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1 by the same or another MRGPRX2 ligand (cross desensitization).
2  changes associated with ASIC activation and desensitization.
3 works to protect nicotinic responses against desensitization.
4  theoretically less likely to cause receptor desensitization.
5 C and c-Jun N-terminal kinase, contribute to desensitization.
6 aling throughout the brain, exhibit profound desensitization.
7 ptic cholinergic response without triggering desensitization.
8 ceptor to initiate apoptosis and not undergo desensitization.
9 gated ion channel (ELIC), and decreases ELIC desensitization.
10 derlying the ABA-induced stress response and desensitization.
11 use for both antibody-mediated rejection and desensitization.
12 nd a subset of these mutations increase ELIC desensitization.
13 ducting pore collapse and subsequent channel desensitization.
14 ssociated beta adrenergic receptor (ADRbeta) desensitization.
15             In total, 102 patients underwent desensitization.
16 ower sensitivity to Mg(2+) block and lack of desensitization.
17 ues, many of these channels can inhibit GPCR desensitization.
18  clustering independent faster recovery from desensitization.
19 s the TRPV1 pain receptors, and causes rapid desensitization.
20 r during ligand-gated channel activation and desensitization.
21  extraordinarily broad effects on gating and desensitization.
22 uncaging current and an increase in receptor desensitization.
23 , might provide similar benefits for allergy desensitization.
24  heterologous adaptation in kinase-dependent desensitization.
25 or kinases (GRKs) that help mediate receptor desensitization.
26 tween the Pre-M1 and the M4 TMD helix during desensitization.
27 ase (GRK2/3) with compound 101 blocked acute desensitization.
28 s lower than 100 mg, should directly undergo desensitization.
29 lyzed in the 167 patients who reacted during desensitization.
30  appropriate procedure between challenge and desensitization.
31 -dependent endocytosis and impaired receptor desensitization.
32 in studied limits, conditioning never caused desensitization.
33 erface of GluK2/K5 heteromers and slow their desensitization.
34 ellular route and, under prolonged exposure, desensitization.
35 anation for the ephemeral nature of clinical desensitization.
36 ntal cortex and protect these responses from desensitization.
37 n is needed for most individuals to maintain desensitization.
38 s) facilitates arrestin binding and receptor desensitization.
39 els, which is a major contributor to channel desensitization.
40 nits can provide activation without inducing desensitization.
41 und 101 was less effective at blocking acute desensitization.
42 ulation of G protein coupled receptor (GPCR) desensitization.
43  produced a receptor with slow recovery from desensitization.
44 ptors are functionally eliminated because of desensitization.
45 n arteries was resistant to activity-induced desensitization.
46 cific alloantibodies are collectively called desensitization.
47  airways, irrespective of beta2-adrenoceptor desensitization.
48 not known whether DAG modulates TRPV1 during desensitization.
49 mory of prior injury, and pain sensitization/desensitization.
50 et of nicotinic signaling without triggering desensitization.
51 ith compound 101 was required to block acute desensitization.
52  control the kinetics of GIRK activation and desensitization(3-5).
53 nhibitors act via the modulation of receptor desensitization, a process initiated by the recruitment
54 dual increase in receptor activity following desensitization accounted for the majority of synaptic t
55 the PSMalpha peptides induce FPR2 homologous desensitization, actin polymerization, and neutrophil re
56 ph node, bone marrow cells, and serum before desensitization, after desensitization, and after kidney
57 ensitizing stimulus from the media following desensitization allowed the cells to recover with half-p
58  the PDE8-RIalpha complex facilitates robust desensitization, allowing the cell to respond to dynamic
59                           We report a Ca(2+) desensitization and a narrowed dynamic range at higher t
60 nt TRPA1 regulation, including potentiation, desensitization and activation by metabotropic receptors
61                        Rituximab is used for desensitization and antibody-mediated rejection (AMR) tr
62  findings support synergism between PI based desensitization and belatacept facilitating transplantat
63  to arterial thrombosis, and 2 to failure of desensitization and development of antibody-mediated rej
64 ble for GPCR phosphorylation and, therefore, desensitization and downregulation of GPCRs.
