ライフサイエンスコーパス: receptor dimerization

1 or, binding of IT1t to this variant promotes receptor dimerization.

2 Two strategies were used to drive receptor dimerization.

3 n, possibly as a result of antibody-mediated receptor dimerization.

4 reventing JAK2 V617F-promoted erythropoietin receptor dimerization.

5 o study the existence and molecular basis of receptor dimerization.

6 eta functions as a regulatory switch for the receptor dimerization.

7 extracellular region (ECR) in ligand-induced receptor dimerization.

8 ortant role for TLR intracellular domains in receptor dimerization.

9 ectively desulfated SOS molecules to promote receptor dimerization.

10 g specificity and how ligand binding induces receptor dimerization.

11 tion analysis is to study relative levels of receptor dimerization.

12 n increasing FGF-FGFR affinity and promoting receptor dimerization.

13 eals that this glycosylation interferes with receptor dimerization.

14 th AP20187, a dimeric F36V ligand, to induce receptor dimerization.

15 d intermolecular disulfide bonds, leading to receptor dimerization.

16 ctivation functions but not on DNA-dependent receptor dimerization.

17 ellular signaling proteins upon PDGF-induced receptor dimerization.

18 -146 on the C140S mutant background restored receptor dimerization.

19 for detecting and monitoring the kinetics of receptor dimerization.

20 e 132 within the C129S/C131S mutant restored receptor dimerization.

21 rmolecular disulfide bond(s) responsible for receptor dimerization.

22 ive with respect to either ligand binding or receptor dimerization.

23 her IGF-II nor the synthetic peptide induced receptor dimerization.

24 (2+) receptor on cell surface expression and receptor dimerization.

25 critical role of the transmembrane domain in receptor dimerization.

26 F and other hematopoietic cytokines on c-kit receptor dimerization.

27 ceptors that are activated by ligand-induced receptor dimerization.

28 y of epidermal growth factor (EGF) to induce receptor dimerization.

29 to allow intermolecular hydrogen bonding and receptor dimerization.

30 ellular domain 3 leads to ligand-independent receptor dimerization.

31 Jak1-dependent event that is independent of receptor dimerization.

32 athematic model describing antibody-mediated receptor dimerization.

33 ue to impairment of either ligand-binding or receptor dimerization.

34 mers, implying that Wnt binding mediates FZD receptor dimerization.

35 ecular disulfide bond formation and covalent receptor dimerization.

36 ed to treat lung cancers but are affected by receptor dimerization.

37 e binding in combination with ligand-induced receptor dimerization.

38 ng receptor-ligand interaction or disrupting receptor dimerization.

39 d CD33 phosphorylation and its signaling via receptor dimerization.

40 N-desulfated heparin does not inhibit Reelin receptor dimerization.

41 indirectly, interacts with FGFRs and induces receptor dimerization.

42 sites, cofactors, membrane localization, and receptor dimerization.

43 R) signalling is activated by ligand-induced receptor dimerization.

44 ved to activate their receptors by mediating receptor dimerization.

45 late the EGFR activation state by modulating receptor dimerization.

46 ptor plasticity is regulated on the level of receptor dimerization.

47 ng, and degradation of Siglec-15 by inducing receptor dimerization.

48 thout reducing ligand affinity or disrupting receptor dimerization.

49 vents O-glycosylation of CSF3R and increases receptor dimerization.

50 ivalent antibodies can mimic HGF agonism via receptor dimerization.

51 face charge differences here directly affect receptor dimerization.

52 ged receptors confirmed that MRAP blocks MC5 receptor dimerization.

53 ase activity, consistent with ligand-induced receptor dimerization.

54 of PDGFRbeta undergoes typical PDGF-induced receptor dimerization.

55 bind and activate SFKs after ligand-induced receptor dimerization.

56 tor tyrosine kinase by binding and promoting receptor dimerization.

57 ctly participate in recruiting the secondary receptor/dimerization.

58 igand binding, receptor phosphorylation, and receptor dimerizations.

59 utations within exon 8 in a region mediating receptor dimerization (2%-13% of cases).

