ライフサイエンスコーパス: desensitization

1 from long-lived, refractory states (O<-->D; 'desensitization').

2 oupling TAS2R14 function ( approximately 65% desensitization).

3 re was no loss of cell surface IgE following desensitization.

4 e but abolished receptor traffic and altered desensitization.

5 d ketamine have contrasting effects on NMDAR desensitization.

6 anges in surface IgE were examined following desensitization.

7 rmational changes during both activation and desensitization.

8 rve and that differentially reflect receptor desensitization.

9 agonist-occupied MC4R to lysosomes and MC4R desensitization.

10 which suggests that IdeS might be useful for desensitization.

11 t it does not block reactions during aspirin desensitization.

12 for eligibility for an ASA challenge and/or desensitization.

13 unologic correlates of food allergy and food desensitization.

14 ring goal-directed efficiency and behavioral desensitization.

15 appropriate procedure between challenge and desensitization.

16 lationship between conformational change and desensitization.

17 , and peanut were associated with successful desensitization.

18 d current (Imax), and time constant (tau) of desensitization.

19 immunogen to restrain health hazards during desensitization.

20 ibutes to sympatho-excitation and baroreflex desensitization.

21 ty, and postsynaptic receptor saturation and desensitization.

22 ough a PKA-dependent enhancement of receptor desensitization.

23 ily reflects receptor activation rather than desensitization.

24 n between subunits results in faster channel desensitization.

25 sure, presumably as a result of steady-state desensitization.

26 e of their high Ca(2+) permeability and fast desensitization.

27 e feedback but is not influenced by receptor desensitization.

28 or internalization, early events in PKCalpha desensitization.

29 d current resulting from AMPAR recovery from desensitization.

30 -dependent endocytosis and impaired receptor desensitization.

31 s that do or do not undergo rapid homologous desensitization.

32 events by an estimated 3% due to cumulative desensitization.

33 ivation, and internalization/agonist-induced desensitization.

34 re domain nearly eliminated Ca(2+)-dependent desensitization.

35 , which exhibit different polarity-dependent desensitization.

36 ing a contribution of PKCdelta to alpha1B-AR desensitization.

37 ge mutation in AMPARs had minimal effects on desensitization.

38 e contractility caused by myofilament Ca(2+) desensitization.

39 ocampal neurons are inwardly rectifying upon desensitization.

40 with the closing of the pore during channel desensitization.

41 in studied limits, conditioning never caused desensitization.

42 els generally exhibit the common response of desensitization.

43 ed CB1R downregulation without altering CB1R desensitization.

44 zation kinetics, and very fast recovery from desensitization.

45 meability in response to OVA challenge after desensitization.

46 htening of the M1 proline kink triggers AChR desensitization.

47 erenol and additional isoproterenol-mediated desensitization.

48 ckground light, rd1/+ rods displayed greater desensitization.

49 ponents during treatment indicated effective desensitization.

50 hetic propofol, increase a rate constant for desensitization.

51 erface of GluK2/K5 heteromers and slow their desensitization.

52 ellular route and, under prolonged exposure, desensitization.

53 anation for the ephemeral nature of clinical desensitization.

54 ght predict reaction severity during aspirin desensitization.

55 AMPA receptor that accompany activation and desensitization.

56 protects GC1 from S-nitrosocysteine-induced desensitization.

57 n, it does contribute to both activation and desensitization.

58 s lower than 100 mg, should directly undergo desensitization.

59 ate the pattern of treatment during clinical desensitization.

60 lyzed in the 167 patients who reacted during desensitization.

61 day 0) who received the same posttransplant desensitization.

