 ing monoclonal antibody directed against TNF-alpha receptor 1 inhibited FHA-associated apoptosis by 4
34 een baseline VCAM-1 or tumor necrosis factor alpha receptor 1 levels and risk of any of the DR end po
35 is essential for tumor necrosis factor (TNF) alpha receptor 1 regulation of intestinal epithelial cel
36 markers examined, only tumor necrosis factor alpha receptor 1 showed a significantly greater increase
38 nsaminase, and soluble tumor necrosis factor alpha receptor 1 were lower after treatment with UDCA th
39 osomal degradation of the IFNAR1 (interferon alpha receptor 1) subunit of the type I interferon (IFN)
41 tibodies to Fas, tumor necrosis factor (TNF)-alpha receptor 1, or TNF-related apoptosis-inducing liga
42 eria toxin receptor (DTR) transgenic and IFN-alpha receptor 1-deficient mice, as well as purified pri
45 control livers, expression of IFN-beta, IFN-alpha receptor 1/2, Jak1, and Tyk2 remained unchanged in
46 centrations of soluble tumor necrosis factor alpha receptors 1 and 2 (sTNF-R1, sTNF-R2), interleukin
47 Activated tumor necrosis factor alpha (TNF-alpha) receptor 1 (TNFR1) recruits TNFR1-associated deat
48 ctivator of tumor necrosis factor alpha (TNF-alpha) receptor 1 (TNFR1) signaling, inducing both chemo
50 asma levels of soluble tumor necrosis factor-alpha receptor-1 (sTNFR-1) and brain natriuretic peptide
51 tumor necrosis factor-alpha (TNF-alpha), TNF-alpha receptor-1 (TNF-alphaR1), TNF-alphaR2, and interle
52 comitantly, the proinflammatory receptor TNF-alpha receptor-1 (TNFR1) was shed from the endothelial s
53 sgenic mice, and tumor necrosis factor (TNF) alpha receptor-1 (TNFR1)(-)(/-) mice underwent nonreperf
54 electively down-regulated the functional IFN-alpha receptor-1 chain of type I, but not type II (IFN-g
55 of tumor necrosis factor (TNF)-alpha and TNF-alpha receptor-1 in the retina of normal and glaucomatou
57 glial cells, whereas immunostaining for TNF-alpha receptor-1 was mainly positive in the retinal gang
58 Both protein and mRNA of TNF-alpha or TNF-alpha receptor-1 were predominantly localized to the inn
59 howed that mRNA signals for TNF-alpha or TNF-alpha receptor-1 were similarly more intense in glaucoma
60 ession and localization of TNF-alpha and TNF-alpha receptor-1 were studied in retina sections from 20
61 eutralizing Ab or to an inhibitor of the TNF-alpha receptor-1, increases proliferative potential, del
62 tile, 2.18; P = .005), tumor necrosis factor-alpha receptor 2 (odds ratio, 1.78; P = .04), and interl
63 ukin 6 (IL-6), soluble tumor necrosis factor alpha receptor 2 (sTNF-R2), E-selectin, soluble intercel
65 seline levels of tumor necrosis factor (TNF)-alpha receptor 2, interleukin (IL)-6, and C-reactive pro
66 ty C-reactive protein, tumor necrosis factor-alpha receptor 2, interleukin-6, and soluble vascular ce
67 ty C-reactive protein, tumor necrosis factor-alpha receptor 2, interleukin-6, and white blood cell co
68 P), interleukin 6, and tumor necrosis factor alpha receptor 2-and risk of invasive epithelial ovarian
69 tation of the RACK-1 binding site in the IFN-alpha receptor 2/beta subunit of the type I IFN receptor
70 a multiprotein complex that includes the IFN-alpha receptor 2/beta-chain of the receptor, STAT1, Janu
71 ers, including soluble tumor necrosis factor-alpha receptor-2 (P<0.001), interleukin-6 (P=0.04), and
72 type peroxisome proliferator-activated (PPAR-alpha) receptors; (2) shifted nicotine self-administrati
75 gh affinity interaction between IL-2 and its alpha receptor, a moderately entropically favorable low
76 TNFR2-/- epidermis, suggesting that the TNF-alpha receptors act independently via different AP-1 com
77 predict that when EGFR is activated with TGF-alpha, receptor activation is biased toward the cell sur
78 ll-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand,
79 .v. treatment prevented the elevation of TNF-alpha, receptor activator of NF-kappaB, and other inflam
80 autoubiquitination of tumor necrosis factor (alpha) receptor adaptor protein 6 (TRAF6), a protein inv
81 dy, the authors hypothesized that either the alpha-receptor agonist phenylephrine or the nitric oxide
82 o generate point mutations in the human PDGF alpha receptor (alphaPDGFR) cDNA, which resulted in sing
83 at the platelet-derived growth factor (PDGF)-alpha receptor (alphaPDGFR) is required for experimental
84 ndicated that platelet-derived growth factor alpha receptor (alphaPDGFR) plays an important role in a
85 e binds to the same site that binds the IL-2 alpha receptor and buries into a groove not seen in the
86 volved the recruitment of PKCbeta to the IFN-alpha receptor and interaction with protein tyrosine pho
87 ed IFN-alpha receptor expression, though IFN-alpha receptor and NKP30 expression was closely associat
88 his report we show, using mice lacking PGF(2)alpha receptor and pregnant rats, that PGF(2)alpha is re
89 ated following stimulation of the interferon-alpha receptor and the TCR in T cells by two different e
91 erleukins, leptin, and tumor necrosis factor-alpha receptors and their downstream molecular adaptors
92 ions of haematopoietic cells on MSCs via TNF-alpha receptors and then activating NF-kappaB signaling
93 ng antibodies, soluble tumor necrosis factor-alpha receptors, and hemin by abolishing both sEng and s
94 lated in response to LPS challenge in an IFN-alpha receptor- and IFN regulatory factor (Irf)9-depende
95 aracterizing pharmaceutical agents including alpha receptor antagonists as medical expulsive agents.
