ライフサイエンスコーパス: spike protein

1 adenovirus expressing full-length SARS-CoV-2 spike protein.

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

3 nding diverse but overlapping regions of the spike protein.

4 eptor-binding domain (RBD) of the SARS-CoV-2 Spike protein.

5 egatively with antibody levels to SARS-CoV-2 spike protein.

6 s 2 binds to cells via the S1 subunit of its spike protein.

7 ey polar and charged contacts with the viral spike protein.

8 ed, membrane-anchored SARS-CoV-2 full-length spike protein.

9 PRSS2, contribute to activate the SARS-CoV-2 spike protein.

10 encodes the stabilized prefusion SARS-CoV-2 spike protein.

11 veral ACE2 orthologs bound to the SARS-CoV-2 spike protein.

12 ing conformational conversion of coronavirus spike protein.

13 ents using a SARS-CoV-2 stabilized prefusion spike protein.

14 and the receptor binding domain (RBD) of the spike protein.

15 ation-dependent binding modality for the M41 spike protein.

16 flow immunoassay (LFI) based on full-length spike protein.

17 ordered, compact, and rigid structure in the spike protein.

18 ect from infection with CoVs using the novel spike protein.

19 antibodies (MAbs) to the ectodomain of HKU1 spike protein.

20 eceptor-binding domain (RBD) of the MERS-CoV Spike protein.

21 proteins, VP6, and two domains from VP4, the spike protein.

22 ing the receptor-binding domain (RBD) of the spike protein.

23 igen-specific T cells against the SARS-CoV-2 spike protein.

24 taneously bind to all three RBDs of a single spike protein.

25 d several high affinity variant forms of the spike protein.

26 mat to cells expressing membrane-bound CoV-2 spike protein.

27 piratory syndrome coronavirus 2 (SARS-CoV-2) spike protein.

28 he SARS-CoV-2 receptor binding domain of the spike protein.

29 hat are inaccessible in the context of whole spike protein.

30 bulin G antibody responses against the viral spike protein.

31 identified an H49Y amino acid change in the Spike protein.

32 plement activation in response to SARS-CoV-2 spike proteins.

33 d with affinities of the receptors for viral spike proteins.

34 tibodies specific for both bat and human CoV Spike proteins.

35 onvoluted extracted ion chromatograms of the spiked proteins.

36 litis replicon particles expressing MERS-CoV spike protein].

37 eptor binding domain (RBD) of the SARS-CoV-2 spike protein(1).

38 piratory syndrome coronavirus-2 (SARS-CoV-2) spike protein(1-5) show promise therapeutically and are

39 cuss structural insights into the SARS-CoV-2 spike protein, a major determinant of transmissibility,

40 sly undergoes genetic changes to its surface spike protein, a major target of neutralizing antibodies

41 total IgG ELISA against trimeric SARS-CoV-2 spike protein, a muliplexed immunoassay, three live SARS

42 its hACE2-dependent transduction by SARS-CoV spike protein, a successful application of the hot spot

43 d Steered MD (SMD) simulations to identify a Spike protein - ACE2 interaction inhibitor.

44 piratory syndrome coronavirus 2 (SARS-CoV-2) spike protein acquired a D614G mutation early in the pan

45 d antibody production against the SARS-CoV-2 spike protein, all of which were clinically associated w

46 A SARS-CoV-2 variant carrying the Spike protein amino acid change D614G has become the mos

47 was non-functional in binding the SARS-CoV-2 spike protein and as a carboxypeptidase.

48 eptor-binding domain (RBD) of IBV strain M41 spike protein and assessed the role of this modification

49 tate both antibody binding to the SARS-CoV-2 spike protein and blocking to the Angiotensin-converting

50 eptor-binding domain (RBD) from the MERS-CoV spike protein and determined its crystal structure.