62 ong patients with successful in-hospital ASA desensitization, 253 patients (80.3%) continued ASA for

63 erwent challenges and 147 subjects underwent desensitizations; 86 of the latter had index reactions t

64 dual increase in receptor activity following desensitization accounted for the majority of synaptic t

65 d by the same cell types, this suggests that desensitization acts at the receptor rather than cellula

66 frequencies because nAChRs exhibit prolonged desensitization after a single pulse of synchronous ChI

67 ealing wound, revealing a period of receptor desensitization after initial exposure to the damage att

68 tion myocardial infarction who underwent the desensitization after primary percutaneous coronary inte

69 ensitizing stimulus from the media following desensitization allowed the cells to recover with half-p

70 the PDE8-RIalpha complex facilitates robust desensitization, allowing the cell to respond to dynamic

71 was also accompanied by slowing of receptor desensitization and an increase in peak currents.

72 osphorylation plays a major role in receptor desensitization and arrestin binding.

73 PKC isoforms abolished fast alpha1B receptor desensitization and augmented IKs reduction, but did not

74 Specific and non-specific desensitization and changes in surface IgE were examined

75 ein kinases and bound by arrestin to trigger desensitization and endocytosis.

76 In conclusion, we report that the slow desensitization and fast deactivation of ASIC1a/2a heter

77 Those with donor-specific antibody requiring desensitization and incompatible live donor kidney trans

78 In addition, niacin induced heterologous desensitization and internalization of FPR1.

79 In addition to their role in desensitization and internalization of G protein-coupled

80 and function, consistent with a mechanism of desensitization and internalization that depends upon dr

81 vestigated the dynamics of dopamine receptor desensitization and internalization, thereby proposing a

82 t non-invasive method for assessing receptor desensitization and internalization.

83 by the receptor is tightly regulated through desensitization and intracellular trafficking.

84 The mechanisms of receptor desensitization and ion permeation, principles of antago

85 peanut components persisted despite clinical desensitization and modulation of allergen-specific immu

86 Clinical desensitization and oral food immunotherapy are therapeu

87 up suggest anti-IL-6R therapy is of value in desensitization and prevention and treatment of antibody

88 vity of acetylcholinesterase minimizes nAChR desensitization and promotes summation.

89 estin recruitment and initiation of receptor desensitization and provide insight into the dysregulati

90 ne, followed by rapid beta-arrestin-mediated desensitization and receptor internalization into endoso

91 ta-arrestin proteins, which then facilitates desensitization and receptor internalization.

92 Eye movement desensitization and reprocessing (EMDR) is an effective

93 nal changes accompanying AMPAR recovery from desensitization and reveal structural bases for regulati

94 oltage-dependent rectification upon receptor desensitization and reveals a physio-molecular signature

95 s of safety but not in outcomes of efficacy (desensitization and SU).

96 tine and ketamine differentially alter NMDAR desensitization and that memantine stabilizes a Ca(2+)-d

97 ils with beta-arrestin 2 in morphine-induced desensitization and tolerance.

98 assessed the efficacy of IdeS with regard to desensitization and transplantation of a kidney from an

99 C1a, leading to the apparent acceleration of desensitization and underestimating its potency; we show

100 sponses, all three compounds reduce receptor desensitization and, consequently, are classed as type I

101 ansplant patients for donor organ selection, desensitization, and assessing the risk for graft reject

102 re well the short time scales of activation, desensitization, and deactivation.

103 ights into the mechanisms of channel gating, desensitization, and ion permeation.

104 The exact mechanisms of aspirin desensitization are not clearly understood.

105 AP) mice does not cause cannabinoid receptor desensitization as previously observed in mice globally

106 hibited TRPA1 sensitivity and promoted TRPA1 desensitization at high Ca(2+).

107 mational changes, kinetics and recovery from desensitization at P2X1Rs.

108 dred seventy-five patients underwent aspirin desensitization at Scripps Clinic between January 2009 a

109 These experiments highlight differences in desensitization between iGluR subtypes and the highly sp

110 Progressive desensitization, both clinically and in basophil reactiv

111 We also found that accelerating ASIC desensitization by anion substitution can induce depress

112 ntional PKCs appear generally insensitive to desensitization by sustained diacylglycerol stimulation.

