ライフサイエンスコーパス: RBD

1 RBD was diagnosed by reported dream-enactment symptoms o

2 RBD-binding IgG concentrations and SARS-CoV-2 neutralizi

3 RBD-CRD exhibits dynamic interactions with the membrane

4 oscopy revealed a higher percentage of the 1-RBD "up" conformation in the G614 spike, suggesting incr

5 divided into 24 RBD-negative (PDRBD-) and 13 RBD-positive cases (PDRBD+) and a comparator group of 22

6 rt III, Geriatric Depression Scale (GDS-15), RBD medication use, total levodopa equivalent daily dose

7 ptide to the binding interface between CoV-2 RBD and ACE2, which we investigate using 20 independent

8 ats showed high binding specificity to CoV-2 RBD and the spike antigens in different assay systems.

9 al discharge were also tested for SARS-CoV-2 RBD antibodies in 95 patients.RESULTSAntibodies develope

10 ion of the coronavirus-2 spike protein CoV-2 RBD at ACE2.

11 that set of simulations, we find that CoV-2 RBD does not bind to ACE2 with the binding motif shown i

12 CoV RBD, an ACE2-binding ridge in SARS-CoV-2 RBD has a more compact conformation; moreover, several r

13 First, SARS-CoV-2 RBD has higher hACE2 binding affinity than SARS-CoV RBD,

14 These structural features of SARS-CoV-2 RBD increase its ACE2-binding affinity.

15 ches to ACE2 so that the activation of CoV-2 RBD might be inhibited in this case.

16 of interactions between ACE2 and SARS-CoV-2 RBD or similar systems.

17 r, several residue changes in the SARS-CoV-2 RBD stabilize two virus-binding hotspots at the RBD-ACE2

18 peptide on the assembly process of the CoV-2 RBD to ACE2 in long-time enhanced correlation guided MD

19 f SARS-CoV spike, suggesting that SARS-CoV-2 RBD, albeit more potent, is less exposed than SARS-CoV R

20 a highly conserved epitope on the SARS-CoV-2 RBD, mainly through a long complementarity-determining r

21 observe that the hexapeptide binds to CoV-2 RBD, which has the effect that this protein only weakly

22 on of the interaction between ACE2 and CoV-2 RBD.

23 zyme 2 (ACE2)-interacting sites on the CoV-2 RBD.

24 ufacturing efforts to advance the SARS-CoV-2-RBD nanoparticle vaccine into the clinic.

25 ith Parkinson's disease were divided into 24 RBD-negative (PDRBD-) and 13 RBD-positive cases (PDRBD+)

26 ects on conversion rate were analyzed in 432 RBD patients with available data using Kaplan-Meier surv

27 108 participants (43 TBI, 26 PD, 8 RBD, 31 controls) were assessed.

28 ll not disrupting the ACE2 homodimer or ACE2-RBD interfaces.

29 We first computationally designed the ACE2-RBD interface using a two-stage flexible protein backbon

30 istic information on attenuation of the ACE2/RBD association by heparin, the study demonstrates the y

31 he role of heparin in destabilizing the ACE2/RBD association to be studied, providing critical inform

32 ve human semisynthetic phage library against RBD, leading to the identification of a high-affinity si

33 and long-lasting antibody responses against RBD from SARS-CoV-2.

34 at the antibodies recognize the closed, 'all RBD-down' conformation of the spike.

35 We structurally defined an RBD antigenic map and serologically quantified serum Abs

36 Here, we designed an RBD mutant that disrupts the ACE2IS and used it to chara

37 Presentation of this cryptic epitope in an RBD-based vaccine might advantageously focus immune resp

38 angstrom-resolution crystal structure of an RBD-EY6A Fab complex identifies the highly conserved epi

39 between angiotensin-converting enzyme 2 and RBD complexes.

40 abs, revealing recognition of both S1(A) and RBD epitopes on SARS-CoV-2 spike.

41 he overall affinity between the membrane and RBD-CRD.