60 ion of downstream signaling pathways, making receptor dimerization a critical determinant of receptor

61 re we show that signaling via ligand-induced receptor dimerization-a very common motif in cellular si

62 R is activated by ligand binding, triggering receptor dimerization, activation of kinase activity, an

63 ographic studies and analyzed the effects on receptor dimerization, activation, and ligand binding.

64 Absence of demonstrable receptor dimerization after the establishment of dual si

65 oring point mutations, which severely impair receptor dimerization, also inhibited efficiently the si

66 RP6 blocked Wnt ligand-induced LRP6-Frizzled receptor dimerization, an essential step in Wnt signalin

67 o key characteristics of the MFEzeta CAR: 1) receptor dimerization and 2) the interaction of the CAR

68 ther, suggesting a possible mechanism of Met receptor dimerization and activation by HGF.

69 of Klotho/FGF receptor assembly that drives receptor dimerization and activation has not been elucid

70 o receptor tyrosine kinases (RTKs) regulates receptor dimerization and activation of the kinase domai

71 F binding to the EGFR and for ligand-induced receptor dimerization and activation that uses this stru

72 complex with the receptor, thereby inducing receptor dimerization and activation, trans-phosphorylat

73 otruding from neighboring receptors mediates receptor dimerization and activation.

74 s of TLR4 and TLR6 have an essential role in receptor dimerization and activation.

75 "beads on a string," mediates FGF-2-induced receptor dimerization and activation.

76 econdary FGFR molecule leading to asymmetric receptor dimerization and activation.

77 M) cysteine residue (Cys(259)) implicated in receptor dimerization and activation.

78 d in structural rearrangements essential for receptor dimerization and activation.

79 that retained VEGFR2 binding, but prevented receptor dimerization and activation.

80 and TLR4, exerting an indirect influence on receptor dimerization and activation.

81 gested mechanisms for growth factor-mediated receptor dimerization and allosteric kinase domain activ

82 ive high-affinity TrkB agonist that provokes receptor dimerization and autophosphorylation and activa

83 of Val664 to glutamate or glutamine induces receptor dimerization and autophosphorylation of the rec

84 , VEGF concentrations to trigger robust VEGF receptor dimerization and autophosphorylation, as well a

85 tibodies that block ligand binding inhibited receptor dimerization and beta-gal complementation.

86 ral model of protein kinases, is enhanced by receptor dimerization and can occur via an intermolecula

87 smembrane (ie, NTRK3L449F) domains increased receptor dimerization and cell-surface abundance.

88 n inhibits EGFR tyrosine phosphorylation and receptor dimerization and concurrently increases both th

89 se system for in vivo imaging changes in EGF receptor dimerization and conformation.

90 EGF-induced receptor dimerization and consequent trans- auto-phospho

91 e results demonstrate how E5 binding induces receptor dimerization and define a molecular mechanism o

92 dim mutant) has been reported as crucial for receptor dimerization and DNA binding, this assumption h

93 ic inhibitors of TNFR1 activation and probed receptor dimerization and function.

94 I-like (FNIII) domains, regions critical for receptor dimerization and function.

95 onstituted an endogenous steric hindrance to receptor dimerization and inhibited EGFR-mediated lung c

96 Ligand binding promotes receptor dimerization and instigates transmembrane signa

97 significant decrease in the rates of the EGF receptor dimerization and its dephosphorylation at 4 deg

98 nterface abolishes the suppressive activity, receptor dimerization and its DNA binding property.

99 and is incompatible with current models for receptor dimerization and ligand activation.

100 Thus, covalent receptor dimerization and ligand oligomerization are two

101 56S, C129S, and C131S, significantly reduces receptor dimerization and markedly inactivates the CaR.

102 will enable further characterization of CB1 receptor dimerization and oligomerization and its functi

103 TRH increased receptor dimerization and phosphorylation within 1 min i

104 omain of Kit is not required for SCF-induced receptor dimerization and provide additional support for

105 ortant for vIL-6 signaling and vIL-6-induced receptor dimerization and show that vIL-6, like hIL-6, c

106 in ligand binding, actively participates in receptor dimerization and signal transduction.

107 RMT1) enhances binding to EGF and subsequent receptor dimerization and signaling activation.

108 -dependent microcompartments sustains robust receptor dimerization and signalling.

109 ely, and that the two sites together mediate receptor dimerization and subsequent activation.

