ライフサイエンスコーパス: virus binding

1 mmediate impact of receptor glycosylation on virus binding.

2 le network for the initial 8 hours following virus binding.

3 d substitution within these areas eliminates virus binding.

4 ment in MHV entry occurs at a step following virus binding.

5 ating a redistribution of membrane following virus binding.

6 G with respect to conformational changes and virus binding.

7 oligosaccharide ligand required for Norwalk virus binding.

8 e airway mucins, which are unable to inhibit virus binding.

9 , cells was dependent on the medium used for virus binding.

10 ), that is required for both viral entry and virus binding.

11 mes more effective than NeuAcGM3 in blocking virus binding.

12 -deficient cells led to a large reduction in virus binding.

13 on of the viral infection process soon after virus binding.

14 bolish adhesion to collagen had no effect on virus binding.

15 loop from the amino terminus is required for virus binding.

16 s were mainly involved in the early steps of virus binding.

17 oline residue found in murine DAF eliminated virus binding.

18 n and a clinical isolate of CHIKV to mediate virus binding.

19 sequently gene expression, without affecting virus binding.

20 2 (SCR2), which is known to be essential for virus binding.

21 ed in tight junctions and not accessible for virus binding.

22 tients' antisera and substantially increased virus binding ability to human cells.

23 ide expressed on the surface of CPMV retains virus-binding activity and is capable of inhibiting vira

24 us receptor binding specificity but enhances virus binding affinity of the H9N2 virus to human cells

25 proach has proven instrumental in bolstering virus-binding affinity on the LFAs.

26 Virus binding also induces several responses by lymphocy

27 Although it facilitated virus binding and affected infection of H7 IAV in cells,

28 or-binding site can reduce the efficiency of virus binding and decrease viral dependence on NA activi

29 Virus binding and DNA internalization studies suggest th

30 Anti-CD98 and xCT antibodies did not block virus binding and entry and nuclear delivery of viral DN

31 ; however, the effects of these molecules on virus binding and entry have not been comprehensively ev

32 ycoprotein (EBOV GP/VSVDeltaG), we evaluated virus binding and entry into cells expressing TIM-4 mole

33 rus virions and is responsible for mediating virus binding and entry into target cells.

34 se results suggest that, besides its role in virus binding and entry into the target cells, KSHV gB a

35 mon key capsid surface residues dictate both virus binding and entry processes, as well as antigenic

36 es as human monoclonal antibodies that block virus binding and entry will be useful in providing pote

37 Activation requires virus binding and entry, as well as de novo infected-cel

38 other data demonstrating minimal effects on virus binding and entry, these data suggest that E2 posi

39 uggesting the involvement of this epitope in virus binding and entry.

40 uence to infection was assessed by measuring virus binding and entry.

41 lls, despite having full capacity to undergo virus binding and fusion.

42 of surface CD4 and were fully susceptible to virus binding and fusion.

43 e apical membrane, and the effects on apical virus binding and gene transfer were minimal.

44 o how virus receptors are organized prior to virus binding and how they assemble into functional plat

45 ence that serum/platelet factors can have on virus binding and identifies CSPGs as alternative cell a

46 This mutation removes a domain critical for virus binding and inactivates amino acid transport activ

47 ive cell line with CAR cDNA led to increased virus binding and increased susceptibility to adenovirus

48 his study, we addressed the initial steps in virus binding and infection and found that the first bin

49 Virus binding and infection experiments were conducted t

50 Virus binding and infection mediated by alphavbeta1 was

51 They may mediate virus binding and infection of cells, or alternatively c

52 In addition, we show that virus binding and infection of the beta6-transfected cel

53 8 in infection was confirmed by showing that virus binding and infection of the transfected cells are

54 as another critical residue that influences virus binding and infection, as well as evidence that th

55 K234) in mATRC1 as a residue that influences virus binding and infection.

56 D84K) of ecotropic Moloney MLV Env abolishes virus binding and infection.

57 kemia virus envelope protein is essential to virus binding and infection.

58 tified residues in the receptor required for virus binding and infection.

59 -1 and -2, for their abilities to facilitate virus binding and infection.

60 o the viral and cellular factors involved in virus binding and infection.

61 carbohydrate chain terminus is important for virus binding and infection.

62 ing predictions have no known involvement in virus binding and instead recapitulate host phylogeny.

