ライフサイエンスコーパス: receptor binding

1 e free hormone) and an active open state (on receptor binding).

2 branes of living cells in the absence of any receptor binding.

3 ins (HC) to hyaluronan (HA), facilitating HA receptor binding.

4 sure in the open Env conformation induced by receptor binding.

5 form, which most likely allows for effective receptor binding.

6 rder to determine its possible role in virus receptor binding.

7 increased euphoria correlated with decreased receptor binding.

8 ng antibodies and two residues essential for receptor binding.

9 near the canyon that might allow alternative receptor binding.

10 inding sites corresponding to glucocorticoid receptor binding.

11 and EIII is believed to play a major role in receptor binding.

12 n, chemokine activity, and G-protein coupled receptor binding.

13 in regions of the virus capsid that control receptor binding.

14 that the GAG-bound hCXCL1 completely occlude receptor binding.

15 h as capsid maturation, genome uncoating and receptor binding.

16 ing, hormone activity, and G-protein coupled receptor binding.

17 es, the ADCs have been engineered to lack Fc-receptor binding.

18 e encephalitic-specific motifs implicated in receptor binding.

19 of the protein that are critical for GTP and receptor binding.

20 loop and can be buffered by avidity in viral receptor binding.

21 (CROP) domain is involved in or required for receptor binding.

22 nthesis capacity, dopamine release, and D2/3 receptor binding.

23 erization interface to the regions mediating receptor binding.

24 ither saturable nor dependent on clathrin or receptor binding.

25 d transendocytosis and Notch activation upon receptor binding.

26 an be much larger than the effects of ligand-receptor binding.

27 the GRK5 RH/catalytic domain interface upon receptor binding.

28 s on the virion surface and are required for receptor binding.

29 e structural basis of the alterations in the receptor binding activities of these mutants is also dis

30 s have described point mutations that confer receptor-binding activity on NA, albeit in laboratory ra

31 ation by all ligands, largely independent of receptor binding affinities, in line with the similar ST

32 itro proteolytic stability while maintaining receptor-binding affinities, with three candidate peptid

33 osylation, which was in turn correlated with receptor binding affinity by surface plasmon resonance a

34 Receptor binding affinity, in vivo tumor uptake, and bio

35 We characterized the virus receptor-binding affinity, pathogenicity, and transmissi

36 neral chemical approach to introduce various receptor binding agents onto the AAV capsid with site se

37 terminal part of the adhesin consists of the receptor-binding amino acid residues which are involved

38 ge in the viral fusion protein, triggered by receptor binding, an environmental change, or both.

39 The in vivo data, together with FGF receptor binding analysis, indicate that the in vivo out

40 HA is composed of a globular head domain for receptor binding and a stem domain for membrane fusion.

41 opamine release by contrasting baseline D2/3 receptor binding and D2/3 receptor binding following met

42 tions and reveal allosteric changes in the G receptor binding and F-activating stalk domains, providi

43 ological interventions to interrogate 5-HT1B receptor binding and function and determined blood-brain

44 the introduction of a W55T mutation impairs receptor binding and function in the rat alpha9 subunit

45 s for the first time a role in TcdB CROPs in receptor binding and further clarifies the relative role

46 strategy to disentangle the two processes of receptor binding and fusion using synthetic DNA-lipid co

47 mer on the surface of HIV is responsible for receptor binding and fusion.

48 ion and murinization of DTA-1 did not affect receptor binding and glucocorticoid-induced TNFR family-

49 he VP2 protein, a major determinant of viral receptor binding and host specificity.

50 sid at VP2 position 300 can profoundly alter receptor binding and infectivity.

51 idonylglycerol, as well as both greater CB1R receptor binding and lower levels of CB1R messenger RNA

52 he early stage of virus infection, including receptor binding and membrane fusion, making it a potent

53 Our data suggest that the MPSR influences receptor binding and neuraminidase activity via an indir

54 over, we found that the MPSR of HN modulates receptor binding and neuraminidase activity without a co

55 olishes cell-cell fusion, whereas HN retains receptor binding and neuraminidase activity.

56 of CC chemokines are shown to be involved in receptor binding and oligomerization.

57 rogressive S protein destabilization through receptor binding and proteolytic cleavage.

