ライフサイエンスコーパス: receptor dimerization

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

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

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

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

5 ortant role for TLR intracellular domains in receptor dimerization.

6 ectively desulfated SOS molecules to promote receptor dimerization.

7 g specificity and how ligand binding induces receptor dimerization.

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

9 eals that this glycosylation interferes with receptor dimerization.

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

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

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

13 ellular signaling proteins upon PDGF-induced receptor dimerization.

14 -146 on the C140S mutant background restored receptor dimerization.

15 for detecting and monitoring the kinetics of receptor dimerization.

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

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

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

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

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

21 (2+) receptor on cell surface expression and receptor dimerization.

22 ved to activate their receptors by mediating receptor dimerization.

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

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

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

26 to allow intermolecular hydrogen bonding and receptor dimerization.

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

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

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

30 athematic model describing antibody-mediated receptor dimerization.

31 late the EGFR activation state by modulating receptor dimerization.

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

33 ecular disulfide bond formation and covalent receptor dimerization.

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

35 d intermolecular disulfide bonds, leading to receptor dimerization.

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

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

38 ivalent antibodies can mimic HGF agonism via receptor dimerization.

39 face charge differences here directly affect receptor dimerization.

40 critical role of the transmembrane domain in receptor dimerization.

41 ged receptors confirmed that MRAP blocks MC5 receptor dimerization.

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

43 of PDGFRbeta undergoes typical PDGF-induced receptor dimerization.

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

45 tor tyrosine kinase by binding and promoting receptor dimerization.

46 Two strategies were used to drive receptor dimerization.

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

48 igand binding, receptor phosphorylation, and receptor dimerizations.

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

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

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

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

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

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

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

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

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

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

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

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

61 otruding from neighboring receptors mediates receptor dimerization and activation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Ligand binding promotes receptor dimerization and instigates transmembrane signa

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

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

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

84 Thus, covalent receptor dimerization and ligand oligomerization are two

85 56S, C129S, and C131S, significantly reduces receptor dimerization and markedly inactivates the CaR.

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

87 TRH increased receptor dimerization and phosphorylation within 1 min i

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

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

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

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

92 -dependent microcompartments sustains robust receptor dimerization and signalling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 Receptor dimerization by soluble MHC oligomers is suffic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Regulated receptor dimerization increases TRH-induced receptor end

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

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

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

159 Receptor dimerization is a critical early step in this p

160 Receptor dimerization is a crucial intermediate step in

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

162 Receptor dimerization is critical for signaling by the e

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

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

165 Receptor dimerization is followed by conformational chan

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

167 Receptor dimerization is generally considered to be the

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

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

170 Receptor dimerization is mediated by receptor-receptor i

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

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

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

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

175 Receptor dimerization is the key signaling event for man

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

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

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

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

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

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

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

183 Cytokine-induced receptor dimerization mediates the trans-phosphorylation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 Receptor dimerization was detectable within 3 minutes af

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

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

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