51 he receptor-binding domain (RBD) of MERS-CoV spike protein and DPP4 was determined by crystallography

52 Viral entry is mediated through viral spike protein and host ACE2 enzyme interaction.

53 3 and detected broad T cell responses to the spike protein and identified 22 targeted peptides.

54 identified key interactions between SARS-CoV spike protein and its host receptor angiotensin-converti

55 ned receptor-binding domain (RBD) on a viral spike protein and its host receptor, angiotensin-convert

56 o remodel the interaction between SARS-CoV-2 spike protein and mouse ACE2 and designed mouse-adapted

57 ometry assay for the detection of SARS-CoV-2 spike protein and nucleoprotein in a relevant biological

58 Recombinant full-length spike protein and nucleoprotein were digested and proteo

59 ercial antibodies generated against SARS-CoV spike protein and nucleoprotein, double stranded RNA, an

60 D-19 patient antibodies primarily recognized spike protein and nucleoprotein.

61 y published cryo-EM structure of the M41 IBV spike protein and our glycosylation results revealed a p

62 e receptor binding domain (RBD) of the viral spike protein and prevent entry into host cells.

63 rs host cells via an interaction between its Spike protein and the host cell receptor angiotensin-con

64 piratory syndrome coronavirus 2 (SARS-CoV-2) spike protein and the human angiotensin-converting enzym

65 o inefficient interactions between the viral spike protein and the mouse orthologue of the human rece

66 eceptor-binding domain (RBD) of the MERS-CoV spike protein and thereby competitively blocks the bindi

67 tained seven proteotypic peptides (four from spike protein and three from nucleoprotein) and the top

68 ction of antibodies to the S1 subunit of the spike protein and to the receptor binding domain of SARS

69 hepatotropism of MHV-JHM depends not on the spike protein and viral entry but rather on a combinatio

70 MAb362 binds to both SARS-CoV and SARS-CoV-2 spike proteins and competitively blocks ACE2 receptor bi

71 structure-function information on the viral spike proteins and the membrane fusion process to provid

72 We expressed different glycoforms of the Spike-protein and ACE2 in CRISPR-Cas9 glycoengineered ce

73 SARS-CoV-2 epitopes in the HR2-domain of the spike-protein and the dengue envelope-protein.

74 ies that specifically bind the S1 SARS-CoV-2 spike protein, and block the interaction with the human

75 ectin from hosts, incorporated it into their spike protein, and evolved it into viral receptor-bindin

76 receptor binding domain (RBD) of SARS-CoV-2 spike protein, and subsequently tested with samples of a

77 s with COVID-19 showed anti-nucleocapsid and spike protein antibodies appearing between days 8 and 14

78 protein of SARS-CoV-2 is more sensitive than spike protein antibody for detecting early infection.

79 ibody tests (99.3% and 99.7%) than using the spike protein antibody test (97.8%; P <= 0.002).

80 Abbott IgG and Roche total antibody) and one spike protein antibody test (DiaSorin IgG) were included

81 antibody tests were more sensitive than the spike protein antibody test overall (70% and 70% versus

82 o nucleocapsid antibody tests outperformed a spike protein antibody test.

83 tes that consisted of the same protruding or spike protein antigens of the three viruses in two forma

84 Glycosylation sites in the spike protein are highly conserved across viral genotype

85 Fusion peptides (FPs) in spike proteins are key players mediating early events in

86 PEDV vaccine antigens.IMPORTANCE Coronavirus spike proteins are large, densely glycosylated macromole

87 ns recognize different receptors and how the spike proteins are regulated to undergo conformational t

88 annose-type glycans (HMTGs) decorating viral spike proteins are targets for virus neutralization.

89 residues, which are conserved in coronavirus spike proteins, are predicted to be electrostatically fr

90 nating disease, and our model identifies the spike protein as a therapeutic target to prevent axonal

91 MHV) uses the N-terminal domain (NTD) of its spike protein as its receptor-binding domain.

92 Many vaccine candidates focus on the Spike protein, as it is targeted by neutralizing antibod

93 were tested for IgG antibodies to SARS-CoV-2 spike protein at least 2 weeks after symptom onset.

