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1 lls transfected with the human high-affinity IgE receptor.
2 ctodomain shedding of CD23, the low affinity IgE receptor.
3 )CPX(2)CYX, for binding to the high-affinity IgE receptor.
4 ion of mast cells by the human high-affinity IgE receptor.
5 ilonRI, the mast cell/basophil high affinity IgE receptor.
6 in basophil expression of the high-affinity IgE receptor.
7 t not the gamma subunit of the high affinity IgE receptor.
8 s, including tryptase, Kit, and a functional IgE receptor.
9 r basophil by binding to their high affinity IgE receptors.
10 induction following aggregation of mast cell IgE receptors.
11 s and basophils through the cross-linking of IgE receptors.
12 antigen-induced aggregation of high affinity IgE receptors.
13 Both FCER2 and FCER1A encode subunits of IgE receptors.
14 endocytic vesicles containing the clustered IgE receptors.
15 downstream signaling processes activated by IgE receptors.
16 classical, antigen-induced cross-linking of IgE receptors.
17 nking of the high-affinity immunoglobulin E (IgE) receptor.
18 ncreased expression of the immunoglobulin E (IgE) receptor.
19 ressing a fully functional immunoglobulin E (IgE) receptor.
20 phorylated SHIP-Grb2-Dok that were lost upon IgE receptor activation but retained under conditions of
22 but, upon activation via their high-affinity IgE receptor, alter their migratory kinetics to persist
24 e selectively endowed with the high-affinity IgE receptor and mediate a range of adaptive and innate
25 nstrate that IgE Abs can engage cell surface IgE receptors and activate effector cells against ovaria
26 very of IgE 50 y ago, followed by studies of IgE receptors and activation mechanisms, this review pro
27 allography interact differently with the two IgE receptors and suggest that temperature influences th
28 th factor, T cell, B cell, and high affinity IgE receptors and the receptor substrates IRS-1 (insulin
29 les, including Ras, PKCbeta activated by the IgE receptor, and Gbetagamma subunits released from acti
30 ecific IgE, nor the presence of a functional IgE receptor, and the clinical occurrence of some allerg
31 lergen exposure, decreases the expression of IgE receptors, and attenuates both immediate and delayed
33 nteractions with both high- and low-affinity IgE receptors, and explains why omalizumab selectively b
34 required for interactions with two distinct IgE receptors, and the structure suggests strategies for
35 idate the effect of rfhSP-D on high-affinity IgE receptor- and CD23-mediated, grass pollen-induced al
36 in response to allergens, anti-IgE, and anti-IgE receptor antibodies was assessed by Griess reagent,
38 ctors activated following stimulation of the IgE receptor as well as in ATP- and GTP-dependent intrac
39 emonstrated little or no cell surface IgE or IgE receptors as analyzed by immunofluorescence and flow
44 proteoform identification was performed and IgE receptor binding capacity and abundance in patient s
45 n-Barr virus gp350/220, and the low-affinity IgE receptor CD23) via the N-terminal two of fifteen or
46 nd to one of its receptors, the low-affinity IgE receptor CD23, which is expressed on activated B cel
47 ation of B cells expressing the low-affinity IgE receptor CD23, which mediates the clearance of IgE a
48 ation of B cells expressing the low-affinity IgE receptor CD23, which mediates the clearance of IgE a
50 Additionally, cleavage of the low affinity IgE receptor, CD23, was profoundly impaired, but subsequ
55 and they inhibit endocytosis of crosslinked IgE receptor complexes, evidently by inhibiting pinching
57 lency trigger degranulation by cross-linking IgE-receptor complexes, whereas smaller DNP-dendrimers a
59 IL-5 and TNF-alpha production in response to IgE receptor cross-linkage, implying a positive feedback
60 ot stimulus specific but is evident for both IgE receptor cross-linking and direct calcium influx.
