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1  determined to be manifested at the level of virus attachment.
2 omplex did block entry even when added after virus attachment.
3  with cell surface glycosaminoglycans during virus attachment.
4 9-201 and 212-216, independently involved in virus attachment.
5 he viral attachment protein, interfered with virus attachment.
6 ate each of the three amino-terminal HBDs in virus attachment.
7 ed that specific polar lipids may facilitate virus attachment.
8 tralization was not associated with blocking virus attachment.
9 fically blocked HCV entry but did not affect virus attachment.
10 face sialic acid groups for transduction and virus attachment.
11 ation, consistent with a role for CD81 after virus attachment.
12  dramatically inhibits infection by reducing virus attachment.
13 and that it, like other polyanions, inhibits virus attachment.
14 xsackie/adenovirus receptor (CAR) needed for virus attachment.
15 equire viral lysis, aggregation, or blocking virus attachment.
16                                              Virus attachment also induced tyrosine phosphorylation o
17  NTD-SA interaction enhances both S-mediated virus attachment and ACE2 binding.
18 strate that RBD has two functions: mediating virus attachment and activating the fusion mechanism.
19 de has potential value as a reagent to study virus attachment and as a future therapeutic.
20  This interaction seems to be independent of virus attachment and cell entry.
21 B does not affect gC-dependent mechanisms of virus attachment and does not block virus attachment at
22 te to open therapeutic avenues to counteract virus attachment and entrance to the body.
23 extracellular domain is sufficient to permit virus attachment and entry and that the presence of a GP
24 eased from specific cell types, and enhances virus attachment and entry into cells.
25 ce glycoprotein (GP1,2) that is required for virus attachment and entry into cells.
26 otein receptor (LDLr) has been implicated in virus attachment and entry into cells.
27 laments serve to increase the probability of virus attachment and entry into host cells.IMPORTANCE Hi
28  is involved in several functions, including virus attachment and entry to target cells, production o
29 de of HIV-1 infection occurs at the level of virus attachment and entry via a unique mechanism that i
30 titis C (HCV) E2 glycoprotein is involved in virus attachment and entry, and its structural organizat
31 n of ECA11 encoding proteins associated with virus attachment and entry, cytoskeletal organization, a
32 ive changes in E1 can have a major effect on virus attachment and entry, furthering our knowledge of
33 ecific antibodies blocking distinct steps of virus attachment and entry, rather than the perspective
34 potentially important differences related to virus attachment and entry.
35 ations also suggest an active role of NTD in virus attachment and entry.
36 ons in both virus and receptor important for virus attachment and entry.
37 l envelope glycoprotein (GP) responsible for virus attachment and entry.
38 d region in the BA strain G protein augments virus attachment and fitness.
39  we show that E1 V156A and E1 K211T modulate virus attachment and fusion and impact binding to hepari
40 y gp120 (Env), a viral protein that mediates virus attachment and fusion to target cells, and also fa
41 utralizes CHIKV infection mainly by blocking virus attachment and fusion.
42 that MMTV/TLR4 interaction is independent of virus attachment and fusion.
43  binding to hematopoietic cells, we analyzed virus attachment and gene delivery to CHO cells expressi
44 ster cells became susceptible to coxsackie B virus attachment and infection.
45 ate and this type of interaction facilitates virus attachment and infectivity.
46 inds directly to VEEV particles and enhances virus attachment and internalization into host cells.
47 es bind RSV F protein, which plays a role in virus attachment and mediates fusion.
48 particles determines the probability of both virus attachment and membrane fusion when viral glycopro
49 while functional domains are responsible for virus attachment and membrane fusion.
50 role in immunity to measles by blocking both virus attachment and subsequent fusion with the host cel
51                                              Virus attachment and subsequent infection of polarized c
52 o analyze membrane fusion events that follow virus attachment and to identify multiple epitopes on VZ
53  complex and insights into the mechanisms of virus attachment and uncoating.
54 cluding reverse transcriptase, protease, and virus attachment, and exhibit no detectable activity aga
55 on by a panel of echoviruses at the stage of virus attachment, and that a blocking antibody to beta2M
56 nisms of virus attachment and does not block virus attachment at 4 degrees C.
57 n early role, uncoating assays showed normal virus attachment but delayed virus entry in the absence
58                            To understand how virus attachment drives entry, we compared infection of
59  When proteasome inhibitors were added after virus attachment, early gene expression was prolonged an
60  conserved MPXV surface proteins involved in virus attachment, entry, and transmission can induce MPX
61                                CD46 mediates virus attachment, entry, and virus-induced cell-to-cell
62               The presence of this efficient virus attachment factor on multiple endothelial cell typ
63 ve contributions of these previously defined virus attachment factors to HIV binding and accumulation
64                                              Virus attachment, fusion, internalization and transport
65 s of EFNB2 specificity for binding the Nipah virus attachment G glycoprotein over Eph receptors.
66                                     A Hendra virus attachment (G) glycoprotein subunit vaccine was te
67  must be present during the initial phase of virus attachment; in contrast, addition of galectin-1 po
68                      We found that influenza virus attachment induced PI3K-dependent FAK-Y397 phospho
69 iously disclosed HIV (human immunodeficiency virus) attachment inhibitors, exemplified by BMS 806 (fo
70 idase (HN) protein, which is responsible for virus attachment, interacts with the fusion protein in a
71 CD34(+) cells and K562 cells on the level of virus attachment, internalization, and replication.
72                         With the caveat that virus attachment is only the first step in the virus rep
73   Integrin alphavbeta6 is the major site for virus attachment on the beta6-transfected cells, and bin
74 ever, HCMV gB is not absolutely required for virus attachment or assembly and egress from infected ce
75 ome disease, whereas resistant birds prevent virus attachment or entry and do not become infected.