65 adverse reactions, and lack of permanence of desensitization and established protocols.
66 PA1 into a distinct conducting state without desensitization and induces persistent pain.
67 analgesic tolerance to opioids was caused by desensitization and internalization of mu-opioid recepto
68 stimulation by its agonist, dopamine, causes desensitization and internalization of the receptor.
69 ivation of downstream effectors and eventual desensitization and internalization, all of which could
70 minus of the mu-opioid receptor alters acute desensitization and internalization, and in measures of
71 on, which, in turn, facilitated NOP receptor desensitization and internalization.
72  and Ser-356, which are involved in receptor desensitization and internalization.
73 on of mu-opioid receptor (MOR) signaling via desensitization and internalization.
74  an incompatible LDKT program, incorporating desensitization and kidney paired donation, was created
75 tes contribute, in varying degrees, to acute desensitization and long-term tolerance.
76 ey step that drives acute mu-opioid receptor desensitization and long-term tolerance.
77 roteins, plays an important role in receptor desensitization and may be important underlying mechanis
78 terminus of MORs almost completely abolished desensitization and one measure of tolerance in locus co
79 ell as practical relevance for generation of desensitization and posttransplant antibody-directed the
80 P(1) on endothelium without causing receptor desensitization and potently activated protection pathwa
81 estin recruitment and initiation of receptor desensitization and provide insight into the dysregulati
82                            We find that both desensitization and recovery can be accelerated by order
83                                 Eye movement desensitization and reprocessing (EMDR) is an effective
84 D movement, which establishes slower channel desensitization and robust regulation by anions and auxi
85 sure of long-term tolerance (increased acute desensitization and slowed recovery from desensitization
86 safer and more effective than allergen rapid desensitization and suppressed anaphylaxis more rapidly
87                                        While desensitization and sustained unresponsiveness (SU) have
88 quaternary structure are sufficient for fast desensitization and that substantial rearrangements like
89 s in the beta(3) subunit, promoting receptor desensitization and the alpha(1) subunit promoting effec
90 cognized as a critical step underlying acute desensitization and the development of cellular toleranc
91                 Although the idea that acute desensitization and tolerance are intimately linked is g
92                                   That acute desensitization and tolerance are not necessarily linked
93 assessed the efficacy of IdeS with regard to desensitization and transplantation of a kidney from an
94 l alanine substitutions (STANT + 7A) reduced desensitization and two measures of long-term tolerance.
95 ted respiratory disease underwent an aspirin desensitization and were placed on high-dose aspirin (1,
96 wo years of low-dose VWG OIT resulted in 30% desensitization, and 13% had sustained unresponsiveness.
97 ter 1 and 2 years of treatment to assess for desensitization, and after 2 years of treatment followed
98 lls, and serum before desensitization, after desensitization, and after kidney transplantation.
99 nding domain plays a key role in activation, desensitization, and ion modulation in kainate receptors
100 , bidirectional locomotor activity, receptor desensitization, and off-target effects.
101 clase activity, receptor internalization and desensitization, and post-endocytic sorting, as well as
102 es, protocols, medical management during the desensitization, and recommendations for maintenance asp
103 eclined, consistent with PAR(2) cleavage and desensitization, and then gradually recovered.
104 persistent manner different from traditional desensitization, and this leads to long-term suppressive
105 ensive review of aspirin challenges, aspirin desensitizations, and maintenance aspirin therapy in pat
106 susceptibility to anaphylaxis, while a rapid desensitization approach safely suppresses disease in mi
107 ns for maintenance aspirin therapy following desensitization are reviewed.
108 s, and cell-surface expression or functional desensitization as indirect measures to investigate CaSR
109 e clinical efficacy of aspirin therapy after desensitization as well as a discussion on the possible
110 hibited TRPA1 sensitivity and promoted TRPA1 desensitization at high Ca(2+).
111 ses beta3-AR transcription and regulates its desensitization behavior.