42 We test whether TBI, PD and RBD have distinct striatal dopamine abnormalities using

43 healthy controls, patients with early PD and RBD.

44 Sensing of S1 and RBD antibodies is specific, which cross-reacts neither w

45 Although anti-RBD immunoglobulin G (IgG) levels generally correlated w

46 al memory CD4(+) T cells and anti-S and anti-RBD, but not anti-NC antibody levels.

47 on of enzyme-linked immunosorbent assay anti-RBD IgG titer facilitated selection and transfusion of t

48 nti-ECD), anti-receptor-binding domain (anti-RBD) IgG titers, and SARS-CoV-2 virus neutralization (VN

49 titers of >=1:160, and all of them had anti-RBD titers of >=1:1350.

50 ositive correlation between both plasma anti-RBD and anti-ECD IgG titers and in vitro VN titers.

51 Plasma anti-RBD or anti-ECD titers of >=1:1350 may provide critical

52 We conclude that anti-RBD or anti-ECD IgG titers can serve as a surrogate for

53 for COVID-19 treatment, was >=80% when anti-RBD or anti-ECD titers were >=1:1350.

54 50 and strong positive correlation with anti-RBD and VN titers.

55 reacts neither with other antibodies such as RBD, S1, and nucleocapsid antibody nor with proteins suc

56 ted nanobodies, H11-D4 and H11-H4, that bind RBD (K(D) of 39 and 12 nM, respectively) and block its i

57 hat neutralize pseudovirus cell entry, block RBD interaction with ACE2, and inhibit live virus replic

58 Surprisingly, both RBD-RNA specificity and disordered segments of key prote

59 ed only 1 sample with seroreactivity to both RBD and S2 that lacked neutralizing antibodies.

60 n their membrane dynamics, with CRD bringing RBD closer to the membrane that impacts its accessibilit

61 ed during natural SARS-CoV-2 infection or by RBD-based vaccines.

62 Using chimeric RBD proteins, we discovered that the region encompassing

63 bable RBD and polysomnographically confirmed RBD were analyzed separately and combined.

64 a-synucleinopathy patients than in controls, RBD was more likely to develop in dementia with Lewy bod

65 In comparison with the SARS-CoV RBD, an ACE2-binding ridge in SARS-CoV-2 RBD has a more

66 higher hACE2 binding affinity than SARS-CoV RBD, supporting efficient cell entry.

67 onally, we tested several published SARS-CoV RBD-specific monoclonal antibodies and found that they d

68 t more potent, is less exposed than SARS-CoV RBD.

69 tom molecular dynamics simulations of a CRAF RBD-CRD construct to investigate the dynamics of the RBD

70 and dynamic interactions between KRAS, CRAF RBD-CRD, and the membrane.

71 Here, we report NMR studies of the KRAS:CRAF RBD-CRD complex.

72 on on the state B membrane interface of CRAF RBD (E125K) stabilized state B and enhanced kinase activ

73 ngineering the Ras/Raf interface of the CRAF-RBD, we identified potent and selective inhibitors of Ra

74 e mapped the membrane interfaces of the CRD, RBD-CRD, and the KRAS:RBD-CRD complex.

75 eye movement (REM) sleep behavior disorder (RBD) in patients who developed alpha-synucleinopathies (

76 Rapid eye movement sleep behavior disorder (RBD) is a prodromal synucleinopathy, as >80% will eventu

77 rapid eye movement sleep behavior disorder (RBD) patients (n = 533) and in controls (n = 1,583).

78 rapid eye movement sleep behavior disorder (RBD), and smoking were associated with beta-diversity.

79 pid eye movement sleep behavioural disorder (RBD) are risk factors for Parkinson's disease (PD).