62 Activation of primary human mast cells by IgE receptor cross-linking or activation of HMC-1 cells
64 rived mast cells stimulated by high affinity IgE receptor cross-linking, direct influx of calcium, an
68 t mice to identify genes activated following IgE receptor crosslinking that were further modulated in
69 adapters that facilitate events initiated by IgE receptor-dependent activation of Src family protein
70 ulation of CD63 following stimulation of the IgE receptor, either specifically with peanut allergen o
74 sociated colitis was dependent on IgE, human IgE receptor-expressing effector cells, and the mediator
75 tic influence appeared central to regulating IgE receptor expression on basophils, whereas expression
78 iants of the beta-chain of the high affinity IgE receptor Fc epsilon RI, I181L-V183L and E237G, have
79 lls transfected with the human high-affinity IgE receptor Fc epsilon RI, we demonstrate that ligands
82 RII or the alpha-chain of the high-affinity IgE receptor Fc-epsilon RI, but did detect transcripts t
83 lysis showed the absence of the low-affinity IgE receptor Fc-epsilon RII (CD23) and Mac-2 and the abs
85 nstrate that engagement of the high affinity IgE receptor (Fc epsilon R1) leads to the tyrosine phosp
88 her hand, cross-linking of the high affinity IgE receptor (Fc epsilon RI) on mast cells induces a set
89 tions this past year to our understanding of IgE receptor (Fc epsilon RI) signaling in mast cells inc
90 IgE and allergens through the high affinity IgE receptor (Fc epsilon RI), play a prominent role in a
91 has revealed a biochemical event proximal to IgE receptor (Fc epsilon RI)-stimulated tyrosine phospho
94 IgE is rapidly bound by the high affinity IgE receptor (Fc epsilonRI), thereby sensitizing Fc epsi
95 pivotal role in mediating the high-affinity IgE receptor (Fc epsilonRI)-induced degranulation of mas
98 ve identified the gene for the high-affinity IgE receptor (FC(epsilon)RI) beta subunit as a candidate
99 mast cells, cross-linking the high-affinity IgE receptor (Fc(epsilon)RI) initiates the Lyn-mediated
102 h antigen receptors, including high-affinity IgE receptors (Fc epsilon RI), is thought to be mediated
103 hrough the cross-linking of the low affinity IgE receptors (Fc epsilon RIIb or CD23) by IgE-allergen
104 , when activated through their high affinity IgE receptors (Fc epsilonRI), release various granule me
105 g of immunoglobulin E (IgE) to high affinity IgE receptors (Fc(epsilon)RI) expressed on the surface o
107 ved the structure of the human high affinity IgE receptor, Fc epsilon RI alpha, in six different crys
108 ity through activation via the high-affinity IgE receptor, Fc epsilon RI, although many other functio
109 tion of Fc gamma RIIB with the high-affinity IgE receptor, Fc epsilon RI, leads to inhibition of Ag-i
110 Antigen stimulation of mast cells via the IgE receptor, Fc epsilon RI, results in recruitment of t
111 express the high-affinity immunoglobulin E (IgE) receptor, Fc epsilon receptor 1 (Fc epsilon RI), ha
112 /-) mice receiving bone marrow from Nhe1- or IgE receptor FcepsilonR1-deficient mice, blunted foam ce
113 dependent of activation of the high-affinity IgE receptor (FcepsilonR1) by antigen, as adenosine is e
114 cells (pDCs) impaired by IgE- high-affinity IgE receptor (FcepsilonR1) cross-linking to induce Tregs
117 ated whether activation of the high-affinity IgE receptor FcepsilonRI elicits release of mast-cell re
118 orescence microscopy to demonstrate that the IgE receptor FcepsilonRI in the plasma membrane can sign
120 ll (MC) activation through the high-affinity IgE receptor FcepsilonRI leads to the release of mediato
121 IgE to prevent its binding to high-affinity IgE receptor FcepsilonRI on basophils and mast cells is
122 E secretion and binding to the high-affinity IgE receptor FcepsilonRI on effector cells are responsib
124 ific IgE, which sensitizes the high-affinity IgE receptor FcepsilonRI on mast cells and basophils and
125 inhibits the activation of the high affinity IgE receptor FcepsilonRI on mast cells and basophils by
126 igen-specific IgE bound to the high-affinity IgE receptor FcepsilonRI on mast cells and basophils.