58 er, the most important feature for efficient receptor binding and signaling was the C-terminal helica

59 igands compete with low affinity ligands for receptor binding and signaling.

60 n domains (T-domains) that are essential for receptor binding and the penetration of the Escherichia

61 al blood sampling and served as measures for receptor binding and thus blood-brain barrier penetratio

62 lation leading to reduced asialoglycoprotein-receptor binding and to improved pharmacokinetic propert

63 Receptor binding and triggering are central in Immunolog

64 n regions containing key residues conferring receptor binding and tropism, which suggests a mechanism

65 Here, we monitor individual ligand:receptor binding and unbinding events in space and time

66 the effect of hemagglutinin glycosylation on receptor binding and virulence of engineered H3N2 viruse

67 vealed that TcdBNAP1 and TcdBNAP1V share the receptor-binding and autoprocessing activities but vary

68 ective motifs in subdomain three outside the receptor-binding and dimerization residues of DBP, and i

69 tes pH-driven conformational changes in both receptor-binding and fusion subunits of Lassa virus, ill

70 lycoprotein S, which forms a trimer carrying receptor-binding and membrane fusion functions.

71 210 degrees rotation of the heterohexameric receptor-binding and tripod protein complexes within its

72 le in contributing to higher fusion, reduced receptor binding, and lower neuraminidase activity, whic

73 ial robustly boosted HIV-1 gp120-specific Fc receptor-binding antibodies and ADCC against HIV-1-infec

74 more potently than the combination of single receptor-binding antibodies.

75 Therefore, mGluR5 receptor binding appears to be an effective biomarker in

76 howing a lower IC50 than aflibercept in VEGF receptor binding assays (RBAs) and retaining activity up

77 bizumab for VEGF binding, inhibition of VEGF receptor binding assays (RBAs), and VEGF-driven in vitro

78 Cell-based receptor binding assays confirm that Q8 is a CysLT1 anta

79 t for the peptide was determined using GLP-1 receptor binding assays, immunocytochemistry for the rec

80 By molecular docking and receptor binding assays, we showed that c-CA itself is n

81 Measurement of EDA levels combined with receptor-binding assays might be of relevance to aid in

82 ypothesis,' VEGF and PlGF do not compete for receptor binding at physiological concentrations, though

83 Upon ligand-receptor binding at synapses the receptor is cleaved in

84 lly human anti-CD73, we demonstrated that Fc receptor binding augmented the production of proinflamma

85 x-based micelles as platforms for presenting receptor-binding biologics in a multivalent format that

86 This switch depended on T-cell receptor binding but was largely independent of downstre

87 Recent biochemical evidence suggests that receptor binding by HN is dispensable for cell-cell fusi

88 VEGFR-3, indicating distinct determinants of receptor binding by these growth factors.

89 ceptor [(C5aR)2/C5L2], a seven-transmembrane receptor binding C5a and C5adesArg, remains ill-defined.

90 Agonist-receptor binding causes GDP-to-GTP exchange and dissocia

91 42J rat pancreatic cancer cells to determine receptor binding characteristics.

92 A receptor binding-competent form of EDA1 was the main for

93 achinery, composed of the fusogen gB and the receptor-binding complex gH/gL.

94 Receptor binding correlated with activity in reporter ce

95 using ToxCast in vitro estrogen and androgen receptor binding data and application in an integrated e

96 tigens by single-chain antibodies fused to a receptor-binding-deficient envelope glycoprotein D (gD).

97 d autoradiographic analyses of CRF1 and CRF2 receptor binding densities in female and male naked mole

98 Sex differences were present in CRF2 receptor binding densities, as is the case in multiple v

99 Removal of complement and/or Fc receptor binding did not affect h2G7 efficacy.

100 Mean DAT, D2, and D1 receptor binding did not differ in suicide.

101 e and electrostatic properties important for receptor binding differ significantly between the peptid

102 mmon yet previously unproven assumption that receptor binding does not produce any clustering or spat

103 h includes a translocation domain (HN) and a receptor binding domain (HC).

104 lly protective H7N7 epitopes close to the HA receptor binding domain (RBD) and neuraminidase (NA) cat

105 sites located on two different domains, the receptor binding domain (RBD) and the F activation domai

106 Finally, using a receptor binding domain protein vaccine and a MERS-CoV f

107 le CL40 binds to a site occupied by the gp42 receptor binding domain.