97 ressin antagonists and tumor necrosis factor-alpha receptor antibody are in phase II and III clinical
98 CV replicon expression, whereas the anti-IFN-alpha receptor antibody could partially block IRF-7-medi
99 e blockade of IFN-alpha receptor by anti-IFN-alpha receptor antibody on the replicon cells increased
101 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
116 otein kinase A with KT5720, but not with the alpha receptor blockers prazosin (alpha1) and/or yohimbi
118 Inhibition of the stromal cell-derived 1 alpha receptor (C-X-C receptor type 4 or CXCR4) using AM
126 have found that TAK1 is recruited to the TNF-alpha receptor complex in a RIP-dependent manner followi
127 as the forced recruitment of NEMO to the TNF-alpha receptor complex is insufficient for TNF-alpha-ind
128 can activate STAT4 by recruitment to the IFN-alpha receptor complex specifically via the carboxy-term
129 is to specifically recruit MEKK3 to the TNF-alpha receptor complex, whereas the forced recruitment o
131 erized by increased expression of the T-cell alpha receptor constant chain and changes in T helper ce
132 NF-alpha monoclonal antibody (MAb) and a TNF-alpha receptor construct (p75-Fc) were compared with tha
133 ody to platelet-derived growth factor (PDGF) alpha receptors coprecipitated STAT5 from extracts of un
134 d to interact with the tumor necrosis factor alpha receptor [corrected].We have identified a locus co
135 es, opioid-mediated down-regulation of MIP-1 alpha receptors could be blocked by the general PKC inhi
136 ly affect FE, nor does FE depend on Fas, TNF-alpha receptor, cytotoxic T-lymphocyte antigen-4, IL-2,
142 ed progesterone, glucocorticoid, or estrogen alpha receptors did not translocate FLAG-beta-catenin to
146 pendency of DCs and Ly6C(+) monocytes on IFN-alpha receptor expression for EmGFP/IL-15 upregulation a
147 efect was not attributable to diminished IFN-alpha receptor expression, though IFN-alpha receptor and
150 the effects of etanercept, a soluble p75 TNF alpha receptor-Fc fusion protein, in 2 patients with HID
151 r a soluble tumor necrosis factor alpha (TNF-alpha) receptor/Fc construct (TNFR-Fc, etanercept).
152 ls that express the NG2 proteoglycan and the alpha receptor for PDGF (NG2 cells, polydendrocytes) mak
153 such as the use of a nonstandard sushi-type alpha receptors for IL-2 and IL-15 in assembling quatern
154 tingly, prostate cancer cells expressing the alpha-receptor for platelet-derived growth factor (PDGFR
155 t, and that these events are mediated by the alpha-receptor for platelet-derived growth factor (PDGFR
156 llebrand factor nor platelet glycoprotein Ib-alpha receptor (GPIb-alpha) is required for RBCs to adhe
157 inflammation (soluble tumor necrosis factor alpha receptor I [sTNF-RI], interleukin 6 [IL-6], and hi
159 interleukin (IL)-8 and tumor necrosis factor-alpha receptor I, were significantly elevated in the cas
160 or-necrosis factor (TNF)-alpha; soluble TNF- alpha receptor I; and C-reactive protein (CRP) were meas
161 sis factor alpha (TNF-alpha) and soluble TNF-alpha receptors I and II; interleukin 1 beta (IL-1 beta)
162 ds to 2 distinct cell-surface receptors: TNF-alpha receptor-I (TNFR-I: p55) and TNF-alpha receptor-II
163 cytes deficient in the interferon-alpha (IFN-alpha) receptor IFN-alphaR showed reduced expression of
164 (NK) cells from mice lacking the type I IFN-alpha receptor (Ifnar(-/-)) or STAT1 (which signals down
165 er, in both CD4 competent, wild-type and IFN-alpha receptor (IFNAR) KO mice, Pneumocystis infection l
167 ties through an evolutionarily conserved IFN-alpha receptor (IFNAR), consisting of IFNAR1 and IFNAR2.