112 ute desensitization and slowed recovery from desensitization) but did not change a second (decreased
113 ain analogs relate to modulation of receptor desensitization, but the cellular and molecular mechanis
114 investigated adrenergic receptor (ADR) beta2 desensitization by administering oral ADRbeta modifiers
115 oplasmic element, the C-cys anchor, prevents desensitization by anchoring the pore-lining helix to th
116     Agonist exposure for 18 h caused minimal desensitization by diphenhydramine (DPD) compared with ~
117                          Currently, although desensitization can be achieved for the majority of indi
118                                 Furthermore, desensitization can be suppressed by trapping the linker
119 these cells, the cellular consequence of MOR desensitization cannot be defined by the activity of a s
120 sensitized mice, which further confirmed the desensitization capability of peanut cutaneous immunothe
121 ect calcium binding mediates stimulus-evoked desensitization, clarifying this important mechanism of
122                           The activation and desensitization data were mechanistically analyzed in th
123 ptor agonist bronchodilators evokes receptor desensitization, decreased efficacy, and an increased ri
124 nts lead to opposite effects, priming versus desensitization, depending on input durations.
125    The results indicate that accumulation of desensitization depends on the level of activity rather
126 sk for AMR in HS patients transplanted after desensitization (DES) who were DSA+ versus DSA- at trans
127 oorly understood, because rapid heat-induced desensitization (Dh) follows tightly heat-induced activa
128                                  The average desensitization duration among reactors was 1.67 days, a
129 king cessation or inadvertently via receptor desensitization during nicotine intake, may be a key tri
130 f ATP to activate P2X4R, slows both receptor desensitization during sustained ATP application and rec
131 he electroporation-induced sensitization and desensitization effects.
132 r interaction critically contributes to GPCR desensitization, endocytosis, and downstream signaling,
133  proteins from GIRK channels to induce rapid desensitization following receptor activation.
134      There are limited data on aspirin (ASA) desensitization for patients with coronary artery diseas
135 otherapy, which may provide a novel route of desensitization for the treatment of peanut allergies.
136          Graft survival was prolonged in the desensitization group (P = .073).
137                                        Thus, desensitization had a twofold effect: It abbreviated sig
138                                              Desensitization has enabled incompatible living donor ki
139 activity under steady-state conditions after desensitization has occurred.
140  and tolerable; however, the adequacy of its desensitization has remained to be determined.
141  In patients, several side effects of S1P(1) desensitization have been attributed to endothelial dama
142 , milk, and peanut allergy, strong levels of desensitization have been shown.
143 ents and novel drug development aimed at HLA desensitization have recently emerged.
144 t and statistically significant induction of desensitization, highest in children ages 4 to 11 years.
145 ation followed by rapid phosphatase-mediated desensitization; however, how degradation events regulat
146 A-543613 (possibly originating from receptor desensitization) implies that agonists may exert neuropr
147 er completion of ketorolac/aspirin challenge/desensitization in 12 patients with AERD.
148           Low- and high-dose VWG OIT induced desensitization in about one half of the subjects after
149 nvestigated whether insulin promotes beta-AR desensitization in airway smooth muscle (ASM) and compro
150 ear has been shown to induce modest clinical desensitization in allergic children.
151 utic modality to prevent or treat beta(2) AR desensitization in ASM.
152 ChR clustering and facilitated recovery from desensitization in both fetal and adult AChRs.
153 ecause rapsyn also facilitated recovery from desensitization in HEK293 cells expressing a delta-R375H
154 anaplastic lymphoma kinase (ALK) blocked D2R desensitization in neurons in the ventral tegmental area
155 beta(2) AR signaling promotes ASM beta(2) AR desensitization in obesity through upregulation of PDE4D
156 ral blood mononuclear cells before and after desensitization in one case revealed a decrease in naive
157 IT) has demonstrated reproducibly successful desensitization in patients with food allergy completing
158                                              Desensitization in pentameric ligand-gated ion channels
159 ot plate antinociceptive tolerance, receptor desensitization in periaqueductal gray, nor a super-sens
160 rinsulinemia plays a crucial role in beta-AR desensitization in the heart.