113 However, desensitization can be done safely and efficiently in an

114 these cells, the cellular consequence of MOR desensitization cannot be defined by the activity of a s

115 ts were re-exposed to taxanes either through desensitization, challenge, or regular infusion based on

116 X4(-/-)) and Ca(2+)/CaM-mediated CNG channel desensitization (CNGB1(DeltaCaM)).

117 se results suggest that the IVIG + rituximab desensitization combined with alemtuzmab induction with

118 ruitment and also demonstrated less receptor desensitization compared to serotonin in both calcium fl

119 zolyl)-urea], which interferes with receptor desensitization, completely eliminated EtOH modulation o

120 R and GlyR pore blocker picrotoxin prevented desensitization, consistent with its deep channel-bindin

121 and amplitude but they also exhibited rapid desensitization, consistent with previous analyses of N3

122 median peanut dose tolerated on the initial desensitization day was 250 mg for omalizumab-treated su

123 ctional characteristics of AMPARs, including desensitization, deactivation or recovery.

124 ted in decreased current amplitudes, altered desensitization decay time constants, and reduced GlyR c

125 Rush desensitization (DS) is a widely used and effective clin

126 The average desensitization duration among reactors was 1.67 days, a

127 al alterations that contribute to baroreflex desensitization during CHF.

128 ransmitter-gated ion channels, ASICs show no desensitization during high-frequency stimulus trains un

129 f ATP to activate P2X4R, slows both receptor desensitization during sustained ATP application and rec

130 of AIT include early mast cell and basophil desensitization effects, regulation of T- and B-cell res

131 he electroporation-induced sensitization and desensitization effects.

132 Beta-arrestins (betaarrs) critically mediate desensitization, endocytosis and signalling of G protein

133 pendent functional outcomes such as receptor desensitization, endocytosis, and G protein-independent

134 We propose that co-adaptative desensitization eventually relies on guidance sensor tra

135 dulation are determined by receptor-specific desensitization, evident at the level of Galphaq activat

136 erexpression of PKCdelta induced M1 receptor desensitization, excluding a contribution of PKC to M1-R

137 The desensitization failure rate was 1.4%.

138 n the palm induce a dramatic acceleration of desensitization followed by the appearance of a sustaine

139 inate alterations during 2 years of allergen desensitization, followed by reversal at 3 years, reflec

140 accelerates the rate of channel opening and desensitization for GluA1/2R channels more pronouncedly

141 There are limited data on aspirin (ASA) desensitization for patients with coronary artery diseas

142 pha2 or alpha3 subunits change upon receptor desensitization from a linear to an inwardly rectifying

143 n and analysis of data on ASA challenges and desensitizations from 10 allergy centers, as well as con

144 channel-binding site overlapping a physical desensitization gate.

145 stratified into those who tolerated aspirin desensitization (group I) and those who did not (group I

146 Patients who developed desensitization had a larger increase in IgG4 levels to

147 Thus, desensitization had a twofold effect: It abbreviated sig

148 Agonists that induce acute desensitization have been shown to induce a noncanonical

149 withdrawal and the frequent reversibility of desensitization if interrupted.

150 er completion of ketorolac/aspirin challenge/desensitization in 12 patients with AERD.

151 Failure to tolerate aspirin desensitization in a subset of patients with AERD is ass

152 mplications for clinical benefits of aspirin desensitization in aspirin-sensitive patients with asthm

153 The baroreflex desensitization in CHF is at least partly the result of

154 uring the establishment of food allergy (FA) desensitization in FA patients is a window into the path

155 whether omalizumab facilitated rapid peanut desensitization in highly allergic patients.

156 GSG1L also speeds up AMPAR deactivation and desensitization in hippocampal CA1 neurons, in contrast

157 fect of the type 2 cytokine IL-13 on beta2AR desensitization in human airway epithelial cells (HAECs)

158 The present studies focused on MOR desensitization in hypothalamic proopiomelanocortin (POM

159 )]-enkephalin (ME) caused significantly less desensitization in KF neurons compared with LC neurons.

