ライフサイエンスコーパス: virus receptor

1 lls and added ganglioside GD1a as a specific virus receptor.

2 ransduction of cells that do not express the virus receptor.

3 ch serves as the amphotropic murine leukemia virus receptor.

4 a tool to study the expression of the visna virus receptor.

5 f interactions between the S protein and the virus receptor.

6 can be achieved by circumventing the normal virus receptor.

7 (HS) moieties of proteoglycans, the initial virus receptor.

8 independent of the use of this protein as a virus receptor.

9 es its receptor, myeloproliferative leukemia virus receptor.

10 lization of HIV in cells lacking the primary virus receptor.

11 ne, which allows it to serve as a functional virus receptor.

12 lly for viral entry, suggest that MYADM is a virus receptor.

13 have acquired a high affinity for human-type virus receptor.

14 man TfR1 into an efficient OCEV and Tacaribe virus receptor.

15 ) a loss of the use of the natural ecotropic virus receptor.

16 x in which a cellular protein is used as the virus receptor.

17 the mammalian alpha2,6Gal-linked sialic acid virus receptor.

18 enza virus receptors and low levels of avian virus receptors.

19 DH82 (histocytosis) cells encode functional virus receptors.

20 izes a conditional allele of the avian tumor virus receptor A (TVA), which allows infection of mouse

21 Adeno-associated virus receptor (AAVR) (also named KIAA0319L) is an essen

22 We discuss the structural basis of virus receptor activities of murine CEACAM1 proteins, bi

23 icities as seen for virus neutralization and virus-receptor activities.

24 d N-terminal domain of MHVR is essential for virus receptor activity and is the binding site for mono

25 r elucidate the regions of MHVR required for virus receptor activity and MAb CC1 binding, we construc

26 Several recombinant glycoproteins exhibited virus receptor activity but did not bind MAb CC1, indica

27 activity are found profoundly influences the virus receptor activity of the glycoprotein.

28 al to the receptor binding site but affected virus-receptor affinity and HA dynamics, allowing the vi

29 Expression of HSV gD, which is known to bind virus receptors, also blocked cell-to-cell spread.

30 omplexes is an important characteristic of a virus receptor and may have exerted a selective pressure

31 been shown to preferentially associate with virus receptors and alter physical properties of the mem

32 tropism is determined by the availability of virus receptors and entry cofactors on the surface of ho

33 hat expresses high levels of human influenza virus receptors and low levels of avian virus receptors.

34 These findings suggest that virus receptors and S protein-cleaving proteases combine

35 alter E2 conformations leading to changes in virus-receptor and -glycosaminoglycan interactions and c

36 ransgenic animals expressing CD46, a measles virus receptor, and lacking interferon type 1 receptor g

37 ry tract is not solely due to the absence of virus receptor, and other factors are involved in determ

38 transmission of HIV by locally concentrating virus, receptor, and coreceptor during the formation of

39 Insight into how virus receptors are organized prior to virus binding and

40 Certain virus receptors are sequestered on the basolateral surfa

41 c acid 237, of the ecotropic murine leukemia virus receptor (ATRC1) have been shown to be essential f

42 tralization epitope(s) and forms part of the virus receptor attachment site.

43 57, 158, 184, 188, and 192 can also modulate virus receptor avidity and that substitutions that incre

44 y and appears to neutralize by blocking both virus receptor binding and postattachment steps.

45 onadherent cells to bind a recombinant Ebola virus receptor binding domain (EboV RBD) and to be infec

46 identified, none of these mutations affected virus receptor binding preference and immunogenicity.

47 parainfluenza virus type 3 (HPIV3) or Nipah virus receptor binding proteins indicates that receptor

48 ution in VP1 loop I adjacent to the putative virus receptor binding site exhibited a large-plaque phe

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

50 onstrate that 190V in the HA does not change virus receptor binding specificity but enhances virus bi

51 Virus sequence analysis and virus receptor binding studies highlighted potential mar

52 epitope but may indirectly impact influenza virus receptor binding, endosomal fusion, or budding.

53 n in order to determine its possible role in virus receptor binding.

54 This indicates that virus receptor binding/attachment to cells, membrane fus

55 mRNA induction by half, while prevention of virus-receptor binding completely inhibited virus-induce

56 Virus-receptor binding is highly specific, and this spec

57 due to viral replication and part was due to virus-receptor binding.