76     Abeta enhanced infection at the stage of virus attachment or entry into the cell.
77 h palivizumab or motavizumab did not inhibit virus attachment or the ability of F protein to interact
78 ainst HIV-1 reverse transcriptase, protease, virus attachment, or nucleocapsid protein zinc fingers.
79 ences described to the S RNA, containing the virus attachment protein glycoprotein 1.
80 ted potential interface areas of the measles virus attachment protein hemagglutinin to begin the inve
81                                              Virus attachment proteins mediate binding to host cell r
82  B Ad fiber knobs that use CD46 as a primary virus attachment receptor.
83  RGD motif in the penton base did not affect virus attachment, regardless of the type of cellular rec
84 fluenza viruses were labeled to identify the virus attachment site in the mouse cornea.
85                          Neither the initial virus attachment site, heparan sulfate proteoglycans, no
86 internalization, but functions merely as the virus attachment site, suggests that the extracellular p
87               Membrane proteins that mediate virus attachment tether virus particles to the cell surf
88                           HIV-1 Env mediates virus attachment to and fusion with target cell membrane
89 ectly to TBEV envelope proteins and promoted virus attachment to and internalization in cells through
90 genome size did not affect the efficiency of virus attachment to and internalization into cells.
91 euraminidase (NA), which are responsible for virus attachment to and release from host cells, respect
92                    PSGL-1 and CD43 inhibited virus attachment to CD4(+) cells irrespective of the pre
93  anti-gp120 mAb IgGb12, an agent that blocks virus attachment to CD4, suggesting that endocytosed vir
94              Infection would proceed through virus attachment to cell surface heparan sulfate (HS) pr
95 eased sensitivity to GAG-based inhibitors of virus attachment to cells and reduced release of viral p
96                                              Virus attachment to cells plays an essential role in vir
97 onstrate that E1 V156A and K211T function in virus attachment to cells, a role that until now has onl
98   A9E generally inhibited prior to or during virus attachment to cells, via virus aggregation, distor
99 t the antibody neutralizes HAstV by blocking virus attachment to cells.
100      They mainly neutralize by inhibition of virus attachment to cells.
101  that the duplicated region functions during virus attachment to cells.
102 0 and the protein itself did not inhibit the virus attachment to cells.
103 ould largely be explained by competition for virus attachment to cellular CD4 rather than other detri
104 tiple modes of action, including blockage of virus attachment to cellular heparan sulfate and enhance
105 determining viral persistence by influencing virus attachment to cellular receptors, such as sialylol
106                Although we found abundant H7 virus attachment to corneal epithelial tissue, this did
107                         Here, we report that virus attachment to DAF on the apical cell surface activ
108              Exposure to flagellin increased virus attachment to epithelial cells in a temperature-de
109 compared MV protein A27, which has a role in virus attachment to glycosaminoglycans on the cell surfa
110  to these glycoproteins, such as gC-mediated virus attachment to heparan sulfate or gE-mediated cell-
111 te that HSV-1 exploits galectin-3 to enhance virus attachment to host cells and support a protective
112 dies neutralize human astrovirus by blocking virus attachment to host cells.
113                         The antibodies block virus attachment to human cells and prevent capsid spike
114 we provide evidence that the antibody blocks virus attachment to human cells.
115 spike domain, however, both antibodies block virus attachment to human cells.
116 h larger amino acids specifically eliminated virus attachment to human DAF but had no effect on attac
117 ike protein at distinct epitopes and blocked virus attachment to its host receptor, human angiotensin
118 rnalization into epithelial cells as well as virus attachment to monocytic cells.
119 epends on intracellular signals triggered by virus attachment to PVR.
120 2161 and G2174 are directly involved in BeAn virus attachment to sialic acid and that substitutions o
121  expected for a process limited by ecotropic virus attachment to single receptors, fusion-from-withou
122 ng activity similar to that observed for KOS virus attachment to sog9 cells, a glycosaminoglycan-defi
123 with resistance to symptomatic infection and virus attachment to such motifs is essential to the infe
124 eplication, at least in part due to improved virus attachment to SUIT-2 cells.
125 eplication, at least in part due to improved virus attachment to SUIT-2 cells.
126 sis may combat virus infection by preventing virus attachment to susceptible cells.
127                           The specificity of virus attachment to target cells is mediated by hemagglu
128 al neutralization, heterotypic immunity, and virus attachment to target cells.
129         While gD has at least two functions, virus attachment to the cell and initiation of the virus
130 chronically infected cells or reduce initial virus attachment to the cell membrane.
131  of uncoating but had little or no effect on virus attachment to the cell surface.
132 rved results from a combination of hindering virus attachment to the host cell, inhibition of one or
133  to the immobilized GAG brushes ensures firm virus attachment to the interface.
134 to cause pneumonia, which is associated with virus attachment to the lower respiratory tract.
135 while polyclonal sera can specifically block virus attachment to the receptor.
136 ssion among humans, which is associated with virus attachment to the upper respiratory tract.
137                     DC-SIGN was required for virus attachment to these cells and DC-SIGN-expressing c
138 rminus of the G protein is also required for virus attachment to this model of the in vivo target cel
139  virus infection, and it does so by blocking virus attachment to TIM1.
140 ese interactions determine the mechanisms of virus attachment, uptake, intracellular trafficking, and
141  entry into host cells is directly linked to virus attachment via CD81 for HCV, this step in the vira
142 -targeting inhibitors typically act prior to virus attachment, whereas gp41 inhibitors are able to ac
143 s due to lower affinity of luminal cells for virus attachment, which can be overcome by pretreating c

 
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