94 y of nsp16 and the endocytosis signal of the spike protein attenuates PEDV yet retains its immunogeni

95 ses, and lung heparan sulfate potently block spike protein binding and/or infection by pseudotyped vi

96 On cells, spike protein binding depends on both heparan sulfate an

97 nteraction surface, which greatly influences Spike protein binding mode.

98 G inhibited angiotensin-converting enzyme 2-spike protein binding to a greater degree than controls.

99 SARS-CoV-2 spike protein binding to angiotensin-converting enzyme 2

100 eutralize the SARS-CoV-2 infection and block Spike protein binding to the ACE2 receptor, and biodistr

101 (SARS-CoV-2) infection begins with the viral spike protein binding to the human receptor protein angi

102 S-CoV-2 receptor binding domain (RBD) of the spike protein binds to the human angiotensin-converting

103 , inhibit cell infection, and cause envelope spike protein breakdown, including gp120 shedding and, f

104 that deletion of this 197-aa fragment in the spike protein can attenuate a highly virulent PEDV, but

105 in the receptor-binding domain (RBD) of the spike protein can neutralize the virus.

106 ored vaccine encoding a prefusion stabilized spike protein (ChAd-SARS-CoV-2-S) in challenge studies w

107 Bacteriophage Mini seems to have lost the spike protein commonly seen in ssDNA phages, suggesting

108 (ChAdOx1 nCoV-19) expressing the SARS-CoV-2 spike protein compared with a meningococcal conjugate va

109 urine ( approximately 1.5 muM total protein; spiked protein concentrations were 0.067% of the overall

110 gn for emerging CoVs should involve chimeric spike protein containing neutralizing epitopes from mult

111 scopy studies illustrate that the SARS-CoV-2 spike protein contains multiple distinct antigenic sites

112 e receptor-binding S1 subunit of coronavirus spike proteins contains two distinctive domains, the N-t

113 In conclusion, SARS-CoV-2 spike proteins convert nonactivator surfaces to activato

114 binding and activation of the coronavirus-2 spike protein CoV-2 RBD at ACE2.

115 This results indicate that spike-protein cross-reactive T cells are present, which

116 However, the presence of spike-protein cross-reactive T cells in a considerable f

117 t al. found that a SARS-CoV-2 variant in the spike protein D614G rapidly became dominant around the w

118 eletion variant observed here.IMPORTANCE The spike protein determines the infectivity and host range

119 n in 3 SARS-CoV-2 IgG immunoassays targeting spike proteins (DiaSorin Liaison, Ortho Vitros, and Euro

120 a, the receptor-binding S1 subunits of their spike proteins differ in primary, secondary, and tertiar

121 novel T cell epitopes were identified, with spike protein dominating total T cell responses.

122 d vaccine expressing a stabilized SARS-CoV-2 spike protein elicited binding and neutralizing antibody

123 self-amplifying RNA encoding the SARS-CoV-2 spike protein encapsulated within a lipid nanoparticle (

124 The spike protein exists in two structurally distinct confor

125 The spike protein expressed on the surface of this virus is

126 myelinating strains of MHV, differing in the spike protein expressed, infect neurons and glial cells

127 y be correlated with the high specificity of spike proteins for such glycans expressed in the intesti

128 was able to detect differential abundance of spiked proteins for expected ratios >/=2, with comparabl

129 rom Novavax, which is based on a full-length spike protein formulated in polysorbate 80 detergent.

130 etic bead assay and a recombinant SARS-CoV-2 spike protein fragment, we tested binding of (131)I-CR30

131 In a prior study, we used a tail spike protein from a bacteriophage (PhiAB6TSP) that dige

132 ribes the atomic-resolution structure of the spike protein from porcine epidemic diarrhea virus, a pa

133 m should include a panel of nucleocapsid and spike proteins from phylogenetically distinct CoVs.