160 In contrast to LC, desensitization in KF neurons was not enhanced by activa

161 s plasma cells, yet has limited efficacy for desensitization in kidney transplant candidates when up

162 When given as an adjunct to oral desensitization in mice with established IgE-mediated hy

163 Active treatment induced desensitization in most and sustained unresponsiveness (

164 IT) has demonstrated reproducibly successful desensitization in patients with food allergy completing

165 Tailored desensitization in pediatric blood group incompatible ki

166 branes, provide novel mechanistic details of desensitization in pentameric channels.

167 Desensitization in pentameric ligand-gated ion channels

168 6 mutant mice lost morphine-induced receptor desensitization in the brain stem and hypothalamus, cons

169 tion, heteromer assembly, ion permeation and desensitization in this prototypical receptor class.

170 M8 channels during menthol- and cold-induced desensitization in vitro.

171 nce of mechanisms that protect PKCalpha from desensitization in vivo.

172 l referred patients), and avoids unnecessary desensitizations in nonhypersensitive patients (30-56% o

173 ve SST receptor [SSTR]) were used to examine desensitization induced by exposure to ME and morphine f

174 t regulate G-protein-coupled receptor (GPCR) desensitization, internalization, trafficking and signal

175 This model yielded in vivo desensitization/internalization rates (0.2/min for quinp

176 Aspirin desensitization is an effective treatment option for asp

177 Modulation of Ca(2+)-dependent NMDAR desensitization is an unexplored mechanism of inhibitory

178 (cryo-EM) at 3.8 A resolution, we show that desensitization is characterized by the establishment of

179 Therefore, efficient Cxcr4 desensitization is critical for lymphoid differentiation

180 ought to determine whether GRK2-mediated DOR desensitization is directed by PKA via AKAP scaffolding.

181 The process of desensitization is dramatically different between subtyp

182 eta2 receptor, suggesting that recovery from desensitization is primarily related to the dissociation

183 We reported that Cxcr4 desensitization is required for quiescence/cycling balan

184 ment with previous reports, Ca(2+)-dependent desensitization is strongly dependent on both intracellu

185 In the majority of subjects, this desensitization is sustained after omalizumab is discont

186 BPAM344 markedly decreased desensitization kinetics (from 5.5 to 775 ms), whereas i

187 dulating ligand-sensitivity, activation, and desensitization kinetics as well as voltage-dependence.

188 displayed diminished pH sensitivity, altered desensitization kinetics, and very fast recovery from de

189 igible, the channel should undergo temporary desensitization (known as adaptation).

190 Alemtuzumab induction with desensitization led to nearly equivalent graft survival

191 dramatic and highly specific effect on NMDAR desensitization, making it AMPAR-like.

192 n in alert fatigue, including the concept of desensitization may not be directly measured and thus co

193 e beta2AR from Cav1.2 is a uniquely specific desensitization mechanism of Cav1.2 regulation by highly

194 observations may implicate sGCs in neuronal desensitization mechanisms far beyond the specific case

195 ed activation by DiC8 failed to engage known desensitization mechanisms, with the enzyme remaining me

196 After desensitization, mice were assessed for clinical sensiti

197 gue was well tolerated with neither signs of desensitization nor behavioral changes.

198 he cocaine-induced plasticity of D2 receptor desensitization observed in wild type mice was not recap

199 model can reproduce the transient changes in desensitization observed upon IVM application, the signi

200 enopus oocytes, we show that PEA reduces the desensitization of acetylcholine-evoked currents after r

201 t membrane PIP2 depletion, whereas the rapid desensitization of alpha1B-AR delimits PIP2 reduction an

202 It was reported that diminazene accelerates desensitization of ASICs, which was, however, not explai

203 dependent ERK1/2 activation and heterologous desensitization of chemoattractant receptors are involve

204 owing a single in vivo cocaine exposure, the desensitization of D2 receptors from neurons expressing

205 Phosphorylative desensitization of G-protein-coupled receptors contribut

206 ine kinase with an important function in the desensitization of G-protein-coupled receptors.