63 CLDN1 acts late in the entry process, after virus binding and interaction with the HCV co-receptor C

64 Finally, this DC-mediated virus binding and internalization are dependent on lipid

65 variable (IgV) domain is essential for both virus binding and internalization by TIM-1.

66 a transmembrane unit (gp41) responsible for virus binding and membrane fusion, respectively.

67 ocesses mediated by the viral Spike protein: virus binding and membrane fusion, which can be distingu

68 in a consistent and significant reduction of virus binding and membrane fusion.

69 terferon-like response in cells that follows virus binding and penetration.

70 h a species-restricted block occurring after virus binding and penetration.

71 induced B-cell immortalization occurs beyond virus binding and penetration.

72 with that of L-SIGN was sufficient to impair virus binding and prevent transmission.

73 orm both a protective barrier that can block virus binding and recruit IAVs to bind cells via the sia

74 nctionality as CVB receptors, examining both virus binding and replication.

75 usceptible to RV-C infection to support both virus binding and replication.

76 Virus binding and RNA replication as well as cellular pr

77 strate that N-sulfation of HS is crucial for virus binding and structural activation by providing hig

78 nt protein and the F fusion protein, mediate virus binding and subsequent membrane fusion, respective

79 uctural determinants of DC-SIGN required for virus binding and transmission to permissive cells.

80 ion but is not required for DC-SIGN-mediated virus binding and transmission.

81 ngliosides as functional receptors mediating virus binding and transport from the plasma membrane to

82 f protective proteins hindering cell surface virus binding and upregulating defensive proteins agains

83 Most substitutions had little effect on virus binding and uptake.

84 Virus binding and vesicle lysis assays revealed that 4-1

85 W142M virus showed a marked reduction in virus binding and was almost noninfectious, suggesting t

86 ons began to appear inside cells 5 min after virus binding and was colocalized with MCAT-1-GFP.

87 n by UV-inactivated HHV-8 suggest a role for virus binding and/or entry but not viral gene expression

88 region(s) within PiT2 that is important for virus binding and/or entry relied on infection results o

89 s that diminish binding to self but preserve virus binding, and 33% had combined 2 or 3 of these muta

90 nous lectin recognition, tumor antigenicity, virus binding, and complement activation.

91 or for T-tropic HIV strains, and thus act as virus binding, and not as fusion, inhibitors.

92 ecreases in CD20+ B cells, failure to elicit virus-binding antibodies in plasma, and high levels of a

93 ctions are regulated by polyclonal influenza virus-binding antibody mixtures in vivo has never been d

94 proteomic analysis indicated that these four virus-binding aphid proteins were specifically inherited

95 ue of 3.519 nM and demonstrated the greatest virus binding as shown by fluorescence imaging.

96 We have used a virus-binding assay to examine conformational changes th

97 By using a virus-binding assay, we demonstrate that L-SIGN and DC-S

98 virions were determined by a newly developed virus-binding assay.

99 In virus binding assays, five of the seven (71%) anti-V3(no

100 The results of virus-binding assays suggested that the observed differe

101 Using RNA transfection and virus-binding assays, we have shown that this requiremen

102 a step of viral infection that occurs after virus binding but before reverse transcription.

103 s, and inhibited viral entry at a step after virus binding but before virus-cell fusion.

104 OCLN overexpression also has no effect on virus binding but enhances virus internalization, cell-t

105 f GD1a has no effect on the overall level of virus binding but mediates the internalization and trans

106 beta-cyclodextrin or filipin did not affect virus binding but reduced virus entry.

107 r, the data may also suggest that D2 affects virus binding by influencing the conformation of D1.

108 Characterization of virus binding by neutralizing antibodies is important bo

109 Virus binding by viral envelope phosphatidylserine is no

110 virus infection by interfering with receptor-virus binding, by virus opsonization, by complement acti

111 how viral capsid protein mechanics influence virus-binding capacity and infectivity.

112 ata, ~2 weeks for DDN design, synthesis, and virus binding characterization, and ~2 weeks for DDN cyt

113 A lysine 234 change alone reduced virus binding, contrary to previous observations that at

114 cytic cells, which lack fiber receptors, and virus binding could be blocked by a soluble penton base

115 In addition to promoting virus binding, DCPD expression was associated with inter

116 omly bred chickens suggests that the altered virus binding domain is not the basis for genetic resist

117 ptor glycoproteins containing the N-terminal virus-binding domain were released into the supernatant

118 ructed chimeric DPP4 receptors that have the virus-binding domains of indigenous Middle Eastern anima

119 sing various modules and generating specific virus-binding domains.