134 The full-length Spike protein functioned inefficiently with all three sy

135 st the CD4 binding site (CD4bs) on the HIV-1 spike protein gp120 can show exceptional potency and bre

136 strains that differ in the gene encoding the spike protein have demonstrated that the spike has a rol

137 Here, we examine the influenza A virus spike protein hemagglutinin (HA), which undergoes a dyna

138 The major spike protein hemagglutinin binds sialic acid residues o

139 hrough multivalent interactions of its major spike proteins, hemagglutinin (HA) and neuraminidase (NA

140 the structures and functions of coronavirus spike proteins, illustrating how the two S1 domains reco

141 the structural integrity of the full-length spike protein immunogen and provides a basis for interpr

142 egree of inhibition was correlated with anti-spike protein immunoglobulin G levels, neutralizing tite

143 ese findings identified a novel role for the spike protein in regulating the uncoating and delivery o

144 sted that T cells specific for the HCoV-NL63 spike protein in this individual could also recognize SA

145 Despite the importance of the spike protein in viral entry and host immune responses,

146 like MHV-2, thus establishing a role for the spike protein in viral growth.

147 h ACE2 and heparin can bind independently to spike protein in vitro, and a ternary complex can be gen

148 ions we compared the SARS-CoV and SARS-CoV-2 Spike proteins in complex with the ACE2 receptor and sho

149 lar responses to membrane, nucleocapsid, and spike proteins in individuals suffering from moderate or

150 of mutations that stabilize Betacoronavirus spike proteins in the prefusion state, improving their e

151 l relative label-free quantification of four spiked proteins in E. coli samples, BSA, beta-lactoglobu

152 an LOQ of 10 ng/mL was achieved for the two spiked proteins in nondepleted human serum.

153 Surprisingly, SARS-CoV-2 trimeric spike protein increased ACE2 proteolytic activity ~3-10

154 higher level of sequence variability in the Spike protein interaction surface, which greatly influen

155 and small molecules targeting the SARS-CoV-2 Spike protein interaction with ACE2.

156 ke protein receptor binding domain and block spike protein interaction with the angiotensin convertin

157 We show that SARS-CoV-2 spike protein interacts with both cellular heparan sulfa

158 eptor-binding domain (RBD) of the SARS-CoV-2 spike protein is a candidate vaccine antigen that binds

159 The coronavirus spike protein is a multifunctional molecular machine tha

160 2'-O-MTase and the endocytosis signal of the spike protein is an approach to designing a promising li

161 at the receptor-binding domain (RBD) of HKU1 spike protein is located in the C domain, where the spik

162 ] and non-P[6] strains suggests that the VP4 spike protein is most likely one of the main reasons pre

163 other class-I membrane-fusion proteins, the spike protein is post-translationally cleaved, in this c

164 The heavily glycosylated IBV spike protein is responsible for binding to host tissues

165 To determine whether the spike protein is responsible for the difference, a recom

166 try mediated by the interaction of ACE2 with spike protein largely determines host range and is the m

167 le neutralizing antibodies against the viral spike protein may correlate with protection, additional

168 ctively inhibit MERS-CoV replication and its spike protein-mediated cell-cell fusion.

169 its CoV entry into cells by interfering with spike protein-mediated membrane fusion.

170 A virus surface spike protein mediates SARS-CoV-2 entry into cells.

171 Coronavirus spike protein mediates viral entry into cells by first b

172 prefusion to postfusion conformation of the spike protein must be triggered, leading to membrane fus

173 ng and ORF1ab sites covarying with the D614G spike protein mutation which has become increasingly pre

174 The spike protein N-terminal domains (NTDs) of bovine corona

175 onses against peptide pools derived from the spike protein of 3 common cold coronaviruses (HCoV-229E,

176 a neutralizing antibody binds to the surface spike protein of coronaviruses like a viral receptor, tr

