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1 ctodomain shedding of CD23, the low affinity IgE receptor.
2 )CPX(2)CYX, for binding to the high-affinity IgE receptor.
3 ion of mast cells by the human high-affinity IgE receptor.
4 t not the gamma subunit of the high affinity IgE receptor.
5 in basophil expression of the high-affinity IgE receptor.
6 s, including tryptase, Kit, and a functional IgE receptor.
7 lls transfected with the human high-affinity IgE receptor.
8 r basophil by binding to their high affinity IgE receptors.
9 induction following aggregation of mast cell IgE receptors.
10 antigen-induced aggregation of high affinity IgE receptors.
11 Both FCER2 and FCER1A encode subunits of IgE receptors.
12 endocytic vesicles containing the clustered IgE receptors.
13 downstream signaling processes activated by IgE receptors.
14 nking of the high-affinity immunoglobulin E (IgE) receptor.
15 ressing a fully functional immunoglobulin E (IgE) receptor.
16 phorylated SHIP-Grb2-Dok that were lost upon IgE receptor activation but retained under conditions of
18 but, upon activation via their high-affinity IgE receptor, alter their migratory kinetics to persist
20 e selectively endowed with the high-affinity IgE receptor and mediate a range of adaptive and innate
21 nstrate that IgE Abs can engage cell surface IgE receptors and activate effector cells against ovaria
22 very of IgE 50 y ago, followed by studies of IgE receptors and activation mechanisms, this review pro
23 allography interact differently with the two IgE receptors and suggest that temperature influences th
24 th factor, T cell, B cell, and high affinity IgE receptors and the receptor substrates IRS-1 (insulin
25 ecific IgE, nor the presence of a functional IgE receptor, and the clinical occurrence of some allerg
26 lergen exposure, decreases the expression of IgE receptors, and attenuates both immediate and delayed
28 nteractions with both high- and low-affinity IgE receptors, and explains why omalizumab selectively b
29 required for interactions with two distinct IgE receptors, and the structure suggests strategies for
30 idate the effect of rfhSP-D on high-affinity IgE receptor- and CD23-mediated, grass pollen-induced al
32 ctors activated following stimulation of the IgE receptor as well as in ATP- and GTP-dependent intrac
33 emonstrated little or no cell surface IgE or IgE receptors as analyzed by immunofluorescence and flow
38 n-Barr virus gp350/220, and the low-affinity IgE receptor CD23) via the N-terminal two of fifteen or
39 ation of B cells expressing the low-affinity IgE receptor CD23, which mediates the clearance of IgE a
40 ation of B cells expressing the low-affinity IgE receptor CD23, which mediates the clearance of IgE a
42 Additionally, cleavage of the low affinity IgE receptor, CD23, was profoundly impaired, but subsequ
46 and they inhibit endocytosis of crosslinked IgE receptor complexes, evidently by inhibiting pinching
48 lency trigger degranulation by cross-linking IgE-receptor complexes, whereas smaller DNP-dendrimers a
50 IL-5 and TNF-alpha production in response to IgE receptor cross-linkage, implying a positive feedback
51 ot stimulus specific but is evident for both IgE receptor cross-linking and direct calcium influx.
53 Activation of primary human mast cells by IgE receptor cross-linking or activation of HMC-1 cells
55 rived mast cells stimulated by high affinity IgE receptor cross-linking, direct influx of calcium, an
58 adapters that facilitate events initiated by IgE receptor-dependent activation of Src family protein
59 ulation of CD63 following stimulation of the IgE receptor, either specifically with peanut allergen o
63 sociated colitis was dependent on IgE, human IgE receptor-expressing effector cells, and the mediator