128 For example, we find that the transmembrane IgE receptor FcepsilonRI preferentially segregates into
129 egranulation following DS, the high-affinity IgE receptor FcepsilonRI was still capable of transducin
130 a neuraminidase enzyme targeted towards the IgE receptor FcepsilonRI, and administering asialylated
131 , leading to activation of the high-affinity IgE receptor FcepsilonRI, and initiating a signaling cas
132 responses, IgE antibodies, the high-affinity IgE receptor FcepsilonRI, and mast cells can contribute
134 c and asthmatic diseases is signaling by the IgE receptor FcepsilonRI, which depends on its interacti
137 rgen immune complexes (IgE-ICs) target the 2 IgE receptors FcepsilonRI and CD23, and we investigated
140 on of the alpha subunit of the high affinity IgE receptor (FcepsilonRI(-/-)) were exposed on 10 conse
141 tyrosine-phosphorylated after high affinity IgE receptor (FcepsilonRI) aggregation in rat basophilic
142 eets, CD9 colocalized with the high-affinity IgE receptor (FcepsilonRI) and NTAL but not with LAT.
143 ur aim was to evaluate whether high-affinity IgE receptor (FcepsilonRI) and the related basophil func
144 ell activation through the IgE:high-affinity IgE receptor (FcepsilonRI) axis appears central to the d
145 ls of FAK and was defective in high affinity IgE receptor (FcepsilonRI) but not Ca2+ ionophore-mediat
146 beta and gamma subunits of the high affinity IgE receptor (FcepsilonRI) contain a consensus sequence
148 to determine whether increased high-affinity IgE receptor (FcepsilonRI) expression and cross-linking
149 onRIbeta) to eliminate surface high-affinity IgE receptor (FcepsilonRI) expression and function, rend
151 rly and downstream signaling mediated by the IgE receptor (FcepsilonRI) in RBL mast cells utilizing s
152 To define the role of the high affinity IgE receptor (FcepsilonRI) in the development of AHR, mi
154 n intact mast cells, including high affinity IgE receptor (FcepsilonRI) internalization and endosome
156 st cell activation through the high affinity IgE receptor (FcepsilonRI) is a critical component of at
164 )-mediated crosslinking of the high-affinity IgE receptor (FcepsilonRI) resulted in genome-wide reorg
165 me thought to be essential for high-affinity IgE receptor (FcepsilonRI) signaling in human cells.
166 ng chemokine, eotaxin, and the high-affinity IgE receptor (FcepsilonRI) were up-regulated >5-fold in
168 mast cells, cross-linking the high affinity IgE receptor (FcepsilonRI) with antigen activates cytoso
172 5 min exposure to UA inhibited high affinity IgE receptor (FcepsilonRI)-mediated degranulation, calci
173 strate Gab2 may play a role in high affinity IgE receptor (FcepsilonRI)-mediated mast cell activation
174 ed SH2 domains to investigate where and when IgE receptor (FcepsilonRI)-mediated tyrosine phosphoryla
178 h the mRNA and protein for the high affinity IgE receptor (FcepsilonRI); it is speculated that this r
179 that expresses both native rat high affinity IgE receptors (FcepsilonRI) and functional human Fcepsil
181 ross-linking of the IgE-bound, high-affinity IgE receptors (FcepsilonRI) by allergens or Ags and the
182 tial observation that antigen stimulation of IgE receptors (FcepsilonRI) causes a significant change
183 pG DNA favors Th1 responses but also possess IgE receptors (FcepsilonRI) implicated in allergen prese
185 tivation mediated through both high-affinity IgE receptors (FcepsilonRI) on mast cells and basophils
186 gic diseases via activation of high-affinity IgE receptors (FcepsilonRI) resulting in release of proi
191 ne kinase has been shown to be necessary for IgE-receptor (FcepsilonRI)-mediated mast cell activation
192 1[EMR1](+)MPs), mast cell MPs (high-affinity IgE receptor [FcepsilonRI](+)c-kit(+)MPs), and basophil
193 Immunoreceptors such as the high affinity IgE receptor, FcepsilonRI, and T-cell receptor-associate
194 induced cross-linking of their high affinity IgE receptor, FcepsilonRI, by releasing histamine and ot
195 step in the activation of the high affinity IgE receptor, FcepsilonRI, is the tyrosine phosphorylati
197 Antigen stimulation of mast cells via the IgE receptor, FcepsilonRI, results in the recruitment of
198 te that IgE antibodies and the high affinity IgE receptor, FcepsilonRI, were essential for such acqui
205 ing of IgE antibodies bound to high-affinity IgE receptors, FcepsilonRI, on the surface of mast cells
207 ling via the high-affinity immunoglobulin E (IgE) receptor, FcepsilonRI, leads to rapid degranulation