58 ion of the virus and abolished by preventing virus-receptor binding.

59 nti-rotavirus peptide that acts by hindering virus-receptor binding.

60 that, at least in tissue culture, influenza virus receptor-binding activity can be entirely shifted

61 We characterized the virus receptor-binding affinity, pathogenicity, and tran

62 05 of the virus capsid protein comprised the virus receptor-binding region and suggested that genotyp

63 ving understanding of the basis of influenza virus receptor-binding.

64 g, we identified genetic factors influencing virus-receptor-binding and predicted GP-NPC1-binding avi

65 dition, our results suggest that multivalent virus-receptor bonds and diffusion in the membrane contr

66 erefore, we studied the distribution of H5N1 virus receptors, by virus and lectin histochemistry, dur

67 we demonstrate that an antibody targeting a virus receptor can cure chronic viral infection and unco

68 omologous human protein that lacks ecotropic virus receptor capability resulted in acquisition of eco

69 nfected cell and triggers degradation of the virus receptor CD4.

70 rotein surface of gp120, one of which is the virus receptor (CD4) binding site.

71 (HIV-1) that promotes the degradation of the virus receptor, CD4, and enhances the release of virus p

72 tially mimics the interaction of the primary virus receptor, CD4, with gp120.

73 tablished by downmodulation of the principal virus receptor, CD4.

74 -unrelated febrile seizures) and the measles virus receptor CD46 (rs1318653: P = 9.6 x 10(-11) versus

75 sive syncytia in cells expressing the normal virus receptor CD46 and also in CD46-negative cells expr

76 r cells expressed high levels of the measles virus receptor CD46.

77 ch ablate recognition of the natural measles virus receptors CD46 and SLAM.

78 Cryo-electron microscopy analysis of the virus-receptor complex and structure-guided mutagenesis

79 We have analyzed the structure of this virus-receptor complex by cryo-electron microscopy and t

80 ch specific structural rearrangements in the virus-receptor complex could help to trigger the irrever

81 alculated, showing for the first time in any virus-receptor complex the nonuniform distribution of RN

82 nd receptor, determined the structure of the virus-receptor complex, and identified residues in the r

83 suggesting that these sites interact in the virus-receptor complex.

84 nd for the subsequent internalization of the virus-receptor complex.

85 yoelectron microscopy reconstructions of the virus-receptor complexes for the 3 PV serotypes.

86 s between the S.CEACAM interaction and other virus-receptor complexes involved in receptor-triggered

87 The intracellular fate of internalized virus-receptor complexes is suspected of influencing the

88 The cryo-EM structures of the two virus-receptor complexes revealed a ring of integrin den

89 o a single receptor, assembly of multivalent virus-receptor complexes, structural changes in viral en

90 s expressing reduced levels of the influenza virus receptor determinant, sialic acid, by selecting Ma

91 e virus, likely due to reduced levels of the virus receptor, dipeptidyl peptidase 4 (DPP4) and higher

92 scuss the most commonly employed methods for virus receptor discovery, specifically highlighting the

93 the intrinsic and extrinsic factors such as virus receptor engagement, adaptive immunity, and virus

94 thoreovirus (reovirus), but the mechanism of virus-receptor engagement is unknown.

95 tter of which is responsible for binding the virus receptors ephrinB2 and ephrinB3.

96 cofactors.IMPORTANCE A factor other than the virus receptor expressed by target cells has been found

97 e heme export by the group C feline leukemia virus receptor (FLVCR).

98 ability resulted in acquisition of ecotropic virus receptor function comparable to that of ATRC1.

99 transport proteins, the gibbon ape leukemia virus receptor Glvr-1 (Pit-1) or the amphotropic retrovi

100 irus strain A59 (MHV-A59), expression of the virus receptor glycoprotein MHVR was markedly reduced.

101 uenza viruses, the distribution of influenza virus receptors have not been studied during influenza v

102 mal models: in mice expressing the essential virus receptor (human transferrin receptor 1; huTfR1) an

103 acids 407 to 547 bound to purified, soluble virus receptor, human aminopeptidase N (hAPN).