65 iants of the beta-chain of the high affinity IgE receptor Fc epsilon RI, I181L-V183L and E237G, have
66 lls transfected with the human high-affinity IgE receptor Fc epsilon RI, we demonstrate that ligands
69 RII or the alpha-chain of the high-affinity IgE receptor Fc-epsilon RI, but did detect transcripts t
70 lysis showed the absence of the low-affinity IgE receptor Fc-epsilon RII (CD23) and Mac-2 and the abs
72 nstrate that engagement of the high affinity IgE receptor (Fc epsilon R1) leads to the tyrosine phosp
75 her hand, cross-linking of the high affinity IgE receptor (Fc epsilon RI) on mast cells induces a set
76 tions this past year to our understanding of IgE receptor (Fc epsilon RI) signaling in mast cells inc
77 IgE and allergens through the high affinity IgE receptor (Fc epsilon RI), play a prominent role in a
78 has revealed a biochemical event proximal to IgE receptor (Fc epsilon RI)-stimulated tyrosine phospho
81 IgE is rapidly bound by the high affinity IgE receptor (Fc epsilonRI), thereby sensitizing Fc epsi
82 pivotal role in mediating the high-affinity IgE receptor (Fc epsilonRI)-induced degranulation of mas
85 ve identified the gene for the high-affinity IgE receptor (FC(epsilon)RI) beta subunit as a candidate
86 mast cells, cross-linking the high-affinity IgE receptor (Fc(epsilon)RI) initiates the Lyn-mediated
89 h antigen receptors, including high-affinity IgE receptors (Fc epsilon RI), is thought to be mediated
90 hrough the cross-linking of the low affinity IgE receptors (Fc epsilon RIIb or CD23) by IgE-allergen
91 , when activated through their high affinity IgE receptors (Fc epsilonRI), release various granule me
92 g of immunoglobulin E (IgE) to high affinity IgE receptors (Fc(epsilon)RI) expressed on the surface o
94 ved the structure of the human high affinity IgE receptor, Fc epsilon RI alpha, in six different crys
95 ity through activation via the high-affinity IgE receptor, Fc epsilon RI, although many other functio
96 tion of Fc gamma RIIB with the high-affinity IgE receptor, Fc epsilon RI, leads to inhibition of Ag-i
97 Antigen stimulation of mast cells via the IgE receptor, Fc epsilon RI, results in recruitment of t
98 express the high-affinity immunoglobulin E (IgE) receptor, Fc epsilon receptor 1 (Fc epsilon RI), ha
99 dependent of activation of the high-affinity IgE receptor (FcepsilonR1) by antigen, as adenosine is e
100 ated whether activation of the high-affinity IgE receptor FcepsilonRI elicits release of mast-cell re
101 orescence microscopy to demonstrate that the IgE receptor FcepsilonRI in the plasma membrane can sign
103 ll (MC) activation through the high-affinity IgE receptor FcepsilonRI leads to the release of mediato
104 IgE to prevent its binding to high-affinity IgE receptor FcepsilonRI on basophils and mast cells is
106 inhibits the activation of the high affinity IgE receptor FcepsilonRI on mast cells and basophils by
107 igen-specific IgE bound to the high-affinity IgE receptor FcepsilonRI on mast cells and basophils.
108 For example, we find that the transmembrane IgE receptor FcepsilonRI preferentially segregates into
109 egranulation following DS, the high-affinity IgE receptor FcepsilonRI was still capable of transducin
110 , leading to activation of the high-affinity IgE receptor FcepsilonRI, and initiating a signaling cas
111 responses, IgE antibodies, the high-affinity IgE receptor FcepsilonRI, and mast cells can contribute
113 c and asthmatic diseases is signaling by the IgE receptor FcepsilonRI, which depends on its interacti
117 on of the alpha subunit of the high affinity IgE receptor (FcepsilonRI(-/-)) were exposed on 10 conse
118 tyrosine-phosphorylated after high affinity IgE receptor (FcepsilonRI) aggregation in rat basophilic
119 eets, CD9 colocalized with the high-affinity IgE receptor (FcepsilonRI) and NTAL but not with LAT.