120 Initially, we investigate the virus binding dynamics to validate the better binding pe

121 ved envelope glycoproteins (gps) involved in virus binding, entry, assembly, and release from infecte

122 otein from 2-20 had greater contributions to virus binding, entry, infectivity, and in vitro growth k

123 in microfilaments did not have any effect on virus binding, entry, nuclear delivery, or infection.

124 of 10 different cell-derived molecules by a virus binding enzyme-linked immunosorbent assay.

125 Glycans within the virus binding face of the apical domain also controlled

126 other N-linked glycosylation sites into the virus binding face of the feline apical domain reduced o

127 Our finding clearly dissects initial virus binding from ADAM17-dependent assembly of a HPV/CD

128 ations deleterious for infection and loss of virus binding has not been established.

129 e 2 (hACE2), and proposed the existence of a virus-binding hot spot on hACE2.

130 or reduce unfavorable interactions with two virus-binding hot spots on ACE2, and by doing so, they e

131 e common ACE2 regions, largely because of a "virus-binding hotspot" on ACE2.

132 changes in the SARS-CoV-2 RBD stabilize two virus-binding hotspots at the RBD-ACE2 interface.

133 sitions 493 and 498 that align well with two virus-binding hotspots on mouse ACE2.

134 m of the MHVR, sMHVR-Ig, which comprised the virus-binding immunoglobulin-like domain of MHVR fused t

135 hrough increases in virus receptor levels or virus binding, indicating that virus fusion is enhanced.

136 s the impact of extended glycan receptors on virus binding, infection, and growth, we have engineered

137 cal membrane glycosphingolipids by toxin- or virus-binding initiates degradation of PARD6B.

138 ates a second glycosylation site on the same virus-binding interface.

139 ves restriction factors to evolve rapidly at virus-binding interfaces to regain defense.

140 e attributed to a role of the H3L protein in virus binding, internalization, or any event prior to la

141 Virus binding involves the mucin-type domain of alpha-DG

142 ARGE-dependent glycosylation of alpha-DG for virus binding is found for several isolates of LCMV, LFV

143 especially novel aspect of human influenza A virus binding is its ability to equivalently recognize g

144 soelectric points and variations in receptor-virus binding kinetics for different conditions.

145 Virus-binding kinetics of H3N2 virus isolates slowly evo

146 f CD4-IgG were completely inactivated, while viruses binding less remained infectious.

147 the survival curve followed a model in which viruses binding more than a threshold level of CD4-IgG w

148 ermit the use of CD46 on host cells by Ad16, virus binding occurs with lower efficiency than with B2

149 LARGE modification required for laminin- and virus-binding occurs on specific Thr residues located at

150 with the host cell range properties of both viruses, binding of 34TF10 gp95-Fc was observed for all

151 During the process of assembly of enveloped viruses, binding of the nucleoprotein core of the virus

152 virus receptors or factors on host cells for virus binding or entry.

153 2-3) linkage of sialic acid had no effect on virus binding or infection.

154 induced gene expression but had no effect on virus binding or uptake.

155 se may be blocked by D4E1 treatment, whereas virus binding, penetration, RNA synthesis, and protein s

156 Expression of either of these artificial virus-binding receptors in fiber receptor-negative cells

157 eover, addition of DGD antibodies soon after virus binding reduced endogenous DGD protein levels and

158 is homologous to the human immunodeficiency virus binding region of CD4 and to the poliovirus bindin

159 In some well-studied cases, the virus-binding region on the receptor has been found to b

160 niquely folded CC' loop that encompasses key virus-binding residues.

161 lly, we generated a new receptor by fusing a virus-binding, single-chain antibody (scAb) to intracell

162 esignated region A, has been proposed as the virus binding site, because mutations in this region abo

163 us, indicating that Pit1 region A is not the virus binding site.

164 cosylation occludes a potentially functional virus-binding site in the CAT-1 protein of hamsters, thu

165 apy with UB-421, an antibody that blocks the virus-binding site on human CD4+ T cells, could induce s

166 These attempts to localize the PiT2 virus-binding site were hampered because they were based

167 onkey cells, suggesting that the IgA and the virus binding sites are in different epitopes on HAVCR1/

168 Similar motifs have been identified in the virus binding sites of other retrovirus receptors, sugge

169 stribution of LSTc, serotonin receptors, and virus binding sites overlapped in kidney and in the chor

170 mouse small intestine was not due to lack of virus binding sites, because poliovirus could attach to

171 viruses, ecotropic MuLV infection eliminates virus-binding sites from cell surfaces and results in co

172 r binding provides a basis for understanding virus-binding specificity, motility, and HA/neuraminidas

173 loop I of hCEA as the region conferring the virus-binding specificity.