80 pid-eye-movement sleep behavioural disorder (RBD) on survival, cognitive impairment and postural stab

81 pid eye movement sleep behavioural disorder (RBD) population is an ideal study population for testing

82 y quantified serum Abs specific for distinct RBD epitopes leading to the identification of two major

83 The RAS-binding domain (RBD) and cysteine-rich domain (CRD) of RAF engage KRAS a

84 (hACE2) through its receptor-binding domain (RBD) and is proteolytically activated by human proteases

85 S-CoV spike protein receptor-binding domain (RBD) and its host receptor angiotensin-converting enzyme

86 th mutations in the receptor-binding domain (RBD) and N-terminal domain that confer resistance to mon

87 with the SARS-CoV-2 receptor-binding domain (RBD) and negative-stain electron microscopy reconstructi

88 RS-CoV-2 Abs to the receptor-binding domain (RBD) and nucleocapsid protein in addition to conventiona

89 irected against the receptor-binding domain (RBD) and those directed against the N-terminal domain (N

90 two epitopes on the receptor binding domain (RBD) and to distinct non-RBD epitopes on the spike (S) p

91 ines, and high anti-receptor binding domain (RBD) antibody levels.

92 he SARS-CoV-2 spike receptor-binding domain (RBD) are being developed as therapeutics and are a major

93 with the S protein receptor-binding domain (RBD) are compared with those between angiotensin-convert

94 Whereas its RAS-binding domain (RBD) contains the main binding interface to the RAS G do

95 , including several receptor-binding domain (RBD) epitopes as well as non-RBD epitopes.

96 s the salivary anti-receptor binding domain (RBD) IgG response yielded 100% specificity.

97 anti-spike protein receptor binding domain (RBD) IgG significantly decreases mortality.

98 unogenic and mobile receptor binding domain (RBD) is either locked in the all-RBDs 'down' position or

99 The receptor-binding domain (RBD) is immunodominant and the target of 90% of the neut

100 o neutralization by receptor-binding domain (RBD) monoclonal antibodies and convalescent sera from pe

101 odies targeting the receptor-binding domain (RBD) of CoV-2.

102 The N-terminal RAS-binding domain (RBD) of ELMO (ELMO(RBD)) interacts with RHOG to modulate

103 , which targets the receptor-binding domain (RBD) of Middle East respiratory syndrome (MERS) coronavi

104 Abs recognizing the receptor-binding domain (RBD) of S.

105 was pre-coated with receptor binding domain (RBD) of SARS-CoV-2 spike protein, and subsequently teste

106 gineered variants of the Ras-binding domain (RBD) of the C-Raf proto-oncogene, Ser/Thr kinase (CRAF).

107 med by ACE2 and the receptor-binding domain (RBD) of the S-protein.

108 panning against the receptor binding domain (RBD) of the SARS-CoV-2 spike (S) glycoprotein.

109 in complex with the receptor binding domain (RBD) of the SARS-CoV-2 spike (S) protein at 3.1-angstrom

110 The receptor binding domain (RBD) of the SARS-CoV-2 spike glycoprotein mediates viral

111 The receptor-binding domain (RBD) of the SARS-CoV-2 spike protein is a candidate vacc

112 ilizing recombinant receptor-binding domain (RBD) of the SARS-CoV-2 spike protein was developed and c

113 NA that encodes the receptor binding domain (RBD) of the SARS-CoV-2 spike protein(1).

114 irected against the receptor-binding domain (RBD) of the SARS-CoV-2 Spike protein.

115 arget the host ACE2 receptor-binding domain (RBD) of the severe acute respiratory syndrome coronaviru

116 ells depends on the receptor-binding domain (RBD) of the spike (S) protein of SARS-CoV-2.

117 odes the trimerized receptor-binding domain (RBD) of the spike glycoprotein of SARS-CoV-2.

118 The SARS-CoV-2 receptor binding domain (RBD) of the spike protein binds to the human angiotensin

119 2IS) located in the receptor-binding domain (RBD) of the spike protein can neutralize the virus.

120 al structure of the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2 (engineered to f

121 specificity to the receptor-binding domain (RBD) of the spike protein.

122 ocapsid (N) and the receptor binding domain (RBD) of the spike protein.

123 e for targeting the receptor-binding domain (RBD) of the spike protein.