110 t stimulates AR transactivation by mediating receptor dimerization and subsequent DNA binding.

111 ivation of ERalpha function through enforced receptor dimerization and suggest dimer disruption as a

112 receptor, the N211Q mutant exhibits enhanced receptor dimerization and sustained activation upon liga

113 ful tools with which to investigate dopamine receptor dimerization and the atypical nature of clozapi

114 have tested the ability of ligand to promote receptor dimerization and the subsequent role of recepto

115 able complex with the receptor, resulting in receptor dimerization and trans-phosphorylation.

116 e kinase domains has been thought to involve receptor dimerization and transphosphorylation of juxtap

117 ase (RTK) activation involves ligand-induced receptor dimerization and transphosphorylation on tyrosi

118 eptor-overexpressing cells, EGF induction of receptor dimerization and tyrosine phosphorylation were

119 in-protein interactions that are involved in receptor dimerization and/or activation of the kinase do

120 hanisms requiring high affinity DNA binding, receptor dimerization, and active silencing.

121 kedly reduces EGFR stability, EGF-stimulated receptor dimerization, and autophosphorylation activity.

122 eceptor (GR) is mediated by hormone binding, receptor dimerization, and coactivator recruitment.

123 ceptor and downstream signaling by enhancing receptor dimerization, and increased expression of matri

124 ltaneously blocked ligand binding, prevented receptor dimerization, and induced substantial conformat

125 etely abolishes the suppressive activity and receptor dimerization, and reduces the DNA-binding affin

126 hallmarks of KIT structures, ligand-induced receptor dimerization, and the critical residues in the

127 are required for this loop to contribute to receptor dimerization, and we identify a set of ligand-i

128 Tyr508 within this domain, and constitutive receptor dimerization are the major molecular determinan

129 y combining the NanoBiT system with androgen receptor dimerization as a reporting mechanism.

130 r in C225-treated cells and does not provoke receptor dimerization as do inhibitors that recognize th

131 regulation and inhibition of growth required receptor dimerization as monovalent Fab fragments only e

132 eolysis paralleled that for its promotion of receptor dimerization (as monitored by formation of GHR

133 all, the results suggest that the FCS & TIRF receptor dimerization assay can assess FGFR dimerization

134 re of ligand-receptor binding, an FCS & TIRF receptor dimerization assay was developed to measure rH(

135 variants in functional, ligand-binding, and receptor dimerization assays.

136 tivate Trk receptor tyrosine kinases through receptor dimerization at the cell surface followed by au

137 tivate Trk receptor tyrosine kinases through receptor dimerization at the cell surface followed by au

138 We present a method for monitoring receptor dimerization at the membrane of live cells.

139 t weak affinities that govern ligand-induced receptor dimerization at the plasma membrane.

140 , it is constitutively active as detected by receptor dimerization, autophosphorylation, and stimulat

141 role for such ligands is to regulate nuclear receptor dimerization both in solution and on DNA.

142 tors, ligand binding is positively linked to receptor dimerization but the linkage is abolished upon

143 e modulators that initiate signaling through receptor dimerization, but natural cytokines have struct

144 s, however, reveals efficient ligand-induced receptor dimerization by all ligands, largely independen

145 Receptor dimerization by soluble MHC oligomers is suffic

146 A dose-dependent inhibition of native erbB receptor dimerization by the erbB peptides has been obse

147 binding (b1b2), and one domain critical for receptor dimerization (c).

148 ial for micro-receptor function, micro-delta receptor dimerization contributes to full micro-agonist

149 We propose a mechanism by which the uPA receptor dimerization could promote autoactivation of sc

150 s for as little as 15 s resulted in chimeric receptor dimerization detectable as beta-gal enzymatic a

151 okine thrombopoietin (Tpo), stimulated c-kit receptor dimerization detectable by FRET, and tyrosine p

152 a confocal-based FRET method for monitoring receptor dimerization directly on the plasma membrane of

153 NH(2)-terminal AB region (but containing the receptor dimerization domain) of RXRalpha was added in p

154 These results reveal how ligand-regulated receptor dimerization dynamics and adaptor protein conce

155 ignaling mechanistically arises from altered receptor dimerization dynamics due to extracellular bind

156 precise molecular details of ligand-induced receptor dimerization, except for studies of the human g

157 s (activation function 1 [AF-1] and AF-2) or receptor dimerization fail to fully inhibit cellular pro

158 ase activity is stimulated by ligand-induced receptor dimerization, FGFR2 LADD mutants may also exert

159 and beta-chains) to RON ectodomain modulates receptor dimerization, followed by autophosphorylation o

160 Despite the reported requirement of estrogen receptor dimerization for hormone-dependent activation,

161 riptional activation but not DNA-binding and receptor dimerization functions.