174 d the virus-alpha3 and -beta1 complexes, and virus binding studies suggest a role for alpha3beta1 in

175 3beta1 integrin via its glycoprotein gB, and virus binding studies suggest that alpha3beta1 is one of

176 upport for this hypothesis was obtained from virus binding studies using mutant or neuraminidase-trea

177 ed the virus alpha3 and beta1 complexes, and virus-binding studies suggest a role for alpha3beta1 in

178 eraction with the cellular receptor CD46 and virus binding, suggesting interference with a yet-uniden

179 4T) that creates a glycosylation site on the virus binding surface of the CD4 receptor.

180 himpanzee CD4 are singly glycosylated at the virus binding surface, and some allelic versions are dou

181 all of these residues correspond to the two virus binding surfaces of TfR1.

182 t-aptamers release fluorescence signals upon virus binding that are easily read with a handheld fluor

183 human chromosome 21 exhibited high levels of virus binding that was specific for the viral fiber prot

184 mature DC with trypsin significantly reduced virus binding, thus demonstrating the role of HIV envelo

185 Rather, virus binding to a receptor on the cell surface induces

186 Thus, virus binding to a sialic acid receptor and to immunoglo

187 inct steps of a common pathway that requires virus binding to a single receptor, assembly of multival

188 /T215I) and NA (E119A) proteins that reduced virus binding to alpha2,3-sialyl receptor and NA activit

189 In contrast, virus binding to alphavbeta6 including the beta8 cytodom

190 ex carbohydrate content greatly increased SB virus binding to and infection of THP-1 cells expressing

191 This technique measures virus binding to and release from a surface coated with

192 st step of virus infection to cause disease: virus binding to angiotensin-converting enzyme 2 (ACE2)

193 eceptor-binding domain (RBD), which mediates virus binding to angiotensin-converting enzyme 2, the fu

194 thymus RNA, called MTVR, was able to confer virus binding to both monkey and human cells; this bindi

195 n E2 that mediate neutralization by blocking virus binding to CD81.

196 Several MAbs efficiently blocked virus binding to cell lines expressing human or rhesus D

197 nic retrovirus infection may be initiated by virus binding to cell receptors or to the virus envelope

198 d hemagglutinin substitutions that increased virus binding to cell surface glycan receptors.

199 in or neuraminidase mutations that increased virus binding to cell surfaces.

200 not alter species tropism but abolished both virus binding to cells and infectivity.

201 he enzymes tested were capable of inhibiting virus binding to cells, but only neuraminidase was capab

202 Virus binding to cells, entry, and nucleocapsid uncoatin

203 erexpression of the human FUT2 gene enhances virus binding to cells, it is not sufficient to allow a

204 n inhibited HVEM-dependent infection but not virus binding to cells.

205 are located on the sites that may influence virus binding to cellular receptors.

206 esidues 289, 291, 324, and 328 may influence virus binding to cellular receptors; and residue 295 may

207 subdomain 2 (P2) of VP1, which may influence virus binding to cellular receptors; and residue 295 was

208 arized Caco-2 cells and is not influenced by virus binding to DAF.

209 Inhibition of virus binding to DC-SIGN, thus, represents an attractive

210 s to the Ad fiber coat protein that redirect virus binding to either alpha(v) integrin [AdZ.F(RGD)] o

211 Western blots using antibodies that inhibit virus binding to either the human or mouse CVB receptors

212 Here we show that virus binding to filopodia induces a rapid and highly or

213 t apolipoprotein E is likely responsible for virus binding to heparan sulfate and that N- and 6-O-sul

214 on of either E2 glycosylation site increased virus binding to heparin and increased replication in BH

215 olecules are detectable intermediates during virus binding to host cell membranes, which probably has

216 d and Western blot assays, and the damage of virus binding to host cells as quantified by RT-qPCR.