171 tion factor signaling through the interferon-alpha receptor (Ifnar1), resulting in the antigen-indepe
172 n (B = 0.27, p < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular
173 d decreased HLA-DR and Tumor necrosis factor-alpha receptor II (CD120b) expression compared with cont
174 s included solubilized tumor necrosis factor-alpha receptor II (sTNF-alphaRII), vascular cell adhesio
175 erleukin-6 (IL-6), and tumor necrosis factor-alpha receptor II (TNF-alpha RII) in the atorvastatin gr
177 10 [IL-10]), placental (TNF-alpha, IL-6, TNF-alpha receptor II [RII], and IL-1beta), and cord (IL-1be
179 C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellul
180 n the AHEI and soluble tumor necrosis factor-alpha receptor II, interleukin-6, soluble intercellular
181 rotein, interleukin-6, tumor necrosis factor-alpha receptor II, pro-brain natriuretic peptide (pro-BN
182 V and caspase 8, and >80% expressed the TNF-alpha receptor II, while Fas, TNFR-I, and CD27 expressio
183 e precursor, as well as sequestration of TNF-alpha receptors II and I, is performed by the zinc-depen
185 of the unliganded form of the interleukin-7 alpha receptor (IL-7Ralpha) extracellular domain (ECD) a
186 ct via the non-signaling membrane-bound IL-6 alpha-receptor (IL-6R) as an agonistic cytokine but also
187 lex, the viral cytokine can engage the human alpha-receptor (IL-6Ralpha) to form a hexameric vIL-6/IL
188 ignaling assembly composed of IL-6, the IL-6 alpha-receptor (IL-6Ralpha), and the shared signaling re
189 ical studies of interleukin-7 (IL-7) and its alpha-receptor (IL-7Ralpha) and comparisons with other g
190 ences in plasma immunological profiles (TNF- alpha receptor, IL-6, IFN-gamma, IL-12, IL-17, IL-22, an
191 s by forming a complex with its cell surface alpha-receptor, IL-11Ralpha, and the beta-subunit recept
192 raction between interleukin-7 (IL-7) and its alpha-receptor, IL-7Ralpha, plays fundamental roles in t
194 ransduction pathways generating from the TNF-alpha receptor in cardiomyocytes and leading preferentia
196 To evaluate the role played by each TNF-alpha receptor in the pathogenesis of this syndrome, mic
197 ions, estradiol up-regulates the level of ER-alpha receptors in keratinocytes and induces keratinocyt
200 ion to canonical beta-alpha-gamma/delta-beta-alpha receptors, including beta-alpha-gamma/delta-alpha-
201 rotective, whereas signaling through the TNF-alpha receptor increases the severity of 1918 virus infe
203 jected into lean mice lacking individual TNF-alpha receptors indicated that TNF-alpha autoamplificati
204 exercise with microspheres before and after alpha-receptor inhibition (phentolamine) and then NPY Y1
206 pathways, such as hypoxia-inducing factor-1-alpha, receptor-interacting protein 1, and apoptosis-ind
207 ibitory effects of roscovitine on STAT5/PDGF alpha receptor interaction, STAT5 activity, and cell sur
208 necrosis factor-alpha, tumor necrosis factor-alpha receptor, interleukin-6 receptor, or L-selectin.
209 licit a calcium flux, failed to induce MIP-1 alpha receptors internalization, and mediated a less pot
210 examined the paradoxical hypothesis that the alpha-receptor inverse agonist doxazosin might produce b
211 e studies thus provide insights into the TNF-alpha receptors involved in mediating and modulating the
218 f NO synthesis and selective blockade of TNF-alpha receptors may provide unique therapeutic approache
220 showed that tumor necrosis factor-alpha (TNF-alpha) receptors mediated cytoprotective signaling again
222 uced NK cell activity and not to altered IFN-alpha receptor, NKP30, NKP44, NKP46, or NKG2D expression
224 receptor, Stat4 activation by the human IFN-alpha receptor occurs through indirect recruitment by in
225 s infection, but the broad expression of IFN-alpha receptors often leads to adverse reactions in many
226 e, a process that required expression of IFN-alpha receptor on the T cells and IL-15 in the host.