161 y peanut SLIT provided clinically meaningful desensitization in the majority of children with peanut
162 ing to properties of receptor activation and desensitization in the presence of muscimol.
163 loss of activatable GABA(A) receptors due to desensitization in the presence of transmitter and the s
164 and c-Jun N-terminal kinase had no effect on desensitization in tissue taken from naive animals.
165  In contrast, a mutation that decreases ELIC desensitization, increases POPG binding.
166 lation of this pathway leads to postreceptor desensitization, indicating the critical balance between
167 our center from 2010 to 2015, categorized by desensitization intensity: none/compatible (n = 260), lo
168  ligand, CXCL13, also mimics CXCL12-mediated desensitization, internalization, ubiquitination, and ly
169 tate 13-acetate (PMA) mimics CXCL12-mediated desensitization, internalization, ubiquitination, and ly
170                                              Desensitization is a canonical property of ligand-gated
171 thus the cPRA change on undiluted serum with desensitization is an insensitive measure of effectivene
172                   Therefore, efficient Cxcr4 desensitization is critical for lymphoid differentiation
173                                Recovery from desensitization is determined by the AChR isoform-specif
174 lamp experiments, we show that recovery from desensitization is faster in the adult AChR isoform.
175                                              Desensitization is inhibited in locus coeruleus neurons
176  activity, but how the receptor could escape desensitization is unknown.
177                   BPAM344 markedly decreased desensitization kinetics (from 5.5 to 775 ms), whereas i
178                   Alemtuzumab induction with desensitization led to nearly equivalent graft survival
179 l of antibody in these patients is such that desensitization may reduce antibody but not cPRA, thus t
180 r 28 months, 44 of 55 subjects passed a 10-g desensitization milk protein challenge; 23 of 55 subject
181 on with humoral-response rebound, suggesting desensitization must be maintained after transplantation
182 r kidney transplants requiring pretransplant desensitization (NCT01399593).
183 gue was well tolerated with neither signs of desensitization nor behavioral changes.
184 treatment with VP250 was well tolerated, and desensitization observed at week 52 persisted between we
185 hloride currents, and accelerated whole-cell desensitization observed in whole-cell recordings.
186        Chronic menthol treatment accelerated desensitization of 100 and 200 muM ACh-evoked currents.
187 inases (GRKs) are responsible for initiating desensitization of activated GPCRs.
188 rning rapid activation, agonist potency, and desensitization of alpha7 nAChRs after exposure to pyrim
189 nge detected after two years of SLIT was the desensitization of effector cells, which was only detect
190 tion, reduced endothelial-NOS expression and desensitization of endothelial-derived hyperpolarizing f
191           Binding of arrestins to KOR causes desensitization of G protein signaling and acts as a sca
192 1 recruitment, receptor internalization, and desensitization of G-protein activation.
193  selectivity for GluK1 subunits, reduces the desensitization of GluK1/GluK2 heteromers and fully abol
194 uK1/GluK2 heteromers and fully abolishes the desensitization of GluK1/GluK5 heteromers.
195 nt with morphine, the acute kinase-dependent desensitization of GPCRs is disrupted such that addition
196 signalling (tonic signalling) and reduce the desensitization of growth factor receptors.
197                                              Desensitization of human muscle AChRs was investigated u
198 duced phosphorylation of MOR, and diminished desensitization of membrane hyperpolarization.
199  surface FcepsilonRI expression and leads to desensitization of mice to IgE-mediated reactions.