207 ived neurotrophic factor (BDNF) increase the desensitization of glucocorticoid receptors (GR) and vul

208 Desensitization of IgE-mediated histamine release from h

209 Desensitization of mast cell responses was readily induc

210 Notably, LPS-induced desensitization of MCs was short term with MC sensitivit

211 surface FcepsilonRI expression and leads to desensitization of mice to IgE-mediated reactions.

212 of C-terminal phosphorylation sites on rapid desensitization of MOPr.

213 Acute desensitization of mu opioid receptors is thought to be

214 Besides activation, Br-BPTC affects desensitization of nAChRs induced by sustained exposure

215 the respiratory system to develop tolerance, desensitization of neurons in the Kolliker-Fuse (KF), a

216 Desensitization of nicotinic receptors, which is a preva

217 ate for acute to chronic pain transition via desensitization of NMDAR.

218 ication of cyclothiazide (CTZ) revealed that desensitization of postsynaptic receptors contributed to

219 ession phenotype by direct receptor:receptor desensitization of TAS2R14 function.

220 96A, S402A) were used, phorbol ester-induced desensitization of the calcium response was markedly dec

221 nockout, caused tonic activation and partial desensitization of the CB1 receptor at PF-PC synapses.

222 y transduction, Ca(2+) removal by NCKX4, and desensitization of the CNG channel by Ca(2+)/CaM, intera

223 potential firing and Ca(2+) activity despite desensitization of the MOR and reduced activation of a p

224 activity as expected.SIGNIFICANCE STATEMENT Desensitization of the mu-opioid receptor (MOR) is thoug

225 he beta-ball-thumb interface accelerates the desensitization of the mutant channels.

226 f Cs(+) , which increased the bleach-induced desensitization of the photovoltage and slowed its tempo

227 embrane voltage measurements showed that the desensitization of the photovoltage was considerably les

228 ction CXCR4 mutations that affect homologous desensitization of the receptor have been reported in th

229 a recovery of neuronal excitability whereby desensitization of the receptor would lead to a new stea

230 ectors that have differential sensitivity to desensitization of the receptor.

231 od photovoltage is not as substantial as the desensitization of the rod outer segment photocurrent.

232 tantial bleaching of the visual pigment, the desensitization of the rod photovoltage is not as substa

233 Physiological signaling and desensitization of the tagged receptors were not differe

234 ils do not respond toward allergens due to a desensitization of their Fc epsilon receptor pathway.

235 the heart; phosphorylation by GRK2 leads to desensitization of these receptors.

236 n by particles, differential activation, and desensitization of TRPV1 by particles and/or other agoni

237 treatment, subjects underwent a rapid 1-day desensitization of up to 250 mg of peanut protein, follo

238 nce arteries with regard to potential Ca(2+) desensitization of VSM contractile apparatus.

239 %) placebo-treated subjects passed the 10-g "desensitization" OFC (P = .18).

240 No patients had a severe immediate HSR with desensitization or challenge.

241 py for food allergies is to induce sustained desensitization or even true long-term oral tolerance to

242 und antibody response in patients undergoing desensitization or treatment for antibody-mediated rejec

243 OIT-only and BF2+OIT mice showed significant desensitization (P<.01 and .001, respectively) at 1 week

244 The desensitization procedure was performed before cardiac c

245 The desensitization procedure was successful in 315 patients

246 l patients underwent a rapid ASA (5.5 hours) desensitization procedure.

247 Recommendations on oral provocation and desensitization procedures have been made.

248 e of the offending colorant as no successful desensitization procedures have been reported.

249 he safety and outcomes of outpatient aspirin desensitization procedures.

250 in recruitment can produce distinct receptor desensitization properties.