124 s mainly target the receptor-binding domain (RBD) of the trimeric spike.

125 actions between the receptor-binding domain (RBD) of the viral attachment protein spike from two IBV

126 EY6A Fab binds the receptor binding domain (RBD) of the viral spike glycoprotein tightly (K(D) of 2

127 ps tightly bind the receptor binding domain (RBD) of the viral spike protein and prevent entry into h

128 irected against the receptor-binding domain (RBD) of the viral spike protein, suggesting that a suita

129 for binding to the receptor-binding domain (RBD) or allosteric interference with conformational chan

130 acts with the spike receptor binding domain (RBD) or docked against the RBD to identify new binding m

131 rimeric spike whose receptor binding domain (RBD) recognizes angiotensin-converting enzyme 2, initiat

132 otably, residues of receptor-binding domain (RBD) showing crucial interactions with angiotensin-conve

133 es in the NS1 N-terminal RNA-binding domain (RBD) that are required for binding double-stranded RNA (

134 G against the spike receptor binding domain (RBD) was predictive of survival and IgA against the vira

135 OSIP) or SARS-CoV-2 receptor-binding domain (RBD) was readily recognized by neutralizing antibodies,

136 the interaction of receptor binding domain (RBD) with angiotensin-converting enzyme 2 (ACE2) recepto

137 of SARS-CoV-2, its receptor-binding domain (RBD), and its primary receptor ACE2 are extensively glyc

138 bodies to the spike receptor binding domain (RBD), S1+S2, nucleocapsid, and ORF6 to ORF10 of SARS-CoV

139 virus spike protein receptor binding domain (RBD), the hexapeptide YKYRYL on the angiotensin-converti

140 oprotein and at the receptor-binding domain (RBD)-receptor interface, suggesting a role in infection.

141 (ACE2) through its receptor-binding domain (RBD).

142 and three bound the receptor-binding domain (RBD).

143 and the SARS-CoV-2 receptor binding domain (RBD).

144 oV-2) spike protein receptor binding domain (RBD).

145 S1 protein and its receptor-binding-domain (RBD) are detected at a limit-of-detection of 2.8 x 10(-1

146 ed from simulations as important for driving RBD association to the membrane.

147 s fidelity could not be achieved with either RBD or S2 alone.

148 minal RAS-binding domain (RBD) of ELMO (ELMO(RBD)) interacts with RHOG to modulate DOCK1/2 activity.

149 r with the crystal structure of a RHOG-ELMO2(RBD) complex.

150 We describe a monomeric, glycan-engineered RBD protein fragment that is expressed at a purified yie

151 The engineered RBD variants closely mimicked the interaction mode of na

152 enhance the membrane affinity of the entire RBD-CRD construct.

153 crystal structure at 2.4 angstrom of the Fab/RBD complex.

154 the ELISAs showed sensitivities of 88.4% for RBD, 89.3% for S1, and 72.9% for N protein, the specific

155 Most mutations are deleterious for RBD expression and ACE2 binding, and we identify constra

156 gress in the development of therapeutics for RBD and associated neurodegenerative disorders.

157 commonly used as symptomatic treatments for RBD, clinical trials of symptomatic treatments are also

158 potentially facilitates immune evasion from RBD-up binding antibody.

159 munogenicity can be accounted for by greater RBD uptake into antigen-presenting cells in particulate

160 furin preactivation of the spike, and hidden RBD in the spike potentially allow SARS-CoV-2 to maintai

161 rules for assigning current and future human RBD-targeting antibodies into classes, evaluating avidit

162 Overall, the hZAP RBD RNA structure provides an atomic-level explanation f

163 erization disclosed how the newly identified RBD mutations cooperate and thereby enhance affinity wit

164 depth analysis of the SNCA locus to identify RBD-specific risk variants.