177 In this study, we showed that for the spike protein of HKU1, the purified C domain, downstream

178 by abolishing the endocytosis signal of the spike protein of KDKE(4A) Compared with icPC22A, the KDK

179 The spike protein of MERS-CoV (MERS-S) facilitates viral ent

180 We found that the spike protein of PDF2180-CoV, a MERS-like virus found in

181 Consistently, recombinant full-length spike protein of SARS-CoV or its receptor-binding domain

182 of the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2 (engineered to facilitate cr

183 replaced the glycoprotein gene (G) with the spike protein of SARS-CoV-2 (VSV-eGFP-SARS-CoV-2) and de

184 igh levels of neutralizing antibodies to the spike protein of SARS-CoV-2 in a safe manner is likely t

185 was also extended to antigen detection (the spike protein of SARS-CoV-2), which presents new possibi

186 d vaccine ChAdOx1 nCoV-19, which encodes the spike protein of SARS-CoV-2, is immunogenic in mice and

187 The Spike protein of SARS-CoV-2, its receptor-binding domain

188 a vaccine encoding the prefusion-stabilized spike protein of SARS-CoV-2, or no vaccine.

189 tored coronavirus vaccine that expresses the spike protein of SARS-CoV-2.

190 Antibodies targeting the spike protein of severe acute respiratory syndrome coron

191 l responses.RESULTSWe found responses to the spike protein of the 3 common cold coronaviruses in many

192 cross-neutralize pseudovirus containing the spike protein of the D614G variant, indicating the poten

193 encodes the prefusion stabilized full-length spike protein of the severe acute respiratory syndrome c

194 rotein is located in the C domain, where the spike proteins of alpha-CoVs and beta-CoVs in groups B a

195 Ds have circulating T cells specific for the spike proteins of HCoV-NL63, HCoV-229E, and HCoV-OC43.

196 estricted the entry mediated by the envelope spike proteins of other human coronaviruses, including t

197 ed similarly to the C-terminal region of the spike proteins of the human endemic coronaviruses 229E a

198 ic acid (SA) receptors and the two principal spike proteins of the influenza A virus (H3N2): hemagglu

199 uman lung tissue and cleave and activate the spike proteins of the Middle East respiratory syndrome a

200 Exchanging the spike proteins of the two viruses neither increased repl

201 The spike protein on the surface of SARS-CoV-2 is a major an

202 red in a murine model a range of recombinant spike protein or inactivated whole-virus vaccine candida

203 his study shows that formulation of SARS-CoV spike protein or inactivated whole-virus vaccines with n

204 vaccines encoding the full-length SARS-CoV-2 spike protein or the spike receptor binding domain in mi

205 osable with that of the tail-less phage PRD1 spike protein P5 and the adenovirus knob, domains that i

206 s individual could also recognize SARS-CoV-2 spike protein peptide pools.CONCLUSIONHDs have circulati

207 Fusion peptides (FPs) in the spike protein play a key role in MHV pathogenesis.

208 ompared N-glycan profiles of the recombinant spike proteins produced from different expression system

209 inhibition of N-glycan biosynthesis enhanced Spike-protein proteolysis.

210 n after hospitalization with high-titer anti-spike protein RBD IgG present in convalescent plasma sig

211 Modeling the binding energies of MERS-CoV spike protein RBD to DPP4 of human (susceptible) or hams

212 Spike-protein-reactive T cell lines generated from SARS-

213 nvalescent plasma containing high-titer anti-spike protein receptor binding domain (RBD) IgG signific

214 g processes of a fragment of the coronavirus spike protein receptor binding domain (RBD), the hexapep

215 piratory syndrome coronavirus 2 (SARS-CoV-2) spike protein receptor binding domain (RBD).

216 lated nanobodies that bind to the SARS-CoV-2 spike protein receptor binding domain and block spike pr

217 hours of admission with plasma with an anti-spike protein receptor binding domain titer of >=1:1350.