120 ur aim was to evaluate whether high-affinity IgE receptor (FcepsilonRI) and the related basophil func
121 ls of FAK and was defective in high affinity IgE receptor (FcepsilonRI) but not Ca2+ ionophore-mediat
122 beta and gamma subunits of the high affinity IgE receptor (FcepsilonRI) contain a consensus sequence
124 to determine whether increased high-affinity IgE receptor (FcepsilonRI) expression and cross-linking
125 onRIbeta) to eliminate surface high-affinity IgE receptor (FcepsilonRI) expression and function, rend
127 rly and downstream signaling mediated by the IgE receptor (FcepsilonRI) in RBL mast cells utilizing s
128 To define the role of the high affinity IgE receptor (FcepsilonRI) in the development of AHR, mi
130 n intact mast cells, including high affinity IgE receptor (FcepsilonRI) internalization and endosome
132 st cell activation through the high affinity IgE receptor (FcepsilonRI) is a critical component of at
140 ng chemokine, eotaxin, and the high-affinity IgE receptor (FcepsilonRI) were up-regulated >5-fold in
142 mast cells, cross-linking the high affinity IgE receptor (FcepsilonRI) with antigen activates cytoso
146 strate Gab2 may play a role in high affinity IgE receptor (FcepsilonRI)-mediated mast cell activation
147 ed SH2 domains to investigate where and when IgE receptor (FcepsilonRI)-mediated tyrosine phosphoryla
151 h the mRNA and protein for the high affinity IgE receptor (FcepsilonRI); it is speculated that this r
152 that expresses both native rat high affinity IgE receptors (FcepsilonRI) and functional human Fcepsil
154 tial observation that antigen stimulation of IgE receptors (FcepsilonRI) causes a significant change
155 pG DNA favors Th1 responses but also possess IgE receptors (FcepsilonRI) implicated in allergen prese
157 tivation mediated through both high-affinity IgE receptors (FcepsilonRI) on mast cells and basophils
158 gic diseases via activation of high-affinity IgE receptors (FcepsilonRI) resulting in release of proi
162 ne kinase has been shown to be necessary for IgE-receptor (FcepsilonRI)-mediated mast cell activation
163 1[EMR1](+)MPs), mast cell MPs (high-affinity IgE receptor [FcepsilonRI](+)c-kit(+)MPs), and basophil
164 Immunoreceptors such as the high affinity IgE receptor, FcepsilonRI, and T-cell receptor-associate
165 induced cross-linking of their high affinity IgE receptor, FcepsilonRI, by releasing histamine and ot
166 step in the activation of the high affinity IgE receptor, FcepsilonRI, is the tyrosine phosphorylati
168 Antigen stimulation of mast cells via the IgE receptor, FcepsilonRI, results in the recruitment of
169 te that IgE antibodies and the high affinity IgE receptor, FcepsilonRI, were essential for such acqui
178 against the alpha-chain of the high-affinity IgE receptor (FcepsilonRIalpha) or IgE on mast cells in
180 ing of the beta-subunit of the high-affinity IgE receptor (FcepsilonRIbeta) to eliminate surface high
184 the membrane topography of the high-affinity IgE receptor, FcstraightepsilonRI, and its associated ty
185 t cells are major effectors in high-affinity IgE receptor (FcvarepsilonRI)-dependent allergic reactio
186 nkage of the high-affinity immunoglobulin E (IgE) receptor (FcvarepsilonRI) on mast cells by antigen
187 stromal lymphopoietin and the high-affinity IgE receptor, FcvarepsilonRI, were required to attain ma
189 , signal transduction from the high affinity IgE receptor for the secretion of histamine was similar
191 , reversing basopenia and improving basophil IgE receptor function, reducing activity of IgG autoanti
193 xamine structural linkages between clustered IgE receptors (IgE-Fc epsilonRI) and the cytoskeleton in
195 hese mice express a tetrameric high affinity IgE receptor, in which the human alpha-chain associates
197 vation of mast cells by aggregation of their IgE receptors induces rapid and transient synthesis of c
200 of allergen-specific IgE-bound high-affinity IgE receptors, leading to immediate mast cell degranulat
202 ains selectively suppressed the induction of IgE receptor-mediated calcium signals as well as the bin
203 to determine the role of STAT6 activation in IgE receptor-mediated mast cell responses using STAT6 kn
204 investigation to determine whether TLR9- and IgE receptor-mediated responses oppose one another in pD
206 showed that aggregation of the high affinity IgE receptor on mast cells, FcepsilonRI, causes this imm
208 mast cells, expression of the high-affinity IgE receptor on other innate immune cells, including mon
210 more, the presence of trimeric high-affinity IgE receptors on leukocytes other than mast cells and ba
211 strate that perturbation of small numbers of IgE receptors on mast cells favors certain signals that
215 nal transduction pathways, including EGF and IgE receptor pathways, have been proposed to be spatiall
216 eceptor tyrosine-based activation motif-free IgE receptor pool, which would fail to induce cell activ
225 ts of btk mutant mast cells in high-affinity IgE receptor-stimulated wild-type mast cells without aff
227 naling proteins (including the high-affinity IgE receptor subunits, spleen tyrosine kinase, and phosp
228 t of antigen activation of the high-affinity IgE receptor, supports an important role for this nucleo
229 with immune cells and in particular with the IgE receptor system, which has been valuable for develop
231 calcium ionophore or by their high affinity IgE receptors, they degranulated in a pattern similar to
232 plasma membrane signaling mechanism by which IgE receptors transiently associate with microdomains an
236 caveolae microdomains, fluorescently labeled IgE receptors were found to be uniformly distributed in
237 ated reduced expression of the high affinity IgE receptor, which was restored to normal levels by the
238 ulation of RBL-2H3 m1 mast cells through the IgE receptor with antigen, or through a G protein-couple
239 s to characterize stimulated interactions of IgE receptors with several signaling proteins, including
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