ライフサイエンスコーパス: receptor binding

1 complex revealed an epitope that blocks ACE2 receptor binding.

2 olved in functional allosteric dynamics upon receptor binding.

3 1T mutations completely abolished human-like receptor binding.

4 sulfate molecule for specific, high affinity receptor binding.

5 for therapies targeted at transient TCR:CD3 receptor binding.

6 utionarily constrained by its involvement in receptor binding.

7 surface protein that increase stability and receptor binding.

8 of which perform essential functions such as receptor binding.

9 HC) administration decreased hippocampal CB1 receptor binding.

10 in "open" state structures formed after CD4 receptor binding.

11 l orientation and conformation to facilitate receptor binding.

12 fibre knob is sufficient to totally abolish receptor binding.

13 he substitutions frequently led to decreased receptor binding.

14 iograms and predominantly exhibited sigma(1)-receptor binding.

15 sessed the role of this modification in host receptor binding.

16 1 structures with fewer clashes and stronger receptor binding.

17 hondroitin-4-sulfate, suggesting a model for receptor binding.

18 not compete with transferrin or ferritin for receptor binding.

19 tinct epitopes, but both VHHs interfere with receptor binding.

20 evealed conformational changes that occur on receptor binding.

21 nderstanding of the basis of influenza virus receptor-binding.

22 ting directional configuration of ligands on receptor binding activities.

23 ine levels in kratom, we compared the opioid receptor binding activity of speciofoline, mitragynine,

24 In this review, we summarize receptor-binding adaptations underlying the emergence of

25 isplayed moderate GAT activities and GABA(A) receptor binding affinities in the mid-nanomolar range (

26 B-chain C-terminal octapeptide, has similar receptor binding affinity to human insulin.

27 a dose-dependent manner determined by opioid receptor binding and [(35)S] guanosine 5'-3-O-(thio)trip

28 e a ligand trap for BMP9, preventing type II receptor binding and BMP9 signaling.

29 The spike (S) protein of SARS-CoV-2 mediates receptor binding and cell entry and is the dominant targ

30 gG responses, accompanied by compromised Fcy receptor binding and Fc effector activity, pointing to d

31 re evaluated for their opioid and adrenergic receptor binding and functional effects, in vivo antinoc

32 h the Fc of IgG is critically important, the receptor binding and functional properties of the Fc are

33 The coronavirus S-protein mediates receptor binding and fusion of the viral and host cell m

34 rge, linker chemistry and ligand identity on receptor binding and internalization.

35 have as AND-gates since they emit only after receptor binding and intracellular activation, showing e

36 , LSD1 inhibition broadly disrupted androgen-receptor binding and its transcriptional output, and dra

37 Both receptor binding and membrane fusion activities are medi

38 HA enables viral entry into host cells via receptor binding and membrane fusion and is a validated

39 Here we investigated receptor binding and protease activation of SARS-CoV-2 s

40 Moving forward, the results argue that both receptor binding and proteolytic cleavage of the spike a

41 s to the molecular mechanism that drives CSP receptor binding and revealed that the pan-group cyclic

42 ssion has been primarily limited to regional receptor binding and single-label transcript expression

43 to HA, which was associated with reducing HA receptor binding and subsequently balancing HA-NA functi

44 y fitted a mathematical model of competitive receptor binding and suggests normalization of OSN ensem

45 ecular events that take place between ligand-receptor binding and target gene transcription.

46 n on gD that is independent of that used for receptor binding and which likely represents the gH/gL i

47 poE have illuminated the physiology of ApoE, receptor binding, and interaction with amyloid-beta (Abe

48 expression across layers, heteromeric nAChR receptor binding, and nAChR excitability of A1 L5 cells.

49 CoV-2 reagents for detecting the presence of receptor-binding antibodies in sera.

50 ation of schizophrenia, SEP-363856, a non-D2-receptor-binding antipsychotic drug, resulted in a great

51 OE and positively charged amino acids at the receptor-binding area suggested that glycosylation inter

52 Human Fc receptor binding assays and analysis of antibody-cell in

53 urfaces, such as membrane remodeling, ligand-receptor binding, assembly of protein complexes, and cha

54 nti-MHC-I mAb that blocks NK cell inhibitory receptor binding at a site distinct from the TCR binding

55 he process must be curtailed by trapping Env-receptor binding at an intermediate stage.

56 ld difference in log-probability of androgen receptor binding at the variant rs2680708 (17q22).