218 ts receiving dialysis in July, 2020, using a spike protein receptor binding domain total antibody che

219 omic-level interactions between the SARS-CoV spike protein receptor-binding domain (RBD) and its host

220 determined the crystal structure of NL63-CoV spike protein receptor-binding domain (RBD) complexed wi

221 piratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike protein receptor.

222 these two critical functions of coronavirus spike proteins, receptor recognition and membrane fusion

223 roperties of genetically engineered isogenic spike protein recombinant demyelinating and nondemyelina

224 city scoring, to assess safety; and IgG anti-spike protein response (in enzyme-linked immunosorbent a

225 es attach to 9-O-acetylated sialoglycans via spike protein S with hemagglutinin-esterase (HE) acting

226 Receptor binding is mediated by spike protein S, the main determinant of coronavirus hos

227 ictive of survival and IgA against the viral spike protein (S protein) associated with rapid virologi

228 Using synthetic biology, we engineered the spike protein (S) from a civet strain, SZ16, into our ep

229 The coronavirus spike protein (S) plays a key role in the early steps of

230 encodes the stabilized prefusion SARS-CoV-2 spike protein (S-2P) in healthy adults.

231 To enter host cells, the viral spike protein (S-protein) binds to its receptor, ACE2, a

232 Both SARS-CoV-2 spike protein (S-protein), a critical element of the vir

233 to produce a prefusion-stabilized SARS-CoV-2 spike protein, S-2P.

234 oV-2 uses the receptor-binding domain of its spike protein S1 to attach to the host angiotensin-conve

235 the nucleoprotein (N), the S1 domain of the spike protein (S1), and a lateral flow immunoassay (LFI)

236 lix bundle fusion core structure of MERS-CoV spike protein S2 subunit by X-ray crystallography and bi

237 evere acute respiratory syndrome coronavirus spike protein (SARS-CoV S) can be primed by a variety of

238 -free top-down quantitation strategies using spiked proteins, spectral counting, along with normalize

239 piratory syndrome coronavirus 2 (SARS-CoV-2) spike protein substitution D614G became dominant during

240 Here, we demonstrate that the SARS-CoV-2 spike protein (subunit 1 and 2), but not the N protein,

241 Spike protein subunits S1 and receptor binding domain, a

242 e receptor-binding domain (RBD) of the viral spike protein, suggesting that a suitable RBD construct

243 n differing from that observed in the intact spike proteins, suggesting that the PEDV receptor-bindin

244 Electron micrographs of spike protein suggests that heparin enhances the open co

245 Because the decoy replicates the spike protein target interface in hACE2, it is intrinsic

246 3, an mRNA vaccine that encodes a SARS-CoV-2 spike protein that is stabilized in the prefusion confor

247 of resistance against four antibodies to the spike protein that potently neutralize SARS-CoV-2, indiv

248 (SARS-CoV-2) has two unique features in its spike protein, the receptor binding domain and an insert

249 se studies on adeno-, corona-, and rotaviral spike proteins, the relationship of these adhesins to ma

250 usly bind the receptor binding domain of the spike protein, thereby providing ideal partners for a th

251 , which is triggered by binding of the viral spike protein to angiotensin-converting enzyme 2.

252 ability of plasma to inhibit the binding of spike protein to angiotensin-converting enzyme 2.

253 n group A, uses the galectin-like NTD in its spike protein to bind its receptor protein, while HCoV-O

254 avirus uses its highly glycosylated trimeric Spike protein to bind to the cell surface receptor angio

255 iated by binding of the viral envelope (Env) spike protein to its receptors, CD4 and CCR5/CXCR4, on t

256 ctor Bb is increased in the supernatant from spike protein-treated cells.

257 s disease 2019 (COVID-19) and expressed anti-spike protein trimer immunoglobulin G inhibited angioten

258 piratory syndrome coronavirus 2 (SARS-CoV-2) spike protein, used in a combined cocktail (REGN-COV2) t

259 to the furin-cleaved form of the SARS-CoV-2 spike protein using cryo-electron microscopy.