200 is study is to explore which kinases mediate desensitization of MOR in brain slices from drug-naive a
201                                        Rapid desensitization of naive, IgE-sensitized huFcepsilonRIal
202 diacylglycerol kinase (DAGK) enzymes reduces desensitization of native TRPV1 in dorsal root ganglion
203 the respiratory system to develop tolerance, desensitization of neurons in the Kolliker-Fuse (KF), a
204                                              Desensitization of nicotinic receptors, which is a preva
205                                        Rapid desensitization of reNSGS mice with anti-FcepsilonRIalph
206                       Here, we show that the desensitization of the ABA signal is achieved by the reg
207                                              Desensitization of the alpha-amino-3-hydroxy-5-methyl-4-
208 potential firing and Ca(2+) activity despite desensitization of the MOR and reduced activation of a p
209                We have previously shown that desensitization of the mu-opioid receptor and interactio
210  after xenobiotic exposure, which leads to a desensitization of the Pdr1-specific response upon repea
211                                        Acute desensitization of the potassium conductance induced by
212  a recovery of neuronal excitability whereby desensitization of the receptor would lead to a new stea
213 ectors that have differential sensitivity to desensitization of the receptor.
214 od photovoltage is not as substantial as the desensitization of the rod outer segment photocurrent.
215 tantial bleaching of the visual pigment, the desensitization of the rod photovoltage is not as substa
216 he combination of kinase inhibitors to block desensitization of the somatostatin receptor in slices f
217 nce arteries with regard to potential Ca(2+) desensitization of VSM contractile apparatus.
218 han 10 ms, reporting movements associated to desensitization on this timescale within LBD dimers in r
219 c polypeptide (GIP) action may occur through desensitization or downregulation of beta-cell GIP recep
220 cium mobilization assay gave no evidence for desensitization or receptor internalization.
221 (2+)-dependent activation results in channel desensitization or rundown, the mechanism of which is un
222 groups in basophil activation at the time of desensitization or sustained unresponsiveness oral food
223 ived none, low, moderate, and high-intensity desensitization (P < .001).
224 luR5, which can decrease mGluR5 activity via desensitization (p < 0.01).
225  Using the estimated affinity, efficacy, and desensitization parameters, we calculated the amount of
226 l patients underwent a rapid ASA (5.5 hours) desensitization procedure.
227 he safety and outcomes of outpatient aspirin desensitization procedures.
228 ly a consequence of, but a necessity for the desensitization process in ASICs.
229 nding domain is an integral component of the desensitization process.
230 ent with a close approach of subunits during desensitization processes, the introduction of bulky ami
231 eromeric iGluRs, namely their activation and desensitization properties.
232  the safety and efficacy of a standard rapid desensitization protocol in patients with ASA sensitivit
233                             A standard rapid desensitization protocol is safe and effective across a
234                                      Aspirin desensitization protocol modifications have improved the
235 .6%) who did not successfully respond to the desensitization protocol, adverse reactions were minor a
236 he United Kingdom, sharing the same tailored desensitization protocol.
237 of signaling parameters such as the receptor desensitization rate constant can be estimated if the me
238 has a stronger effect on slowing the channel desensitization rate than gamma-2; yet, gamma-2 causes a
239 f AMPA receptors on slow time scale, such as desensitization rate.
240 tified specific residues that underlie acute desensitization, receptor internalization, and tolerance
241  of the ion channel (e.g., faster whole-cell desensitization) reduced unitary conductance and spontan
242               Although effective, parenteral desensitization regimens require use of costly venom ext
243  (TMD) underlying ion channel activation and desensitization remain poorly understood.
244 Ms 3-5, which mediate channel activation and desensitization, respectively.
245 se to continued signaling MORs undergo acute desensitization resulting in robust reduction in the pea
246 nt (mv) anti-FcepsilonRIalpha mAbs increases desensitization safety without loss of efficacy.
247 ation of signaling mechanisms (e.g. receptor desensitization, signal degradation).
248 y SHB1 and CCA1 under red light represents a desensitization step.
249                                     Although desensitization strategies permit transplantation via lo
250 as a whole and their response to our current desensitization strategies.
251 rminal center response and plasma cells as a desensitization strategy, we sensitized maximally MHC-mi
252 increases from week 52 to week 130 in either desensitization success or successfully consumed dose.