57 51T substitutions in HA, resulted in reduced receptor-binding avidity toward both human and avian-lik

58 The entirely different receptor binding behavior of (R)- (11)C-Me-NB1 and (S)-

59 ABM300 was characterized in vitro (receptor binding, beta-arrestin2 recruitment, ERK1/2 pho

60 spike proteins and competitively blocks ACE2 receptor binding, by overlapping the ACE2 structural bin

61 in of SARS-CoV-2 has a 10- to 20-fold higher receptor-binding capacity compared with previous pandemi

62 Host cell receptor binding causes conformational changes in the at

63 onds (NGO-BBN-AF750), and investigated their receptor binding, cell uptake and internalization in HSC

64 Based on known receptor binding characteristics, we hypothesized that t

65 nization, mast cell activation, CC-chemokine receptor binding, circulating immunoglobulin complex, se

66 its receptor to explain its weaker FcgammaRI receptor binding compared to our best-fit IgG1 structure

67 Whilst receptor binding contributes to the viral host range, S-

68 ing antibodies (nAbs) to two epitopes on the receptor binding domain (RBD) and to distinct non-RBD ep

69 a, pro-inflammatory cytokines, and high anti-receptor binding domain (RBD) antibody levels.

70 ptom onset (DPSO), whereas the salivary anti-receptor binding domain (RBD) IgG response yielded 100%

71 sma containing high-titer anti-spike protein receptor binding domain (RBD) IgG significantly decrease

72 , in which the highly immunogenic and mobile receptor binding domain (RBD) is either locked in the al

73 ining sensing electrodes was pre-coated with receptor binding domain (RBD) of SARS-CoV-2 spike protei

74 nvalescent SARS patient, in complex with the receptor binding domain (RBD) of the SARS-CoV-2 spike (S

75 cFv, and VH libraries by panning against the receptor binding domain (RBD) of the SARS-CoV-2 spike (S

76 The receptor binding domain (RBD) of the SARS-CoV-2 spike gl

77 ed nucleoside-modified mRNA that encodes the receptor binding domain (RBD) of the SARS-CoV-2 spike pr

78 The SARS-CoV-2 receptor binding domain (RBD) of the spike protein binds

79 ibodies against the nucleocapsid (N) and the receptor binding domain (RBD) of the spike protein.

80 EY6A Fab binds the receptor binding domain (RBD) of the viral spike glycopr

81 se optimized receptor traps tightly bind the receptor binding domain (RBD) of the viral spike protein

82 an ACE2 helix that interacts with the spike receptor binding domain (RBD) or docked against the RBD

83 binds host cells via a trimeric spike whose receptor binding domain (RBD) recognizes angiotensin-con

84 Notably, IgG against the spike receptor binding domain (RBD) was predictive of survival

85 ng activity by disrupting the interaction of receptor binding domain (RBD) with angiotensin-convertin

86 ed IgG, IgM, and IgA antibodies to the spike receptor binding domain (RBD), S1+S2, nucleocapsid, and

87 a fragment of the coronavirus spike protein receptor binding domain (RBD), the hexapeptide YKYRYL on

88 interaction between ACE2 and the SARS-CoV-2 receptor binding domain (RBD).

89 ome coronavirus 2 (SARS-CoV-2) spike protein receptor binding domain (RBD).

90 ously identified betacoronaviruses include a receptor binding domain and a unique insertion of 12 nuc

91 wo unique features in its spike protein, the receptor binding domain and an insertion of 12 nucleotid

92 es that bind to the SARS-CoV-2 spike protein receptor binding domain and block spike protein interact

93 st that treatment of COVID-19 with high anti-receptor binding domain IgG titer convalescent plasma is

94 length SARS-CoV-2 spike protein or the spike receptor binding domain in mice.

95 e S1 subunit of the spike protein and to the receptor binding domain of SARS-CoV-2 in human serum and

96 dual antibodies that simultaneously bind the receptor binding domain of the spike protein, thereby pr

97 isotypes that are specific to the SARS-CoV-2 receptor binding domain of the spike protein.

98 rs that neutralize SARS-CoV-2 and target the receptor binding domain that engages human angiotensin-c

99 ssion with plasma with an anti-spike protein receptor binding domain titer of >=1:1350.