217 se of soluble rhinovirus receptor to inhibit virus binding to host cells should be feasible in humans

218 oxygen damaged the virus genome and impaired virus binding to host cells, which elucidated the mechan

219 AcGM3 displayed dose-dependent inhibition of virus binding to host cells.

220 RSV and influenza A, in vitro, by inhibiting virus binding to host cells.

221 nfluenza virus-infected cells in addition to virus binding to host cells.

222 known host-range determinant as it mediates virus binding to host-specific cellular receptors.

223 sus repeat 2 (SCR2) with murine SCR2 ablated virus binding to human DAF, as did deletion of human SCR

224 These data demonstrate that JC virus binding to human glial cells induces an intracellu

225 identified that increases 2009 pandemic H1N1 virus binding to human-like alpha2,6-linked sialic acids

226 tter understand the molecular details of the virus binding to its host cell and to develop anti-viral

227 SLPI binding neither prevented virus binding to monocytes nor attenuated the infectivit

228 raction between JCV and glial cells involves virus binding to N-linked glycoproteins containing termi

229 ifferent species and quantified by measuring virus binding to receptor analogs using surface biolayer

230 amount of reference sera required to prevent virus binding to red blood cells.

231 This mechanism may reduce SARS-CoV-2 virus binding to respiratory epithelial cells and decrea

232 binds to sialic acid, which enhances overall virus binding to sialic acid receptor analogues.

233 Infection by PV is initiated by virus binding to specific cell receptors, which results

234 arly important since the disruption of plant virus binding to such a receptor may enable the developm

235 HIV-1), gp120(SU) plays an essential role in virus binding to target CD4+ T-cells and is a major vacc

236 ell surface receptor CD4, thus impairing the virus binding to target cells.

237 s of virus-producing cells, and second after virus binding to target-cell receptors.

238 e coronavirus 2 (SARS-CoV-2) is initiated by virus binding to the ACE2 cell-surface receptors(1-4), f

239 The antagonism of activation of TLRs and virus binding to the alveolar epithelium by resident con

240 rdiovascular injury is the interplay between virus binding to the angiotensin-converting enzyme 2 rec

241 gation of virion particles preventing normal virus binding to the cell surface and uptake into cells.

242 viruses (HIV and SIV, respectively) mediate virus binding to the cell surface receptor CD4 on target

243 wed that all monoclonal antibodies inhibited virus binding to the cell surface.

244 without affecting CD4 or CXCR4 expression or virus binding to the cell surface.

245 ce receptor is not necessary for the initial virus binding to the cells but is required for subsequen

246 eriments showed that MAb vpg15 did not block virus binding to the cells.

247 Therefore, virus binding to the cellular receptor CD46 and subseque

248 on the surface of mammalian cells, inhibits virus binding to the host cell and infection with the pe

249 The biological implications in regard to virus binding to the host cell and the release of new vi

250 restricted to mice and rats at the level of virus binding to the host cell receptor.

251 on virus internalization, fiber shedding and virus binding to the nuclear envelope.

252 Neuraminidase also contributes to virus binding to the sialic acid groups of cell glycopro

253 This suggests that virus binding to the surface of CD4(-) cells is an impor

254 uced the virus infectivity without affecting virus binding to the target cells.

255 tep for efficient gene transfer is effective virus binding to the target cells.

256 , indicating the involvement of P antigen in virus binding to these cells.

257 development of novel therapeutics targeting virus binding to this cell surface receptor.

258 a a poorly defined mechanism, which involves virus binding to vitamin K-dependent blood coagulation f

259 e, disrupting viral particles and decreasing virus binding to, and infection of, human epithelial cel

260 For many enveloped viruses, binding to a receptor(s) on a host cell acts as

261 elated with neutralizing antibody titers and virus-binding total IgG and IgG1 concentrations.

262 surface receptors TIM-1 and -4 also enhance virus binding/transduction.

263 heparin inhibited radiolabeled A2 and cp-52 virus binding up to 90%.

264 DC draining from the skin occurs soon after virus binding via the caspase 8 pathway and is not assoc

265 In contrast, there was little difference in virus binding, virus infection rate, or cell cycle distr

266 Virus binding was not affected by CA-074 Me, whereas syn

267 reverse transcription-PCR assay to quantify virus binding, we found that HLA-DR+/DC-SIGN+ cells can

268 ecific antibodies were effective at blocking virus binding, we propose that spinoculation works by de

269 , anti-DC-SIGN antibodies blocked 90% of the virus binding when more-physiologic amounts of virus ino

270 n pH-dependent conformational changes and in virus binding, which could partially explain the defects