108 on of the three variable regions from the E2 receptor-binding domain (Delta123) increases the ability

109 th chimeric E proteins in which the putative receptor-binding domain (EIII) sequences of other mosqui

110 Efforts focused solely on the receptor-binding domain (RBD) of the viral Spike (S) gly

111 Mutations in its spike (S) protein receptor-binding domain (RBD), a key vaccine target, hav

112 t to shield conserved regions of the EBOV GP receptor-binding domain (RBD), thereby blocking epitopes

113 peptidase 4 (DPP4) via the spike (S) protein receptor-binding domain (RBD).

114 de evidence that the HAstV capsid spike is a receptor-binding domain and that the antibody neutralize

115 nt epitopes on an immunogen comprised of the receptor-binding domain from MERS coronavirus (MERS-CoV)

116 ormational states of the trimer wherein each receptor-binding domain is either tightly packed at the

117 stal structure of ciA-C2 in complex with the receptor-binding domain of BoNT/A1 (HCA1) at 1.68 A reso

118 cted in spike (S) protein are located in its receptor-binding domain which is in direct contact with

119 hat the GAG-binding domain overlaps with the receptor-binding domain, indicating that a GAG-bound che

120 tutions in HA antigenic sites at or near the receptor-binding domain.

121 d there is extensive overlap between GAG and receptor-binding domains.

122 o show that the N9 NA can also contribute to receptor binding due to unusual kinetic characteristics

123 giogenesis have focused on uni-family ligand-receptor binding, e.g., VEGFs bind to VEGF receptors, PD

124 cell function through a multistep process of receptor binding, endocytosis, low pH-induced pore forma

125 ll function through a multistep mechanism of receptor binding, endocytosis, pore formation, autoprote

126 ism for fusion initiation through sequential receptor-binding events and provide a foundation for the

127 ch can promote antibody multimerization upon receptor binding, facilitated anti-OX40 antibody to have

128 show that a putative fifth subunit, nuclear receptor binding factor 2 (NRBF2), is a tightly bound co

129 The attachment (H) protein mediates receptor binding, followed by triggering of the fusion (

130 ting baseline D2/3 receptor binding and D2/3 receptor binding following methylphenidate.

131 2-fold reduction in the level of FcgammaIIIa receptor binding for Remsima.

132 ochemically ER-positive metastases that lack receptor-binding functionality.

133 in human immunity and may act by inhibiting receptor-binding functions of key merozoite invasion lig

134 s, morphologic assessment, Western blotting, receptor binding, gene expression, small interfering RNA

135 arenavirus GPC that consists of an SSP, the receptor-binding GP1, and transmembrane GP2 protein subu

136 magglutinin globular head, and hemagglutinin receptor binding has changed from recognition of a broad

137 Moreover, the receptor binding head group stabilizes the 4HB stalk as

138 Our data suggest that the receptor binding head serves to stabilize the stalk to r

139 From DNA base pairs to drug-receptor binding, hydrogen (H-)bonding and aromaticity a

140 highly conserved substitution that regulates receptor binding in different subtypes.

141 nstream assays were used to characterize ELA receptor binding in human heart and signaling in cells e

142 ully to quantify N-methyl-d-aspartate (NMDA) receptor binding in humans.

143 d point to a multifaceted role for chemokine receptor binding in promoting HIV-1 entry.

144 was a positive correlation between D1 and D2 receptor binding in the dorsal striatum of control subje

145 ide reductase (TorA) signal peptide in TatBC receptor binding in vivo and in vitro We show that besid

146 y a dominance of 5-HT2C on 5-HT2A and 5-HT2B receptor binding; in 5-HT2C-containing heterodimers, lig

147 naptotagmin II, demonstrating that enhancing receptor binding increases the overall efficacy at funct

148 diate and provide the molecular basis of the receptor-binding-induced conformational change required

149 f the trimerous symmetry and distortion at a receptor-binding interface.

150 responsible for skin color, with a vitamin D receptor-binding interval.

