ライフサイエンスコーパス: virus receptor

1 ch serves as the amphotropic murine leukemia virus receptor.

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

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

4 can be achieved by circumventing the normal virus receptor.

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

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

7 es its receptor, myeloproliferative leukemia virus receptor.

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

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

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

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

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

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

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

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

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

17 DH82 (histocytosis) cells encode functional virus receptors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Certain virus receptors are sequestered on the basolateral surfa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 05 of the virus capsid protein comprised the virus receptor-binding region and suggested that genotyp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 We first characterized this virus-receptor interaction crystallographically.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 These virus-receptor interactions can be highly species specif

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

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

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

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

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

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

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

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

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

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

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

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

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

132 tructural changes can dramatically influence virus-receptor interactions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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