100 ialysis in July, 2020, using a spike protein receptor binding domain total antibody chemiluminescence

101 (enzymatic domain, translocation domain and receptor binding domain) are targets for neutralizing an

102 cans, with the notable exception of the ACE2 receptor binding domain, and also that the degree of shi

103 Spike protein subunits S1 and receptor binding domain, and nucleoprotein were coupled

104 with serum neutralization assays as well as receptor binding domain-specific IgA; however, the frequ

105 nfected with SARS-CoV-2, in complex with the receptor binding domain.

106 , which is located in close proximity to the receptor binding domain.

107 among anti-spike ectodomain (anti-ECD), anti-receptor-binding domain (anti-RBD) IgG titers, and SARS-

108 eceptors, an extended loop in the C-terminal receptor-binding domain (HC) of BoNT/B (HC/B) has been p

109 its receptor human ACE2 (hACE2) through its receptor-binding domain (RBD) and is proteolytically act

110 eractions between the SARS-CoV spike protein receptor-binding domain (RBD) and its host receptor angi

111 V-2 S protein variants with mutations in the receptor-binding domain (RBD) and N-terminal domain that

112 antibody fragment (Fab) with the SARS-CoV-2 receptor-binding domain (RBD) and negative-stain electro

113 ssays for detection of SARS-CoV-2 Abs to the receptor-binding domain (RBD) and nucleocapsid protein i

114 y divided between those directed against the receptor-binding domain (RBD) and those directed against

115 Antibodies targeting the SARS-CoV-2 spike receptor-binding domain (RBD) are being developed as the

116 tions of these antibodies with the S protein receptor-binding domain (RBD) are compared with those be

117 distinct antigenic sites, including several receptor-binding domain (RBD) epitopes as well as non-RB

118 The receptor-binding domain (RBD) is immunodominant and the

119 so was more susceptible to neutralization by receptor-binding domain (RBD) monoclonal antibodies and

120 ology to search for antibodies targeting the receptor-binding domain (RBD) of CoV-2.

121 Here, we analyzed the N-glycosylation of the receptor-binding domain (RBD) of IBV strain M41 spike pr

122 monoclonal antibody (MAb), which targets the receptor-binding domain (RBD) of Middle East respiratory

123 with most neutralizing mAbs recognizing the receptor-binding domain (RBD) of S.

124 noncovalent complexes formed by ACE2 and the receptor-binding domain (RBD) of the S-protein.

125 The receptor-binding domain (RBD) of the SARS-CoV-2 spike pr

126 on of ultrapotent sdAbs directed against the receptor-binding domain (RBD) of the SARS-CoV-2 Spike pr

127 ed immunosorbent assay utilizing recombinant receptor-binding domain (RBD) of the SARS-CoV-2 spike pr

128 alizing antibodies that target the host ACE2 receptor-binding domain (RBD) of the severe acute respir

129 entry of the virus into cells depends on the receptor-binding domain (RBD) of the spike (S) protein o

130 ied mRNA vaccine that encodes the trimerized receptor-binding domain (RBD) of the spike glycoprotein

131 -interacting surface (ACE2IS) located in the receptor-binding domain (RBD) of the spike protein can n

132 e we determined the crystal structure of the receptor-binding domain (RBD) of the spike protein of SA

133 nomolar affinity and high specificity to the receptor-binding domain (RBD) of the spike protein.

134 frequently used IGHV gene for targeting the receptor-binding domain (RBD) of the spike protein.

135 responses to coronaviruses mainly target the receptor-binding domain (RBD) of the trimeric spike.

136 tropism by studying interactions between the receptor-binding domain (RBD) of the viral attachment pr

137 RS-CoV-2, are primarily directed against the receptor-binding domain (RBD) of the viral spike protein

138 er competition with hACE2 for binding to the receptor-binding domain (RBD) or allosteric interference

139 Notably, residues of receptor-binding domain (RBD) showing crucial interactio

140 d with BG505.SOSIP.664 (SOSIP) or SARS-CoV-2 receptor-binding domain (RBD) was readily recognized by

141 The Spike protein of SARS-CoV-2, its receptor-binding domain (RBD), and its primary receptor

142 extracellular spike glycoprotein and at the receptor-binding domain (RBD)-receptor interface, sugges

143 imited clonal expansion, and three bound the receptor-binding domain (RBD).

144 ensin-converting enzyme 2 (ACE2) through its receptor-binding domain (RBD).