104 nositol 3-kinase (PI3K)/Akt pathway, and the virus receptor hyaluronidase 2 (Hyal2) is not involved.

105 nt factor, is not sufficient as an influenza virus receptor in vivo.

106 all species, we observed a decrease of H5N1 virus receptors in influenza virus-infected and neighbor

107 ransmission would allow for crop protection, virus receptors in insect vectors are unknown.

108 epresents the functional equivalent of other virus receptors in its interaction with processed viral

109 We studied the distribution of virus receptors in kidney and brain using lectins, antib

110 ugh studies on the distribution of influenza virus receptors in normal respiratory tract tissues have

111 ecognition of both avian and human influenza virus receptors in the absence of other changes.

112 partly be explained by the presence of H5N1 virus receptors in the human alveoli, which are the site

113 The distribution of influenza virus receptors in the respiratory tract of the micromin

114 host specificity, transmission barriers, and virus receptors in the vectors.

115 s exploits extracellular vesicles to mediate virus receptor-independent transmission to host cells an

116 This finding provides a novel aspect to virus receptor interaction and host manipulation by path

117 To test the effect of structural virus receptor interaction on infection, two chimeric re

118 demonstrate that miR-28-3p does not prevent virus receptor interaction or virus entry but, instead,

119 In contrast to influenza A virus, receptor interaction plays an essential role in p

120 tes a critical hydrophobic side chain to the virus-receptor interaction (14).

121 sults of our structural investigation of the virus-receptor interaction and ensuing conformational ch

122 We first characterized this virus-receptor interaction crystallographically.

123 may be the result of steric hindrance of the virus-receptor interaction following the interaction bet

124 Our finding that the mode of virus-receptor interaction in EV12 is distinct from that

125 studies provide an insight into theoretical virus-receptor interaction points, structure of immunoge

126 This review examines the contribution of the virus-receptor interaction to replication in vivo as wel

127 nomolar affinity using a unique mechanism of virus-receptor interaction, which is coordinated by mult

128 in will provide useful information about the virus-receptor interaction.

129 rate antibodies which do not block influenza virus-receptor interaction.

130 ntribution of these residues in a productive virus-receptor interaction.

131 ing at low pH may mimic those occurring upon virus-receptor interaction.

132 t these antibodies block different facets of virus-receptor interaction.

133 , the techniques described may be applied to virus:receptor interaction studies or antiviral drug:vir

134 at the south rim of the canyon dominates the virus-receptor interactions and may correspond to the in

135 residues needed for EBOV entry clarifies the virus-receptor interactions and paves the way for the de

136 nalysis, and will be valuable for studies of virus-receptor interactions and potentially for vaccine

137 Although the virus-receptor interactions are believed to trigger vira

138 range and better inform our understanding of virus-receptor interactions associated with disease emer

139 While there have been extensive studies of virus-receptor interactions at the cell surface, our und

140 myr-preS1-NTCP complex were used to analyze virus-receptor interactions at the molecular level.

141 These virus-receptor interactions can be highly species specif

142 inant of viral tropism and pathogenesis, and virus-receptor interactions can be therapeutic targets.

143 These virus-receptor interactions can therefore dictate viral

144 Understanding the nature of virus-receptor interactions could also be important for

145 ons during budding and of virus assembly and virus-receptor interactions during virus uptake into inf

146 To understand the virus-receptor interactions for HPV infection, we determ

147 that, compared with human rhinoviruses, the virus-receptor interactions for PVs have a greater depen

148 Understanding the virus-receptor interactions for these DPP4 orthologs wil

149 which is different from previously reported virus-receptor interactions in which a single type of bi

150 f the cryo-EM structure identifies important virus-receptor interactions that are conserved across pi

151 build an atomic-level iterative framework of virus-receptor interactions to facilitate epidemic surve

152 y PVR-Fc but not by D1-Fc indicated that the virus-receptor interactions were specific.

153 y can therefore regulate binding by reducing virus-receptor interactions when the concentration of re

154 by a variety of mechanisms, such as low pH, virus-receptor interactions, and virus-host chaperone in

155 tion, where bacterial glycans can facilitate virus-receptor interactions, enhance viral replication,

156 he early events of KSHV infection, including virus-receptor interactions, involved envelope glycoprot

157 d T(H)2 immunoglobulin G subclasses, blocked virus-receptor interactions, neutralized viral infection

158 protein encoded by a viral circRNA modulates virus-receptor interactions, resulting in blocking of vi

159 an escape mechanism would be compatible with virus-receptor interactions, we tested a soluble dodecam

160 pioneering paradigm for the consequences of virus-receptor interactions.