228 of TNF-alpha, which, acting through the TNF-alpha receptor p55, augments macrophage colony-stimulati
229 ng a probe to platelet-derived growth factor-alpha receptor (PDGF alpha R), an OPC-expressed mRNA.
230 of the mouse platelet-derived growth factor alpha receptor (PDGFalphaR) is fused to the cytosolic do
231 we show that platelet-derived growth factor-alpha receptor (PDGFR-alpha) is specifically phosphoryla
232 ects are mediated through activation of PDGF-alpha receptors (PDGFR-alpha) on perivascular astrocytes
234 brain express platelet-derived growth factor alpha-receptors (PDGFRA), as they do in more caudal regi
235 utside of the PDGF family activated the PDGF alpha receptor (PDGFRalpha) and promoted disease progres
236 disease, the platelet-derived growth factor alpha receptor (PDGFRalpha) is dramatically more capable
241 alpha (TNF-alpha), acting via the type 1 TNF-alpha receptor, promotes fibrin deposition, while gamma
242 eukin-6 must first complex with its specific alpha-receptor (Ralpha) in order to bind and activate gp
243 s contain one of five chimeric retinoic acid alpha-receptor (RAR alpha) genes (X-RAR alpha) created b
244 ption factors CCAAT/enhancer binding protein-alpha, receptor retinoid X receptor-alpha, and peroxisom
245 olabeling for androgen (AR) and estrogen (ER alpha) receptors revealed no colocalization of hcrt/orx
246 a converting enzyme (TACE) prevented the TNF-alpha receptor shedding response, which suggests that ex
247 Ob/ob male but not female mice lacking TNF-alpha receptors showed significantly lower levels of adi
249 cytosis activity, indicating that intact TNF-alpha receptor signaling is critical for microglial-medi
253 body response requires B cell-autonomous IFN-alpha receptor signaling, it is independent of B cell-in
255 RY produced "classic" inverse agonism at all alpha receptor subtypes; thus, a neutral efficacy was no
257 to construct IL-2 mutants that bind the IL-2 alpha receptor subunit (IL-2Ralpha, CD25) with affinitie
258 indicate that reduced expression of the RXR-alpha receptor subunit may represent a mechanism for res
259 of the cytokine subunit p19 and the soluble alpha receptor subunit p40, binds to a receptor complex
260 in that it does not require the nonsignaling alpha-receptor subunit for the formation of gp130-based
267 Cs with the antibody against the type II TNF-alpha receptor (TNF-RII), but not by the antibody agains
268 are primarily mediated through the major TNF-alpha receptor, TNF-R1, which is constitutively expresse
269 lacking either of the tumor necrosis factor-alpha receptor (TNFR) genes were also studied; the induc
270 in a subset of peripheral glia, and the TNF-alpha receptor (TNFR), Wengen, is expressed in motoneuro
271 mpared delivery of the tumor necrosis factor alpha receptor (TNFR)-immunoglobulin G1 (IgG1) Fc fusion
272 cluding the tumor necrosis factor alpha (TNF-alpha) receptor (TNFR), Fas, and death domain receptors
277 b/ob mice, p55 and p75 tumor necrosis factor-alpha receptors (TNFRs) act cooperatively to induce PAI-
278 seases; however, the precise role of the TNF-alpha receptors (TNFRs) has not been well defined using
279 t in TTP and either or both of the known TNF-alpha receptors (TNFRs), type 1 (TNFR1) and type 2 (TNFR
280 ce deficient in TNFR-I, TNFR-II, or both TNF-alpha receptors (TNFRs), we determined that AQARSAASKVKV
282 s, including the redistribution of the SDF-1 alpha receptor, to the basal surface and leading edge of
283 ceptor complex composed of an IL-15-specific alpha receptor, together with beta and gammac receptors
284 s of type 1 tumor necrosis factor alpha (TNF-alpha) receptor transcription in gastrointestinal cells
285 hain of the tumor necrosis factor alpha (TNF-alpha) receptor transcripts with IFN-gamma activation.
286 ptosis, because macrophages deficient in IFN-alpha receptor type I (IFNAR1) are highly resistant to n
287 ith adenoviral vector expressing soluble TNF-alpha receptor type I attenuated both MMP-2 and MMP-9 ac
288 , resistin and soluble tumor necrosis factor alpha receptor type II) in peripheral blood were measure
289 of soluble tumor necrosis factor alpha (TNF-alpha) receptors types 1 and 2 (sTNF-R1 and sTNF-R2), C-
291 studies demonstrate that activation of PPAR-alpha receptors using a selective PPAR-alpha ligand resu
292 th factor, soluble p75 tumor necrosis factor alpha receptor, vascular cell adhesion molecule 1, and m
293 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