151 eyond the realm of 1:1 stoichiometric ligand-receptor binding into a new and immense field of applica

152 e bonds within variable regions required for receptor binding is found within natural gammaretroviral

153 The anchor point for receptor binding is the embrace of an ABO fucose residue

154 mer not only retains similar bioactivity and receptor binding kinetics as native TRAIL in vitro which

155 Ligand-receptor binding kinetics is an emerging topic in the dr

156 Determining how viruses infect new hosts via receptor-binding mechanisms is important for understandi

157 bly located on the apex of the molecule; the receptor-binding mode might be different from that of re

158 A revised toxin-receptor binding model is presented, which is consistent

159 RBDs mutated in multiple key residues in the receptor-binding motif (RBM) of RBD and demonstrated the

160 paviruses, the absence of a conserved ephrin receptor-binding motif in the MojV attachment glycoprote

161 mately 80 residues and has three activities: receptor binding, neuraminidase, and fusion activation.

162 density of mGluR1 transcript allows specific receptor binding of a radioligand to be quantified witho

163 s not clear how the immune system reconciles receptor binding of self-proteins with self/non-self-dis

164 e structures will facilitate studies of EPR3 receptor binding of symbiotically compatible and incompa

165 is suggests two distinct roles for chemokine receptor binding, one to trigger formation of the FI-sen

166 unctionally conserved epitopes important for receptor binding or DBP dimerization.

167 ly less infectious, possibly due to impaired receptor binding or endosomal processing.

168 These residues may participate in receptor binding or provide the protease, lipase, or est

169 ed by blocking any of the following: Fcgamma receptor binding (P = 0.048), eosinophil adhesion (P = 0

170 Scaffold proteins in the PSD are abundant receptor binding partners, yet electron microscopy sugge

171 receptor, the near-complete occupancy of the receptor binding pocket, the dense network of intermolec

172 While antibodies targeting the receptor-binding pocket of HA possess strong neutralizat

173 inant protein design to target the conserved receptor-binding pocket of the hemagglutinin protein and

174 d that these neutralizing mAbs bind near the receptor-binding pocket on HA.

175 ical conformation as it sits deep within the receptor-binding pocket.

176 and calls for investigation of other ligand-receptor binding possibilities.

177 tivity pattern and extrastriatal baseline D2 receptor binding potential and its change after amphetam

178 tic amino acid decarboxylase), baseline D2/3 receptor-binding potential using [(11)C]raclopride (a we

179 reater synthesis capacity showed higher D2/3 receptor-binding potential.

180 onsible for mammalian adaptation and a mixed receptor binding preference.

181 Receptor-binding preference and stability of hemagglutin

182 se, BoNT/A recognizes motoneurons via a dual-receptor binding process in which it engages both the ne

183 eG, and each features a related yet distinct receptor binding profile.

184 nhanced sialic acid content and differential receptor-binding profiles.

185 N9 NA has previously been shown to have receptor binding properties mediated by a sialic acid bi

186 nd even driven the acquisition of altered HA receptor-binding properties and may have contributed to

187 hemical influenza A viral biosensor in which receptor-binding properties have been based on NA was de

188 s in hemagglutinin (HA), causing the altered receptor-binding properties mentioned above.

189 Analysis of the receptor-binding properties of the H7 protein of a human

190 ection of substitutions in H7 that modify H7 receptor-binding properties.

191 of Notch ligands, which has both lipid- and receptor-binding properties.

192 racis, which expresses lethal factor and the receptor-binding protective antigen.

193 usion is orchestrated via interaction of the receptor binding protein (HN, H, or G) with the viral fu

194 Gp45 was identified as the receptor binding protein (RBP) involved in this process

195 The molecular adapter growth factor receptor binding protein 14 (Grb14) is an inhibitor of i

196 Fusion is orchestrated by the receptor binding protein hemagglutinin-neuraminidase (HN

197 virus type and substrate]), which acts as a receptor binding protein, and a fusion (F) protein, whic

198 tinct lineages defined by the immunodominant receptor binding protein, haemagglutinin.