161 tructural changes can dramatically influence virus-receptor interactions.

162 ropism, which is thought to be influenced by virus-receptor interactions.

163 basis for understanding viral evolution and virus-receptor interactions.

164 ing virus-host cell interactions, especially virus-receptor interactions.

165 heir association has a synergistic effect in virus-receptor interactions.

166 urface molecule influences FMDV tropism, and virus/receptor interactions appear to be responsible, in

167 t spot structure have significant effects on virus/receptor interactions, revealing critical energy c

168 ve selection in bat NPC1 concentrated at the virus-receptor interface, with the strongest signal at t

169 e identity of the amino acid residues in the virus-receptor interface.

170 o imbalanced salt bridges at the hydrophobic virus/receptor interface, and that SARS-CoV has evolved

171 IMPORTANCE The knowledge about a virus receptor is useful to better understand the uptake

172 nfection does not occur through increases in virus receptor levels or virus binding, indicating that

173 e cell lines that express very low levels of virus receptor MHVR and which also have and may express

174 Mouse hepatitis virus receptor (MHVR) is a murine biliary glycoprotein (

175 , our data suggest that the decrease of H5N1 virus receptors might be part of a defense mechanism tha

176 delivery by using an appropriate nanobody or virus receptor mimic.

177 t1) but also the amphotropic murine leukemia virus receptor (MolPit2).

178 lls expressing HVEM, but not the other major virus receptor, nectin-1.

179 pression in cell lines, drug-target, protein-virus receptor networks, and immune cell infiltration of

180 en shown to destabilize the complex with the virus receptor NPC1.

181 which also have and may express alternative virus receptors of lesser efficiency, there is a strong

182 cell line clone, suggesting that it binds to virus receptor on host cells.

183 surface protein recognizes and binds to the virus receptor on host cells.

184 ecent demonstration of the clustering of the virus receptor on rat cells suggested a possible interac

185 ruses from entry owing to a lack of archaeal virus receptors on the external membranes.

186 necessary cellular molecules serving as the virus receptors or factors on host cells for virus bindi

187 effectively than conventional MDCK or human virus receptor-overexpressing (AX4) cells.

188 iruses (FeLV-Bs) use the gibbon ape leukemia virus receptor, Pit1, as a receptor for entry.

189 gy modeling and computational docking of the virus-receptor protein-protein interaction.

190 have been identified include genes encoding virus receptors, receptor-modifying enzymes, and a wide

191 y the presence of specific membrane-embedded virus receptors required for virus entry.

192 This effect does not abrogate virus receptor requirements, is specific to PS compared

193 expressing human dipeptidyl peptidase 4, the virus receptor, showed that the single deletion of the E

194 nin, does not bind the canonical influenza A virus receptor, sialic acid or any other glycan(1,3,4),

195 may contribute to the formation of a single virus receptor site.

196 rease in the abundance of apically localized virus receptors such as ACE2.

197 develop a nanodisc incorporated with a decoy virus receptor that inhibits virus infection.

198 moter of the CD155 gene specifying the polio virus receptor that is bound by the nuclear respiratory

199 esentation may result from the virus using a virus receptor that is expressed predominantly in the lu

200 piratory syndrome coronavirus 2 [SARS-CoV-2] virus "receptor") that results in tissue injury from ang

201 tion treatment consisting of a proteinaceous virus receptor trap and an RNA interference-based compon

202 expression of the subgroup A avian leukosis virus receptor, TVA.

203 rs serve as a powerful tool for the study of virus receptor usage and entry.

204 ient induction of apoptosis and suggest that virus receptor utilization plays an important role in re

205 The observed decrease of H5N1 virus receptors was associated with the presence of MxA,

206 h the functional assay in that expression of virus receptors was predominantly on the more-committed

207 ere potent and nearly equally effective MERS virus receptors, while goat and bat receptors were consi

208 Detection of the mouse hepatitis virus receptor within the central nervous system (CNS) h