145 SAs to detect the full-length S protein or S receptor-binding domain (S-RBD); and an IgG avidity assa

146 d CDTb were of particular interest since the receptor-binding domain 1 lacks sequence homology to any

147 e homology to any other known toxin, and the receptor-binding domain 2 is completely absent in other

148 A neurotoxin-like sequence motif on the receptor-binding domain also exhibits a high tendency to

149 antibodies developed against the MERS spike receptor-binding domain and S2 portion are ineffective i

150 that the IgM, A, and G Ab responses against receptor-binding domain are significantly correlated to

151 s of two mAbs in complex with the SARS-CoV-2 receptor-binding domain at 2.55 and 2.70 angstrom reveal

152 Here, the glycan interacts with the receptor-binding domain D of the toxin.

153 d high-molecular-weight (HMW) form of the E2 receptor-binding domain lacking three variable regions,

154 says, we found that cross-linking the sigma1 receptor-binding domain modulates reovirus attachment bu

155 SARS-CoV-2 uses the receptor-binding domain of its spike protein S1 to attac

156 The receptor-binding domain of SARS-CoV-2 has a 10- to 20-fo

157 t the introduction of a cysteine pair in the receptor-binding domain of sigma1 yielded a virus that r

158 ell as authentic SARS-CoV-2, by engaging the receptor-binding domain of the S glycoprotein.

159 nt neutralizing activity and fully block the receptor-binding domain of the S protein (S(RBD)) from i

160 owed that Simeprevir and Lumacaftor bind the receptor-binding domain of the Spike protein with high a

161 S-CoV-2, and prevents the interaction of the receptor-binding domain of the viral spike protein with

162 assays with both the trimeric spike and the receptor-binding domain proteins.

163 2+) binding site was discovered in the first receptor-binding domain that is important for its stabil

164 important for its stability, and the second receptor-binding domain was found to be critical for hos

165 otency of antibodies targeting the S protein receptor-binding domain was not attenuated.

166 virus enters host cells through binding of a receptor-binding domain within its trimeric spike glycop

167 etection of human SARS-CoV-2 Abs against the receptor-binding domain, including an Ag sandwich ELISA

168 sible 3686 future mutations on the S protein receptor-binding domain, we show that most likely future

169 ss-reactive antibody titers specific for the receptor-binding domain.

170 a panel of murine mAbs directed against the receptor-binding domain.

171 ich encodes a secreted trimerized SARS-CoV-2 receptor-binding domain; or BNT162b2, which encodes a me

172 odies to SARS-CoV-2 spike S1 protein and its receptor-binding-domain (RBD) are detected at a limit-of

173 ke in a fully inactive conformation with its receptor binding domains locked into their inaccessible

174 oV-2 spike (S) glycoprotein reveals that the receptor binding domains tightly bind the essential free

175 article vaccines display 60 SARS-CoV-2 spike receptor-binding domains (RBDs) in a highly immunogenic

176 ant state of the trimer has one of the three receptor-binding domains (RBDs) rotated up in a receptor

177 The SARS-CoV-2 spike employs mobile receptor-binding domains (RBDs) to engage the human ACE2

178 The prefusion trimer has three receptor-binding domains clamped down by a segment adjac

179 Roles played by 2 receptor-binding domains of activated CDTb were of parti

180 oV-2 S uses ACE2 to enter cells and that the receptor-binding domains of SARS-CoV-2 S and SARS-CoV S

181 erent regions of the shell domain, including receptor-binding domains.

182 f a quaternary epitope spanning two adjacent receptor-binding domains.

183 e the role of cholesterol in IAV fusion from receptor binding effects.

184 and Nrg3 in this process is not due to their receptor-binding EGF-like domain, but rather to their di

185 MYDGF and identify its functionally relevant receptor binding epitope.

186 raminidase (HN) functionality, it presents a receptor-binding face incongruent with sialic acid recog

187 ssion, animal models, and molecular basis of receptor binding for SARS-CoV-2.

188 f complement and ability to mediate FC-gamma-receptor binding, for immunotherapeutically enhanced hK2

189 plex stability, beta167-169 RGD loop, T-cell receptor binding, formation of homodimer of alpha-beta h

190 1, IgG2, and IgG4 subclasses and explain the receptor-binding functions of IgG2.

191 ibody m102.4 binds to the immunodominant NiV receptor-binding glycoprotein (GP), and potently neutral

192 In the case of influenza, the receptor-binding glycoprotein is the haemagglutinin (HA)

193 f entry glycoproteins, including the diverse receptor-binding glycoproteins (HSV-1 glycoprotein D (gD

194 es, each species uses distinct receptors and receptor-binding glycoproteins.