165 of SNCA was performed in isolated/idiopathic RBD (iRBD, n = 1,076), Parkinson disease (PD, n = 1,013)

166 The prevalence of idiopathic RBD at alpha-synucleinopathy diagnosis was 3.4%, increas

167 pattern of association at the SNCA locus in RBD as compared to PD, with an opposite direction of eff

168 odifying and symptomatic treatment trials in RBD is described, including potential treatments in the

169 that MAFI alone is not sufficient to induce RBD-mediated RAS inhibition.

170 c antibody levels against the S-protein, its RBD-subunit, and viral nucleocapsid in a cohort of COVID

171 We found that the nucleotide-dependent KRAS-RBD interaction results in transient electrostatic inter

172 interfaces of the CRD, RBD-CRD, and the KRAS:RBD-CRD complex.

173 structural insight into this tripartite KRAS:RBD-CRD:membrane complex has relied on molecular dynamic

174 Next, we show that membrane-localized RBD has its RAS-binding interface mostly inaccessible be

175 e predicted N-glycosylation sites of the M41-RBD were evaluated along with two control Val-to-Ala sub

176 as retained compared with the unmodified M41-RBD construct.

177 matic structural rearrangements and mediated RBD positioning through coordinated movements of the ent

178 Crystal structures of each nanobody-RBD complex revealed how both nanobodies recognize the s

179 First, the sequence of 2019-nCoV RBD, including its receptor-binding motif (RBM) that dir

180 binding domain (RBD) epitopes as well as non-RBD epitopes.

181 tor binding domain (RBD) and to distinct non-RBD epitopes on the spike (S) protein.

182 OH, but not RBD, correlated with reduced survival in PD, DLB and MSA

183 ence of a dsRNA platform that binds both NS1 RBD and DHX30N.

184 bacteria-expressed proteins: the DHX30N-NS1 RBD interaction in vitro requires the presence of a dsRN

185 ame two amino-acid residues required for NS1 RBD dsRNA-binding activity.

186 -binding activity of both DHX30N and the NS1 RBD.

187 viously that the NS1 RNA-binding domain (NS1(RBD)) interacts directly with the second caspase activat

188 he interaction between NS1 and TRIM25 or NS1(RBD)'s ability to bind RNA.

189 ngle strain-specific polymorphism in the NS1(RBD) (R21Q) completely abrogates this interaction.

190 B involved the C terminus of CRD, beta3-5 of RBD, and part of KRAS alpha5.

191 Increasing awareness of RBD among the general public and medical community coupl

192 beta6 and the C terminus of CRD and beta2 of RBD.

193 quencing revealed the expansion of clones of RBD-specific memory B cells that expressed closely relat

194 We found that only a small fraction of RBD-binding antibodies targeted the ACE2IS.

195 on-gamma was produced by a large fraction of RBD-specific CD8(+) and CD4(+) T cells.

196 echnology to enable objective measurement of RBD episodes in the ambulatory setting, and advances in

197 objective polysomnogram-based measurement of RBD-related movements and vocalisations should be the pr

198 hat showed stronger liposome partitioning of RBD-CRD relative to CRD alone.

199 esidues reduced the liposome partitioning of RBD-CRD.

200 , simulations indicated that the presence of RBD near the membrane led to a local enrichment of anion

201 Plasma IgGs differed in their focus on RBD epitopes, recognition of alpha- and beta-coronavirus

202 Using these optimized RBD variants, we stratified patient-derived colorectal c

203 complex with the SARS-CoV-2 spike trimer or RBD.

204 Overall RBD increased to 23.8% after 15 years, with an overall i

205 Whereas overall RBD-specific serum IgG titers waned with a half-life of

206 to constipation, physical activity, possible RBD, smoking, and subthreshold parkinsonism.

207 Probable RBD (pRBD) was assessed with the RBD Screening Questionn

208 Probable RBD and polysomnographically confirmed RBD were analyzed

209 rt from 23andMe of PD patients with probable RBD (pRBD) was also analyzed (n = 1,782 cases; n = 131,2

210 alization with high-titer anti-spike protein RBD IgG present in convalescent plasma significantly red

211 SA), demonstrating that tissue binding of QX-RBD is dependent on a different sialylated glycan recept

212 The lack of binding of QX-RBD to a previously identified IBV-M41 receptor was conf

213 f all proteins to all tissues, binding of QX-RBD to trachea and kidney could not be blocked by preinc

214 ion encompassing amino acids 99 to 159 of QX-RBD was required to establish kidney binding.