251 the safety and efficacy of a standard rapid desensitization protocol in patients with ASA sensitivit

252 A standard rapid desensitization protocol is safe and effective across a

253 Aspirin desensitization protocol modifications have improved the

254 ve crossmatch, who received a posttransplant desensitization protocol starting at day 0 with high-dos

255 62 patients (19.7%) who had responded to the desensitization protocol was because of medical decision

256 An endovenous desensitization protocol was performed on one of them, w

257 .6%) who did not successfully respond to the desensitization protocol, adverse reactions were minor a

258 he United Kingdom, sharing the same tailored desensitization protocol.

259 Despite the previous safety data, desensitization protocols were adopted by only 42% of su

260 omes have been described, notably because of desensitization protocols, but mid- and long-term data a

261 ure, patients were then treated with shorter desensitization protocols, challenge, or both with the a

262 Receptor-specific desensitization provides a mechanism of effector modulat

263 Aspirin desensitization provides long-term clinical benefits.

264 d state, not responsive to ATP, and that its desensitization rate can be altered by each of the three

265 at lower concentrations but with more rapid desensitization relative to alpha6*-nAChRs.

266 Alteration in Cxcr4 desensitization resulted in decrease of circulating HSPC

267 se to continued signaling MORs undergo acute desensitization resulting in robust reduction in the pea

268 Disruption of the desensitization ring is probably the key switch that ena

269 Formation of this 'desensitization ring' is mediated by staggered helix con

270 t D2L receptors, exhibited calcium-dependent desensitization similar to that exhibited by endogenous

271 patients receiving omalizumab reacted during desensitization, suggesting that it does not block react

272 mediate and gradual protocols, but not rapid desensitization, suppressed splenocyte proliferation and

273 Unexpectedly, upon desensitization the tagged D2 receptors were not interna

274 Before desensitization, the median isoagglutinin titer of 34 AB

275 that for the LBD mutant L483Y, known to lack desensitization, the postulated active state of the LBD

276 and protein kinase A in salmeterol-mediated desensitization through bioluminescence resonance energy

277 ine-binding protein 1 (PEBP1) contributes to desensitization through release of G protein receptor ki

278 ta-ball, and thumb domains to activation and desensitization through the analysis of chimeras and the

279 -modulating treatment that is able to induce desensitization to food allergens, to increase tolerance

280 Natural desensitization to milk and egg can occur.

281 in basal GC1 activity and prevent/rescue GC1 desensitization to NO.

282 ot after chronic alcohol-feeding, suggesting desensitization to the inhibitory actions of ethanol.

283 istered to mice undergoing sensitization and desensitization to the model food allergen ovalbumin.

284 mice, we demonstrate loss of TC-PTP led to a desensitization to tumor initiator 7,12-dimethylbenz[a]a

285 that prolonged stimulation leads to PKCalpha desensitization via dephosphorylation and/or degradation

286 Recovery from desensitization was also studied.

287 posure to AT-1001, the time to recovery from desensitization was longest for the human alpha3beta4 nA

288 to assess salmeterol efficacy for functional desensitization, we examined the kinetics of salmeterol-

289 There was little or no non-specific desensitization when lung mast cells were exposed to ant

290 ution of Ca(2+)-dependent PKCs to alpha1B-AR desensitization, whereas IKs facilitation is induced by

291 ronary syndrome (ACS), 101 of whom underwent desensitizations, whereas 172 suffered from a chronic is

292 APP attenuates alpha2AAR internalization and desensitization, which are arrestin-dependent processes.

293 IL-13 treatment of HAECs leads to beta2AR desensitization, which involves 15LO1/PEBP1 interactions

294 greatly increases the rate of recovery from desensitization, while biochemical analysis reveals a la

295 Most patients undergoing aspirin desensitization will have symptoms.

296 2 g/kg x2 doses)/rituximab (375 mg/m x1) for desensitization with alemtuzumab induction (15-30 mg, 1

297 roaches are intended to induce some level of desensitization with chronic or repeated exposure to the

298 Desensitization with IVIG + rituximab combined with alem

299 oltage thereby eliminating its difference in desensitization with the rod outer segment photocurrent.

300 rant exposure triggers dephosphorylation and desensitization without altering receptor localization.