195 tortion that is imposed by the biophysics of receptor binding, here we show that it also plays an imp

196 Following receptor binding, IFN-I is siloed into endosomal compart

197 , and intramolecular RNA tetraloop-tetraloop receptor binding, illustrating the potential general uti

198 uses (CoVs) has been attributed to a gain in receptor binding in a new host.

199 The assay allowed kinetic analysis of ligand-receptor binding in living HEK293 cells, competition bin

200 ontaining both a stabilized HA and alpha-2,6 receptor binding in tandem pose greater pandemic risk.

201 nbound and expanded virus particles suggests receptor binding initiates a cascade of conformational c

202 acement of G29, a residue at the edge of the receptor binding interface and the center of the structu

203 Exchanging the receptor-binding interfaces between TcsL and TcdB switch

204 several differences between the ligand- and receptor-binding interfaces, providing an explanation fo

205 of a ligand configure conditions for ligand-receptor binding is a key to accurate assessment of toxi

206 Fusion activation after receptor binding is proposed to involve the exposure of

207 that proteolytic cleavage of the spike, not receptor binding, is the primary infection barrier for t

208 pe and limitations, and also enlighten their receptor binding mode.

209 d by natural mutations via modulation of the receptor-binding mode.

210 relatively low amino acid similarity in the receptor binding module.

211 produced by Bacillus anthracis, comprises a receptor-binding moiety, protective antigen and the leth

212 an epitope that overlaps with the human ACE2 receptor binding motif providing a structural basis for

213 the sequence of 2019-nCoV RBD, including its receptor-binding motif (RBM) that directly contacts ACE2

214 r results explain the immunodominance of the receptor-binding motif and will guide the design of COVI

215 s leading to the identification of two major receptor-binding motif antigenic sites.

216 ation, we predict that a few residues on the receptor-binding motif, i.e., 452, 489, 500, 501, and 50

217 any sarbecoviruses detected to date, and its receptor-binding motif, important for specificity to hum

218 nstrate that O-glycans positioned within the receptor binding motifs of members of the neuropeptide Y

219 n have been described, little is known about receptor binding of TcAs.

220 CXCR4 also results in monomerization of the receptor, binding of IT1t to this variant promotes recep

221 changes of the S protein triggered by either receptor binding or high pH.

222 on of C1q binding did not compromise Fcgamma-receptor binding or in vitro phagocytosis.

223 al changes of S proteins triggered by either receptor binding or pH 8.0.

224 it is unclear whether modulation of cytokine-receptor binding parameters can modify biological outcom

225 s, either individually or in combination, on receptor binding, pH of fusion, thermal stability, and v

226 y structures, changes in the 220-loop of the receptor-binding pocket caused similar interactions with

227 raction of the chemokine N terminus with the receptor-binding pocket is the key driver of signaling,

228 ssion tomography were used to measure D(2/3) receptor binding potential in cortical regions of intere

229 It is not determined by receptor binding preference but is determined by other m

230 und that this phenotype is determined not by receptor binding preference but is determined by other m

231 pdm09 harboring the D222G substitution has a receptor-binding preference for alpha-2,3-linked sialic

232 iliated with drift have implications for the receptor binding properties of these viruses, affecting

233 Receptor binding properties, pH thresholds for HA activa

234 st in correlating peptide heterogeneity with receptor-binding properties.

235 man monoclonal antibodies (mAbs) against HeV receptor binding protein (RBP).

236 less dependence on interaction by the viral receptor-binding protein with known MeV receptors.

237 n IAVs into humans is the specificity of the receptor-binding protein, hemagglutinin (HA), which reco

238 subunit transcript expression (message) and receptor binding (protein) were observed in L2-6, most p

239 such as high-affinity, environmentally hardy receptor-binding proteins.

240 Coupled with receptor binding, proteolytic activation offers a new pa

241 to have a highly unusual structure with the receptor binding protruding (P) domain only loosely teth

242 identity and concentration using an odorant-receptor binding rate tensor, modulated by the odorant c

243 TLR2-mediated response to HBV, suggesting a receptor binding-related mechanism.

244 rs with a human IgG1 Fc part competent in Fc receptor binding resulted in an almost 10-fold superior

245 ng basic amino acids at the interface of the receptor binding (S1) and fusion (S2) domains.

246 Loss of HE receptor binding selected for second-site mutations in S

247 specific substitutions within the C-terminal receptor-binding sequence, reduced metabolization and im

248 ture, which revealed enrichment for androgen receptor binding sequences and hypomethylation of these

249 Histone methyltransferases of the nuclear receptor-binding SET domain protein (NSD) family, includ

250 neutralizing Ab MR78 that is specific to the receptor binding site (RBS) of MARV glycoprotein (GP).