215 In contrast, only QX-RBD binds more extensively to cells of the digestive tra

216 In particular, QX-RBD amino acids 110 to 112 (KIP) were sufficient to rend

217 oint mutation that improves binding of c-Raf-RBD to KRas in its active, GTP-bound state (KRasGTP).

218 han the previous best-binding variant, c-Raf-RBD(RK).

219 We measured the binding affinity of c-Raf-RBD(RKY) using a bio-layer interferometry (BLI) assay, a

220 to create a new variant of c-Raf-RBD, c-Raf-RBD(RKY).

221 ng domain of the protein kinase c-Raf (c-Raf-RBD) is the tightest known binder of KRas, a protein imp

222 n the design starting point (wild-type c-Raf-RBD).

223 by osprey) to create a new variant of c-Raf-RBD, c-Raf-RBD(RKY).

224 nt sets of mutations in the PPI of the c-Raf-RBD:KRas complex.

225 protein-protein interface (PPI) of the c-Raf-RBD:KRas complex.

226 n linked RAS nucleotide exchange and RAS/RAF-RBD interaction assays.

227 t Eu(3+)-GTP-loaded RAS interaction with RAF-RBD-Alexa680 monitored at 730 nm.

228 Using the RAS-RBD (CRAF RAS binding domain) interaction as a model sys

229 s shown that rapid conversion of recombinant RBD into particulate form via admixing with liposomes co

230 ing CoPoP liposomes admixed with recombinant RBD induces multiple orders of magnitude higher levels o

231 Nevertheless, rare but recurring RBD-specific antibodies with potent antiviral activity w

232 This could reduce RBD presentation on virus, lowering binding to host ACE2

233 The robust RBD-specific antibody, T cell and favourable cytokine re

234 receptor-binding domain of the S protein (S(RBD)) from interacting with human angiotensin-converting

235 esults identify protective epitopes on the S(RBD) and provide a structure-based framework for rationa

236 es that recognize distinct epitopes on the S(RBD), as well as distinct conformational states of the S

237 M or IgA titers for S1, full-length S, and S-RBD in the overall population.

238 th S protein or S receptor-binding domain (S-RBD); and an IgG avidity assay.

239 ibodies that compete for binding to the same RBD surface but have different escape mutations.

240 ying treatments for synucleinopathies, since RBD represents an early prodromal stage of synucleinopat

241 In the absence of ACE2, single-RBD-up conformations dominated at pH 5.5, resolving into

242 Spike RBD and S2 and neutralizing antibodies remained detectab

243 mediated by the binding of SARS-CoV-2 spike RBD domain.

244 itivity for IgG against the SARS-CoV-2 spike RBD was predictive of survival.CONCLUSIONThe measurement

245 bound ACE2 receptor in both an apo and spike RBD-bound state to probe the intrinsic dynamics of the A

246 atisfactory immunogenicity suggest that such RBD subunit vaccine formulations hold great promise to c

247 al spike protein, suggesting that a suitable RBD construct might serve as a more accessible vaccine i

248 ELISAs targeting RBD and S1 protein of SARS-CoV-2 are promising immunoass

249 ted with the MF59-like adjuvant AddaVax, the RBD derivative elicited neutralizing antibodies with an

250 r binding domain (RBD) or docked against the RBD to identify new binding modes, and their amino acid

251 tro antibody selection for the spike and the RBD proteins using both unbiased and biased selection st

252 stabilize two virus-binding hotspots at the RBD-ACE2 interface.