162 ghlight how ligand dimerization, rather than receptor dimerization, governs PTH(1)R activation dynami

163 ding to its receptor is oligomerization, and receptor dimerization has been correlated with mitogenic

164 Ligand-induced receptor dimerization has traditionally been viewed as t

165 humanized monoclonal antibody that inhibits receptor dimerization, has a mechanism of action that is

166 Prior biochemical studies of c-kit receptor dimerization have mainly used affinity cross-li

167 meric proteins are prominent in biology, and receptor dimerization (homo- or heterodimerization) is c

168 demonstrating that the peptide also promotes receptor dimerization in a cellular context.

169 opioid receptors to dimerize and the role of receptor dimerization in agonist-induced internalization

170 To monitor receptor dimerization in cell-based assays and living an

171 tates real-time monitoring of ligand-induced receptor dimerization in complex biological fluids, offe

172 yzing function and therapeutic modulation of receptor dimerization in intact cells and living mice.

173 n the single molecule level, and IFN-induced receptor dimerization in micropatterns could be monitore

174 trophin interface resulted from the need for receptor dimerization in signal initiation.

175 r in cis and disclose an obligatory role for receptor dimerization in substrate phosphorylation in ad

176 eric construct, indicating a requirement for receptor dimerization in the DDR1-collagen interaction.

177 These data identify a role of receptor dimerization in the mechanism of DOR and MOR fe

178 ontains the major determinants which inhibit receptor dimerization in the quiescent cells and that th

179 ition of the EGFR kinase, induced reversible receptor dimerization in vitro and in intact A431 cells.

180 show that specific mutations that disrupted receptor dimerization in vitro reduced the rate of prote

181 Regulated receptor dimerization increases TRH-induced receptor end

182 Since Csf1r signaling requires receptor dimerization initiated by CSF1 binding, the dat

183 ded manipulation of residues involved in the receptor dimerization interface identified one residue (

184 monomer binds to one sEGFR monomer, and that receptor dimerization involves subsequent association of

185 Receptor dimerization is a critical early step in this p

186 Receptor dimerization is a crucial intermediate step in

187 Membrane receptor dimerization is a well-established event for in

188 We also show that the asymmetric mode of receptor dimerization is applicable to paracrine FGFs th

189 Receptor dimerization is critical for signaling by the e

190 re-function studies and a mechanism in which receptor dimerization is critical for signaling, we cons

191 ing the strategy of dimer dilution, where WT receptor dimerization is disrupted by increasing express

192 Receptor dimerization is followed by conformational chan

193 Thus, the mechanism of receptor dimerization is fundamentally different than th

194 Receptor dimerization is generally considered to be the

195 dies using artificial membranes confirm that receptor dimerization is governed by the two-dimensional

196 atively consistent with a mechanism in which receptor dimerization is initially mediated by the assoc

197 Receptor dimerization is mediated by receptor-receptor i

198 our knowledge) aspect of our results is that receptor dimerization is modulated by membrane cholester

199 metry allowed us to conclude that the leptin receptor dimerization is not induced by ligand binding.

200 The conclusion is that receptor dimerization is not required to activate the ty

201 g only a single FKBP12 domain confirmed that receptor dimerization is sufficient for proliferative si

202 Receptor dimerization is the key signaling event for man

203 or dimerization; when G-CSF is bound to both receptors, dimerization is enhanced 2000-fold, while the

204 Although the monomers can activate chemokine receptors, dimerization is required for leukocyte recrui

205 olor single quantum dot tracking to quantify receptor dimerization kinetics on living cells and show

206 hus the results indicate that CSF-1-mediated receptor dimerization leads to a Tyr-559/SFK/c-Cbl pathw

207 Similarly, in vivo, opioid receptor dimerization, ligand binding of receptors, and

208 This suggests that inhibitor-dependent receptor dimerization may facilitate C225-induced recept

209 dicating that the paradigm of ligand-induced receptor dimerization may not apply to the DDRs.