251 21 mutant viruses, most substitutions in the receptor binding site (RBS) resulted in viable virus, bu

252 standing the specific amino acids around the receptor binding site (RBS) that were important in elici

253 volving the fastest, that are closest to the receptor binding site (RBS), and that are exposed to sol

254 idues in the Sa antigenic region, around the receptor binding site (RBS), served as signatures for th

255 ing host receptor-induced exposure of the co-receptor binding site and fusion elements.

256 tudy showed substantial diversity within the receptor binding site of H5N1 during human infection.

257 al genetic diversity was detected within the receptor binding site of hemagglutinin of HPAI A/H5N1 vi

258 some of the positions were located near the receptor binding site of the HA protein, as they are in

259 e divergence in the amino acids at the Spike receptor binding site on these proteins.

260 n GDF5 signaling, RGMs occupy the BMP type 1 receptor binding site similar to the observed interactio

261 a highly conserved epitope, distal from the receptor binding site, that enables cross-reactive bindi

262 T epitope on SEB overlapped with the T-cell receptor binding site, whereas other evidence suggested

263 directly to gD at sites distinct from the gD receptor binding site.

264 binding sites, and within or close to the HA receptor binding site.

265 highly conserved epitope, away from the ACE2 receptor binding site.

266 HA stem domain [2-12], the less conserved HA receptor-binding site (RBS) [13-16], as well as conserve

267 P increased accessibility of epitopes in the receptor-binding site (RBS) for neutralizing mAbs, resul

268 al flexibility: it modulates exposure of its receptor-binding site and subsequently undergoes complet

269 m closed to open conformations to expose its receptor-binding site and, subsequently, from prefusion

270 ural analysis of both RBDs suggests that the receptor-binding site for QX is located at a different l

271 of SEMA6A/6B via a region homologous to the receptor-binding site in Clostridioides difficile toxin

272 The CedV G receptor-binding site is structurally distinct from othe

273 et positive charge around the haemagglutinin receptor-binding site show increases and decreases in av

274 er loop, at a site that is distinct from the receptor-binding site.

275 the E2 domain B and overlaps with the Mxra8 receptor-binding site.

276 n immunodominant site, which may overlap the receptor-binding site.

277 elements of both the allosteric ligands and receptor binding sites important for these allosteric ac

278 along their complete sequences and providing receptor binding sites on both membrane sides.

279 age-specific transcription factors, estrogen receptor binding sites were also found to have elevated

280 es in this factor were enriched for androgen receptor binding sites.

281 (Fabs) and preserves steric accessibility to receptor-binding sites, likely influencing antigen bindi

282 n in vitro All substitution mutants retained receptor binding specificity, but the substitutions freq

283 that supports adaptation of human-preferred receptor-binding specificity by the hemagglutinin (HA) s

284 erfaces between TcsL and TcdB switches their receptor-binding specificity.

285 nd virion incorporation of glycoprotein O, a receptor binding subunit for an envelope glycoprotein co

286 ists of the stable signal peptide (SSP), the receptor-binding subunit GP1, and the transmembrane subu

287 t cholesterol compositions is independent of receptor binding, suggesting that cholesterol-mediated s

288 IP(6) interacts with the receptor-binding surface of arrestin-3, induces arrestin

289 ins are organized and interact to create the receptor-binding surface, limiting efforts to exploit it

290 g-range allosteric communication between the receptor binding surfaces and the core of the IL-2 struc

291 developed a neurochemical model of dopamine receptor binding taking into account the different kinet

292 larger, virus-membrane-distal, HA1 mediates receptor binding; the smaller, membrane-proximal, HA2 an

293 oline fragments that disrupt TNFalpha ligand-receptor binding through an allosteric desymmetrization

294 of toxic potencies, linking molecular ligand-receptor binding to in vitro responses.

295 -located GRP78 has been reported to act as a receptor binding to the active form of alpha(2)-macroglo

296 y, interactions with HSPG, and Lrp5-mediated receptor binding, to regulate zebrafish brain developmen

297 and leads to reduced [(11)C]raclopride D2/3 receptor binding via competitive displacement.

298 In all of the mAbs, Fc receptor binding was abrogated by Trx activity, with sig

299 CD47 receptor binding was demonstrated by immunofluorescence.

300 Receptor binding was studied with activated human periph