210 against the alpha-chain of the high-affinity IgE receptor (FcepsilonRIalpha) or IgE on mast cells in
211 says and in vivo using a human high-affinity IgE receptor (FcepsilonRIalpha)-transgenic mouse model o
214 ing of the beta-subunit of the high-affinity IgE receptor (FcepsilonRIbeta) to eliminate surface high
218 x ganglion neurons express the high-affinity IgE receptor FceR1, the levels of which increase in OVA-
219 E secretion and binding to the high-affinity IgE receptor FceRI on effector cells are responsible for
220 ross-linking of the IgE-bound, high-affinity IgE receptors (FceRI) by allergens or Ags and the bindin
222 IgG autoantibodies against the high-affinity IgE receptor, FceRIalpha, contribute the pathogenesis of
223 the membrane topography of the high-affinity IgE receptor, FcstraightepsilonRI, and its associated ty
224 t cells are major effectors in high-affinity IgE receptor (FcvarepsilonRI)-dependent allergic reactio
225 nkage of the high-affinity immunoglobulin E (IgE) receptor (FcvarepsilonRI) on mast cells by antigen
226 stromal lymphopoietin and the high-affinity IgE receptor, FcvarepsilonRI, were required to attain ma
228 , signal transduction from the high affinity IgE receptor for the secretion of histamine was similar
231 , reversing basopenia and improving basophil IgE receptor function, reducing activity of IgG autoanti
232 phism in the high-affinity Immunoglobulin E (IgE) receptor (GC and non-GC haplotypes) that has sex-de
234 xamine structural linkages between clustered IgE receptors (IgE-Fc epsilonRI) and the cytoskeleton in
236 hese mice express a tetrameric high affinity IgE receptor, in which the human alpha-chain associates
237 Similarly, cis-epoxysuccinate aggravated IgE-receptor-induced contraction of human bronchi, which
240 vation of mast cells by aggregation of their IgE receptors induces rapid and transient synthesis of c
246 of allergen-specific IgE-bound high-affinity IgE receptors, leading to immediate mast cell degranulat
248 ains selectively suppressed the induction of IgE receptor-mediated calcium signals as well as the bin
249 to determine the role of STAT6 activation in IgE receptor-mediated mast cell responses using STAT6 kn
250 ed capacity to elicit high- and low-affinity IgE receptor-mediated responses compared to Ara h 2 or w
251 investigation to determine whether TLR9- and IgE receptor-mediated responses oppose one another in pD
253 showed that aggregation of the high affinity IgE receptor on mast cells, FcepsilonRI, causes this imm
255 mast cells, expression of the high-affinity IgE receptor on other innate immune cells, including mon
256 mediates cross-linking of the high-affinity IgE receptor on various cells, causing release of inflam
258 more, the presence of trimeric high-affinity IgE receptors on leukocytes other than mast cells and ba
259 strate that perturbation of small numbers of IgE receptors on mast cells favors certain signals that
263 nal transduction pathways, including EGF and IgE receptor pathways, have been proposed to be spatiall
264 eceptor tyrosine-based activation motif-free IgE receptor pool, which would fail to induce cell activ
267 soluble isoform of FceRI, the high-affinity IgE receptor (sFcepsilonRI), is a protein of the IgE net
274 yzed a published model for immunoglobulin E (IgE) receptor signaling using synthetic qualitative and
275 d MC activation, including the high affinity IgE receptor, stem cell factor (SCF) receptor KIT/CD117,
276 ts of btk mutant mast cells in high-affinity IgE receptor-stimulated wild-type mast cells without aff
278 naling proteins (including the high-affinity IgE receptor subunits, spleen tyrosine kinase, and phosp
279 t of antigen activation of the high-affinity IgE receptor, supports an important role for this nucleo
280 with immune cells and in particular with the IgE receptor system, which has been valuable for develop
283 calcium ionophore or by their high affinity IgE receptors, they degranulated in a pattern similar to
285 plasma membrane signaling mechanism by which IgE receptors transiently associate with microdomains an
289 caveolae microdomains, fluorescently labeled IgE receptors were found to be uniformly distributed in
290 ated reduced expression of the high affinity IgE receptor, which was restored to normal levels by the
291 ulation of RBL-2H3 m1 mast cells through the IgE receptor with antigen, or through a G protein-couple
292 s to characterize stimulated interactions of IgE receptors with several signaling proteins, including