253 hat the monoclonal antibody CR3022 binds the RBD tightly, neutralizing SARS-CoV-2, and report the cry

254 The most potent antibody bound the RBD and prevented binding to the ACE2 receptor, while th

255 Ten designs bound the RBD, with affinities ranging from 100 picomolar to 10 na

256 Antibodies elicited by the RBD nanoparticles target multiple distinct epitopes, sug

257 esign process that improved affinity for the RBD by up to 12-fold.

258 particulate presentation strategies for the RBD immunogen should be considered for inducing strongly

259 d to map how all amino-acid mutations in the RBD affect antibody binding and apply this method to 10

260 OVID-19-suspect cases, seroconversion in the RBD bridging assay could be demonstrated before day 12;

261 iral variants that harbored mutations in the RBD, D510G and I529T, was observed.

262 e and conformationally intact display of the RBD on the liposome surface.

263 6 binds to a flexible up conformation of the RBD on the spike and relies on antibody avidity for neut

264 eparin enhances the open conformation of the RBD that binds ACE2.

265 mutations cluster on several surfaces of the RBD that broadly correspond to structurally defined anti

266 construct to investigate the dynamics of the RBD when it is tethered to CRD that is anchored to a POP

267 The high hACE2 binding affinity of the RBD, furin preactivation of the spike, and hidden RBD in

268 ding surface, explaining the blocking of the RBD-ACE2 interaction.

269 antibodies to three distinct epitopes on the RBD neutralized the virus with half-maximal inhibitory c

270 ntiguous patch of the positive charge on the RBD surface), resulting in a notable decrease in its abi

271 the heparin segments not accommodated on the RBD surface.

272 , and we identify constrained regions on the RBD's surface that may be desirable targets for vaccines

273 receptor, while the other bound outside the RBD.

274 neutralizing and target epitopes outside the RBD.

275 Across populations, the RBD bridging assay identified most patients correctly as

276 nstructions of one antibody that targets the RBD, a second that targets the NTD, and a third that bri

277 These findings thus suggest that the RBD and CRD have synergistic effects on their membrane d

278 First, we show that the RBD positioning is very dynamic with a preferential loca

279 ed seven amino acid changes and bound to the RBD 170-fold more tightly than wild-type ACE2.

280 measure how all amino acid mutations to the RBD affect expression of folded protein and its affinity

281 y 4 weeks after symptom onset and IgG to the RBD increased until the third month of follow-up.

282 ibodies from an unbiased selection using the RBD preferentially bound to the surfaces that are inacce

283 Probable RBD (pRBD) was assessed with the RBD Screening Questionnaire (RBDSQ) and dichotomized usi

284 e of the most potent Nbs in complex with the RBD.

285 asurements confirmed that mutations of these RBD residues reduced the liposome partitioning of RBD-CR

286 cancer cells showed that expression of these RBD variants inhibits Ras signaling, reducing cell growt

287 ired for ACE2 interaction, primarily through RBD movement combined with smaller alterations in neighb

288 hich competed with human ACE2 for binding to RBD.

289 nonhospitalized patients, the Ab response to RBD is weaker but follows similar kinetics, as has been

290 at impacts its accessibility to RAS and with RBD causing local anionic lipid enrichment that enhances

291 of two IGHV3-53-neutralizing antibodies with RBD, with or without Fab CR3022, at 2.33- to 3.20-angstr

292 ith PD, and p.M393T was also associated with RBD (OR = 1.59, p = 0.001).

293 e) heparin oligomers form 1:1 complexes with RBD, indicating the presence of a single binding site.

294 einopathy, 86 were clinically diagnosed with RBD (19.8%), including 30 (35%) by polysomnography and 5

295 The iRBD cases were diagnosed with RBD prior to neurodegeneration, although some have since

296 Furthermore, mice immunized with RBD-NVP induced robust and long-lasting antibody respons

297 Patients with RBD had reduced DaT levels in the putamen (12.8%) but no

298 (T(H)1)-skewed T cell immune responses with RBD-specific CD8(+) and CD4(+) T cell expansion.

299 esponses and strong antibody responses, with RBD-binding IgG concentrations clearly above those seen

300 ffector-binding site in Ras compared with WT RBD.