253              Median age (years) for week 130 desensitization success was 6.2 years (interquartile ran
254                                 At week 130, desensitization success was achieved in 1 of 20 (5%) PLB
255 e emerging role of the beta11-12 linker as a desensitization switch or 'molecular clutch'.
256  allyl isothiocyanate, which elicits channel desensitization, tachyphylaxis, and transient pain, GNE5
257 sion medicine approach using biologics, oral desensitization, targeted gut microbiome alterations, an
258  unresponsiveness (SU), and 13 had transient desensitization (TD).
259 ptor (MOR) results in the induction of acute desensitization that is thought to be a precursor for th
260 tion parameters, we calculated the amount of desensitization that would accumulate during a long (2-m
261                           Unexpectedly, upon desensitization the tagged D2 receptors were not interna
262            Although immunotherapy can induce desensitization, the mechanisms underlying this process
263             Despite its good track record of desensitization, the safety and tolerability of OIT has
264              Rather than using pretransplant desensitization therapies, we used a posttransplant prop
265                                              Desensitization therapy-mediated DSA reductions approach
266 al center (GC) response may limit bortezomib desensitization therapy.
267  a prerequisite for effective prevention and desensitization, this review article focuses on the most
268   Although the canonical mechanism for acute desensitization through phosphorylation by G protein-cou
269                                              Desensitization time constants were similar with both AC
270 t help explain the phenomenon of therapeutic desensitization to aspirin by nonselective COX inhibitor
271  contribute to the therapeutic properties of desensitization to aspirin in aspirin-exacerbated respir
272 09, which confers intracellular pH-dependent desensitization to OTOP channels.
273  feedback loops, enabling duration-dependent desensitization to repetitive stimulations.
274 ot after chronic alcohol-feeding, suggesting desensitization to the inhibitory actions of ethanol.
275 istered to mice undergoing sensitization and desensitization to the model food allergen ovalbumin.
276  and a monitoring tool to assess efficacy of desensitization treatment.
277 duction, calculated per antibody titer, as a desensitization trial endpoint.
278 plex antibody data and an ideal endpoint for desensitization trials.
279                                              Desensitization using proteasome inhibition and costimul
280 ent outcomes, and to differentiate transient desensitization versus sustained unresponsiveness after
281 2)) regulates TMEM16A channel activation and desensitization via binding to a putative binding site a
282                                              Desensitization was assessed through a double-blind, pla
283 imeric experiments showed that recovery from desensitization was determined by the M3-M4 cytoplasmic
284 SST sequence (TSST-4E), an increase in acute desensitization was present after chronic morphine treat
285            Anti-huFcepsilonRIalpha mAb rapid desensitization was safer and more effective than allerg
286 ng from Chrna5 disruption without triggering desensitization, we enhanced nicotinic receptor affinity
287 ict which patients are better candidates for desensitization, we studied 38 patients from 3 centers (
288                                          For desensitization, we used anti-huFcepsilonRIalpha mAbs th
289 ronary syndrome (ACS), 101 of whom underwent desensitizations, whereas 172 suffered from a chronic is
290 APP attenuates alpha2AAR internalization and desensitization, which are arrestin-dependent processes.
291 n GLP-1r density, leads to functional portal desensitization with a consequent suppression of vagal s
292 2 g/kg x2 doses)/rituximab (375 mg/m x1) for desensitization with alemtuzumab induction (15-30 mg, 1
293  by diphenhydramine (DPD) compared with ~50% desensitization with all other agonists.
294                                        Rapid desensitization with anti-FcepsilonRIalpha mAbs may be a
295  global suppression of this process by rapid desensitization with anti-FcepsilonRIalpha mAbs.
296  prevented in wild-type BALB/c mice by rapid desensitization with anti-mouse FcepsilonRIalpha mAb.
297 t augmenting proteasome inhibitor (PI) based desensitization with costimulation blockade (belatacept)
298                                              Desensitization with IVIG + rituximab combined with alem
299 g efferent actuation demonstrated an overall desensitization with respect to those of unstimulated ce
300 ishes the course of addiction, consisting of desensitization, withdrawal, resensitization, and associ

 
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