260 e N-glycosylation profiles of the SARS-CoV-2 spike proteins using signature ions-triggered electron-t

261 eutralizing antibody treatment or a MERS-CoV spike protein vaccine protected the engineered mice agai

262 l and increasing frequency of the SARS-CoV-2 spike protein variant D614G are suggestive of a selectiv

263 istally located VP8* domain of the rotavirus spike protein VP4 (ref. 5) mediates such interactions.

264 Interaction of the VP8* domain of the spike protein VP4 with sialic acid was thought to be the

265 quence alterations in the VP8* domain of the spike protein VP4.

266 h a series of intersubunit interactions, the spike protein (VP4) adopts a dimeric appearance above th

267 us for efficient infectivity by cleaving the spike protein, VP4, into VP8* and VP5*.

268 Mechanisms by which the viral spike protein, VP4, mediates receptor binding and membra

269 t the VP5 cleavage fragment of the rotavirus spike protein, VP4, undergoes a foldback rearrangement t

270 tryptic cleavage product of the outer capsid spike protein, VP4.

271 structures of the ectodomains of the 57-kDa spike protein VP5 from two related HRPVs revealing a pre

272 Our results suggest that the spike protein VP8* of RVs is involved in the recognition

273 this study, we demonstrated that the surface spike protein VP8* of the major P genotypes of human RVs

274 The distal portion of rotavirus (RV) VP4 spike protein (VP8*) is implicated in binding to cellula

275 eptor-binding domain (RBD) of the SARS-CoV-2 spike protein was developed and compared to three commer

276 ariant that contained mutations in the viral spike protein was observed.

277 Based on the sequence of 2019-nCoV spike protein, we apply this predictive framework to pro

278 ar high affinity between ACE2 and SARS-CoV-2 spike protein, we investigated how this interaction woul

279 the immunogenicity of different parts of the spike protein, we performed in vitro antibody selection

280 Using immunoassays specific for SARS-CoV-2 spike proteins, we determined SARS-CoV-2-specific IgA an

281 ectodomain and S1 subunit of the SARS-CoV-2 spike protein were characterized using this approach.

282 um IgG and IgA antibodies against SARS-CoV-2 spike protein were detected by using enzyme-linked immun

283 and 100% specificity, whereas antibodies to spike protein were detected with 91% sensitivity and 100

284 or serum antibodies to the nucleocapsid and spike proteins were analyzed using luciferase immunoprec

285 eight common HCPs into antibody product, all spiked proteins were positively identified.

286 f the 29 shared epitopes were located in the spike protein, whereas most epitopes were located in ORF

287 ssion of strains with a H49Y mutation in the Spike protein, which could be further used as a molecula

288 utralizing antibodies against the SARS-CoV-2 spike protein, which engages with host ACE2 receptor for

289 ss immunogenic than the other regions of the spike protein, which has important implications in the d

290 y, the Wuhan-Hu-1 reference sequence for the Spike protein, which is the basis for different vaccine

291 ly active against C-terminal epitopes in the spike protein, which show a higher homology to spike gly

292 piratory syndrome coronavirus 2 (SARS-CoV-2) spike protein, which yielded a large collection of fully

293 h-yield production of a stabilized prefusion spike protein will accelerate the development of vaccine

294 of the receptor-binding domain of the viral spike protein with ACE2.

295 Replacement of the signal peptide of the Spike protein with an optimal signal peptide did not enh

296 cking of the ACE2 receptor to the SARS-CoV-2 spike protein with antispike antibodies.

297 ftor bind the receptor-binding domain of the Spike protein with high affinity and prevent ACE2 intera

298 affinities and block the binding of MERS-CoV Spike protein with its hDPP4 receptor.

299 noviral vectored vaccine expressing MERS-CoV spike protein, with further groups receiving control vac

300 nd highlights the potential of including non-spike proteins within future COVID-19 vaccine design.