199 E2, the receptor binding protein, has been implicated as a deter

200 ficance: These findings identify an estrogen receptor-binding protein as a critical mediator of HER2-

201 re mediated by the coordinated action of the receptor-binding protein, hemagglutinin-neuraminidase (H

202 This rotation reorients the receptor-binding proteins to point away from the phage h

203 in combination with an antibody that blocks receptor binding, provided full protection against all p

204 s no correlation between striatal DAT and D1 receptor binding (R(2)=0.07, p=0.33), although DAT and D

205 Our data provide insights into the ligand-receptor binding reaction for rhodopsin in particular, a

206 role in the viral life cycle for the second receptor binding region of the HN protein, which is cons

207 , a second intermolecular bridge between the receptor-binding region of the HA and sialic acid on eff

208 cture limited to loops located away from the receptor-binding regions.

209 s as a genomic enhancer where glucocorticoid receptor binding regulates Kappa expression, unraveling

210 ow that the spatial orientation of gp120-CD4 receptor binding relative to the site of TCR engagement

211 gulatory filings, our glycoform analysis and receptor binding results appear to be somewhat different

212 We show that receptor-binding scFvs or small antibody mimetics that h

213 Nuclear receptor-binding SET domain protein 2 (NSD2) is a histon

214 tural and functional similarities of the GP1 receptor binding site (RBS) of these viruses and the rec

215 ith JUNV monoclonal antibodies targeting the receptor binding site (RBS).

216 his change at position 149 was distal to the receptor binding site but affected virus-receptor affini

217 positions 151 to 159 located adjacent to the receptor binding site caused escape from ferret and huma

218 gp350 sequences, noting that the gp350 host receptor binding site is remarkably stable across patien

219 le the HN169R mutation located at the second receptor binding site of the HN protein contributed to a

220 A2, whose promoter has a predicted vitamin D receptor binding site, and XPR1), and one unassociated (

221 alization determinants including the primary receptor binding site, CD4 binding site (CD4bs), is a ma

222 HA) head domain and function by blocking the receptor binding site, preventing infection of host cell

223 ne at position 226 in the hemagglutinin (HA) receptor binding site, which is critical for binding hum

224 tide stretch constitutes part of the CCR5 co-receptor binding site, with the high-mannose patch glyca

225 mino acid deletions within the hemagglutinin receptor binding site.

226 luenza A hemagglutinin (HA) at its conserved receptor binding site.

227 vaccine design, including the conserved CD81 receptor-binding site (CD81bs) that is a key target of b

228 equence space of bnAb C05, which targets the receptor-binding site (RBS) of influenza haemagglutinin

229 The receptor-binding site (RBS) on the HA "head" and a regio

230 ing host receptor sialylated glycans via its receptor-binding site (RBS).

231 t bind conserved viral epitopes, such as the receptor-binding site (RBS).

232 aling lymphocytic activation molecule (SLAM) receptor-binding site and has been implicated in the eme

233 Nonetheless, the evolution of the receptor-binding site and the stem region on HA is sever

234 n, in which mAbs specific for NPC1 or the GP receptor-binding site are coupled to a mAb against a con

235 loop (loop beginning at position 150) of the receptor-binding site common to this subgroup and a uniq

236 ctivity and that antibodies specific for the receptor-binding site located in the head domain of HA t

237 ite in a region homologous to the muscarinic receptor-binding site of Tau suggests that MAP2c also ma

238 the receptor and, conversely, binding to the receptor-binding site of the ligand.

239 structures also augment our understanding of receptor-binding site recognition by antibodies that neu

240 ng to infectious virions at the exposed MARV receptor-binding site, revealing a mechanism of filoviru

241 uitment and structural plasticity within the receptor-binding site.

242 ts of regions distinct from the melanocortin receptor-binding site.

243 ites that extensively overlap the poliovirus receptor-binding site.

244 ultidrug efflux systems MexAB and MexXY as a receptor-binding site.

245 RV GP at or near the predicted region of the receptor-binding site.

246 rlap the antibody epitope and may comprise a receptor-binding site.

247 To date, a receptor/binding site for 20-HETE has been implicated ba

248 to a 1-site model, and the maximum number of receptor binding sites (Bmax) values were derived from b

249 ons of amino acids in the 220 loop of the HA receptor binding sites (RBSs).

250 s border sequences carrying aryl hydrocarbon receptor binding sites and enhancer-specific histone mod

251 sults highlight the subtle interplay between receptor binding sites in IgE-Fc and their affinities, t

252 aphic studies to map the distribution of CRF receptor binding sites in the mouse brain.