210 rane receptors to better understand specific receptor dimerization mechanisms.

211 Cytokine-induced receptor dimerization mediates the trans-phosphorylation

212 s with 2:1 stoichiometry reconciles a common receptor dimerization mode for ALK and LTK and provides

213 Receptor tyrosine kinase activation requires receptor dimerization/multimerization, which, for many r

214 receptor pre-dimerization to ligand-induced receptor dimerization occurring only after receptor upta

215 Receptor dimerization of urokinase-type plasminogen acti

216 ssential for its activity, interference with receptor dimerization offers a new opportunity to exploi

217 analyzed the significance of this domain for receptor dimerization/oligomerization in detail.

218 and molecular diversity of G protein-coupled receptor dimerization/oligomerization.

219 ptor dimerization and the subsequent role of receptor dimerization on its intracellular trafficking.

220 ue is sufficiently sensitive to detect c-kit receptor dimerization on normal human hematopoietic cell

221 mbined with confocal microscopy to visualize receptor dimerization on the plasma membrane, and there

222 No discernible difference in Neu receptor dimerization or activation was detected in MMTV

223 sine residues, without measurable effects on receptor dimerization or ligand binding.

224 s of transcription factor activation such as receptor dimerization or tolerance.

225 Further, we examine the effect of receptor dimerization patterns on biological response us

226 expressing varying levels of HERs 1-3 on the receptor dimerization patterns using a detailed kinetic

227 ition to simply mediating ligand binding and receptor dimerization, perhaps by helping to recruit NMJ

228 PDGF beta receptor tyrosine kinase, causing receptor dimerization, phosphorylation, and cell transfo

229 ing its ability to dimerize, indicating that receptor dimerization property can be functionally uncou

230 These data support the view that steroid receptor dimerization provides an important mechanism fa

231 -once activated upon ligand binding-leads to receptor dimerization, recruitment of protein complexes,

232 neu-pertuzumab complex demonstrated that the receptor dimerization region encompassed residues 266-33

233 mistry, and molecular modeling, we find that receptor dimerization relies upon covalent and noncovale

234 ing to its transmembrane domain and inducing receptor dimerization, resulting in cellular transformat

235 a a conformational change that exposes a key receptor dimerization site in the fourth of the five imm

236 s that hold the kinase domain inactive until receptor dimerization stimulates transition to an active

237 ses to different EGFR ligands are defined by receptor dimerization strength and signaling dynamics.

238 R modules of TLR4 in a manner that precludes receptor dimerization; such dimerization is a prerequisi

239 mply exposing this arm is not sufficient for receptor dimerization, suggesting that additional ligand

240 F induced a dose-dependent increase in c-kit receptor dimerization that correlated well with the conc

241 intermolecular N-C interaction occurs during receptor dimerization that results in an antiparallel ar

242 ternary structure reveal novel mechanisms of receptor dimerization, the existence of tetrameric chrom

243 its productive conformation is stabilized by receptor dimerization.The hormone binding site of the re

244 ur by the common mechanism of ligand-induced receptor dimerization: the DDRs form stable noncovalent

245 Because ligand binding is coupled to receptor dimerization, this coupling lends complexity to

246 hich may be indicative of mechanisms such as receptor dimerization, tolerance mechanisms which are ev

247 EGFR signalling is preceded by receptor dimerization, typically thought to result from

248 lar signaling is initiated by ligand-induced receptor dimerization, tyrosine phosphorylation of the T

249 Here, we investigated ET-receptor dimerization using fluorescence resonance energ

250 specific JAK2 V617F inhibitory mutations on receptor dimerization using the NanoBiT protein compleme

251 The ability of SCF to induce c-kit receptor dimerization was assessed by flow cytometric an

252 Receptor dimerization was detectable within 3 minutes af

253 Significant FRET signal indicative of receptor dimerization was found even in the absence of c

254 ation of the complex between [3H]EGF and EGF receptor, dimerization was measured by quantitative cros

255 binding of G-CSF also enhances the receptor-receptor dimerization; when G-CSF is bound to both recep