253 The ability to bind two distinct receptor binding sites simultaneously can allow the sele

254 scribes recent efforts to target alternative receptor binding sites with drugs that act as allosteric

255 To define CGRP receptor binding sites, in vitro autoradiography was per

256 interactions of the Env protein at host cell receptor binding sites, inhibit cell infection, and caus

257 /EBPbeta, retinoid X receptor, and vitamin D receptor binding sites, whereas adipocyte differentiatio

258 get cells or eliminating competent chemokine receptor-binding sites on Env trimers resulted in a loss

259 is allosteric communication between the two receptor-binding sites, which we now know are located at

260 riched for both enhancer marks and oestrogen receptor-binding sites.

261 usion behavior across viruses with different receptor binding specificities.

262 The 190V in HA does not affect virus receptor binding specificity but enhances binding affini

263 te that 190V in the HA does not change virus receptor binding specificity but enhances virus binding

264 seal H3N8 virus has retained its avian-like receptor binding specificity, but could potentially esta

265 c traits of influenza viruses (hemagglutinin receptor binding specificity, hemagglutinin pH of activa

266 ults demonstrate that the CTR domain confers receptor-binding specificity of RELN.

267 irmed these findings and revealed avian-like receptor-binding specificity.

268 Virus sequence analysis and virus receptor binding studies highlighted potential markers r

269 Neutralisation of the high-affinity IL-15 receptor binding subunit, IL-15ralpha in elderly myotube

270 fusion subunit, one-fourth recognize the GP1 receptor-binding subunit and the remaining fourth are sp

271 lex consisting of a stable-signal peptide, a receptor-binding subunit, GP1, and a viral-host membrane

272 In the pre-fusion conformation, the receptor-binding subunits, S1, rest above the fusion-med

273 xing kinetics are found to be independent of receptor binding, supporting the common yet previously u

274 nto the Skint family, identifying a putative receptor binding surface that directly implicates Skint-

275 , disrupts this interaction by targeting the receptor-binding surface of the GP1 glycoprotein from Ju

276 conserved IR domains, unmasking an invariant receptor-binding surface that spans both insulin A and B

277 Thus, although Tyr(B26) is part of insulin's receptor-binding surface, our results suggest that its c

278 the trimerization surface, which is also the receptor-binding surface, suggests a feature called the

279 achment glycoproteins, in particular at host receptor-binding surfaces.

280 In vitro receptor-binding techniques were used to measure alpha1-

281 The structures reveal a unique mode of receptor binding that is dependent on the oligomeric ass

282 hat residues B24-B30 detach from the core on receptor binding, the environment of 3-I-Tyr(B26) in a r

283 ns of the protein surface to antibody or CD4 receptor binding; the number of glycans that can potenti

284 affinity and can be appreciably depleted by receptor binding, then negative cooperativity produces a

285 rmational changes introduced by antibody and receptor binding to be deciphered.

286 of use to elucidate the kinetics of integrin receptor binding to ECM proteins for homeostatic and dis

287 echanistic details regarding the coupling of receptor binding to F activation are not fully understoo

288 riments to evaluate the kinetics of integrin receptor binding to hepatic ECM proteins.

289 tional regulation by the GR requires dynamic receptor binding to specific target sites located across

290 paradigm for IL-23 and IL-12 whereby cognate receptor binding to the helical cytokine subunits primes

291 and enhanced the affinity of glucocorticoid receptor binding to the promoter region of KLF15 In thre

292 affinity and the stoichiometry of chemokine receptor binding to trimeric Env.

293 te receptor for the P4 region, but the other receptor, binding to P2 region, remained unknown.

294 operties of the sialidase site which promote receptor binding via this site and which enhance binding

295 In the rostral cortex, D1 receptor binding was 22% lower in zQ175 than WT animals.

296 ing (R(2)=0.07, p=0.33), although DAT and D1 receptor binding was positively correlated in subjects w

297 transporter (DAT)-binding sites, but D2-like receptor binding was unaffected.

298 ly reported data on altered phospholipid and receptor binding, we hypothesize that mutations destabil

299 Images of mGluR5 receptor binding were acquired in 14 long-term ex-smoker

300 rged; the sCT C-terminal Pro was crucial for receptor binding, whereas the AC413/rAmy C-terminal Tyr