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1 nt binding, causing a shift toward CSPGs for viral attachment.
2 his led to elevated sialylation and enhanced viral attachment.
3 ced JCPyV internalization but did not affect viral attachment.
4 1-positive cells and occurs within 60 min of viral attachment.
5 nize a variety of host receptors, leading to viral attachment.
6 ks the normal hemagglutinin-mediated mode of viral attachment.
7 nt of the identity of the receptors used for viral attachment.
8 tion by modulating gangliosides required for viral attachment.
9 paran sulfate proteoglycan (HSPG), promoting viral attachment.
10                                     To block viral attachment, 15C5 binds three forms of capsids, and
11                         Drugs that can block viral attachment and cell entry independent of antigenic
12                       Finally, we found that viral attachment and disassembly must occur within the s
13 capsid proteins that play important roles in viral attachment and disassembly.
14 e glycoprotein, E, of these viruses mediates viral attachment and entry by membrane fusion.
15 The major envelope glycoprotein, E, mediates viral attachment and entry by membrane fusion.
16 Its major envelope glycoprotein, E, mediates viral attachment and entry by membrane fusion.
17  many of the molecular processes involved in viral attachment and entry have been resolved, the popul
18  strategies such as microbicides that target viral attachment and entry into mucosa-resident target c
19 oprotein of hepatitis C virus (HCV) mediates viral attachment and entry into target hepatocytes and e
20 eins, VP4 and VP7, which are responsible for viral attachment and entry, are targets for protective n
21 ays are widely used to measure inhibition of viral attachment and entry, the ability of diverse antib
22 ss of apoptotic mimicry, they interfere with viral attachment and entry.
23 of molecular components and their synergy in viral attachment and entry.
24  the conformation of Spike, thereby reducing viral attachment and entry.
25    A single viral glycoprotein (GP) mediates viral attachment and entry.
26  to cellular receptors, thereby facilitating viral attachment and entry.
27 r of human semen itself, was at the level of viral attachment and entry.
28 rliest stages of viral infection, preventing viral attachment and exerting a mild virucidal action.
29 dase (HN), an envelope protein essential for viral attachment and for fusion mediated by the other en
30 that determine reciprocal specificity of the viral attachment and fusion (F) proteins have not been i
31 oviruses requires an interaction between the viral attachment and fusion (F) proteins to enable recep
32 ur as transient conformational states during viral attachment and fusion.
33 where they play important roles in mediating viral attachment and host cell entry.
34                  We suggest a model in which viral attachment and infection involves heparan sulfate-
35 oV-NL63 to heparan sulfates was required for viral attachment and infection of target cells, showing
36 virus and adenovirus receptor (CAR) mediates viral attachment and infection, but its physiologic func
37 ctly to the TBEV E glycoprotein and mediated viral attachment and internalization into cells.
38                          In paramyxoviruses, viral attachment and membrane fusion are governed by the
39  comparable to that of acyclovir by blocking viral attachment and penetration into host cells.
40 then used a genetic approach to identify the viral attachment and penetration protein, VP4, as a dete
41 avirus/vector interactions, serves a role in viral attachment and possibly in entry into arthropod ve
42 otavirus were used to test the importance of viral attachment and replication.
43  extracellular matrix, yet they also promote viral attachment and/or entry.
44 SCRs bind viral envelope N-glycans, blocking viral attachment and/or fusion.
45  usually requires an interaction between the viral-attachment and -fusion proteins.
46                        Retrocyclin 2 blocked viral attachment, and its addition during the binding or
47                  One of these loops mediates viral attachment, and the other participates in making t
48  steps in reovirus replication subsequent to viral attachment are required for reovirus-induced apopt
49 ycoprotein with the ACE2 receptor and higher viral attachment at low temperatures.
50 mation by competing with cell surface HS for viral attachment, binding studies were also performed.
51  that receptor affinity has little impact on viral attachment but is nevertheless a key determinant o
52              Confocal analysis revealed that viral attachment, cell entry, and intracellular transpor
53    Entry of HIV-1 into target cells involves viral attachment, co-receptor binding, and fusion.
54  entry is a multistep process that comprises viral attachment, co-receptor interactions and fusion.
55                                        After viral attachment, endocytosis, and fusion mediated by th
56 e trimeric SARS-CoV-2 Spike protein mediates viral attachment facilitating cell entry.
57                          Moreover, levels of viral attachment factors and ZIKV are significantly incr
58 ied up to a 10,480-fold higher expression of viral attachment factors AXL, GAS6, and PROS1 and a 3880
59 tain cell surface sialoglycans that serve as viral attachment factors for cell entry.
60 nfection and suggest that further studies of viral attachment factors in NPCs are needed.
61  of cells coordinated by interactions of the viral attachment (G) and fusion (F) glycoproteins.
62 ate binding and fusion in the absence of the viral attachment (G) protein.
63 le of fusing membranes in the absence of the viral attachment (G) protein.
64         Previous reports have shown that the viral attachment glycoprotein (G) modulates innate and a
65 receptors ephrin B2 and/or ephrin B3 via the viral attachment glycoprotein G, and the concerted effor
66 in alpha(v)beta3 on the COOH terminus of the viral attachment (H) protein and rescued the replication
67                  These findings suggest that viral attachment induces MHCII clustering, a process sim
68               Successful infection following viral attachment, internalization, and nuclear transport
69 t receptor ACE2, mechanical stability of the viral attachment is a crucial fitness advantage.
70 ycans (HSPG), the highly conserved target of viral attachment ligands (VALs).
71 ery of functional virus, indicating that the viral attachment mechanism is a primary distinguishing f
72 ucleopolyhedrovirus (AcMNPV), is involved in viral attachment, mediates membrane fusion during virus
73                     To measure the impact of viral attachment on the dynamics of MHCII, we employ an
74 inhibits infection primarily at a step after viral attachment, potentially by blocking envelope glyco
75 wo mutations, an amino acid change in the E2 viral attachment protein and a deletion within the 3'-UT
76           Outer-capsid protein sigma1 is the viral attachment protein and binds carbohydrate molecule
77 fy thrips proteins that bind directly to the viral attachment protein and thus may play a role in the
78                     The relationship between viral attachment protein encapsidation efficiency and vi
79 s provide evidence of a relationship between viral attachment protein encapsidation efficiency and vi
80  is known about the biological importance of viral attachment protein encapsidation efficiency.
81                                   Binding of viral attachment protein final sigma 1 to both sialic ac
82 plinary approach to study the binding of the viral attachment protein G to its host receptor ephrinB2
83                                          The viral attachment protein of RSV has many surprising feat
84 hment to cells is mediated by the binding of viral attachment protein sigma 1 to junctional adhesion
85 he S1 gene is bicistronic, encoding both the viral attachment protein sigma-1 and the nonstructural p
86  First, while the S1 gene. which encodes the viral attachment protein sigma1 (as well as a nonstructu
87     The S1 gene is bicistronic, encoding the viral attachment protein sigma1 and the nonstructural pr
88 s infections are initiated by the binding of viral attachment protein sigma1 to receptors on the surf
89                               The binding of viral attachment protein sigma1 to unidentified receptor
90                          The S1 gene encodes viral attachment protein sigma1, and the S4 gene encodes
91 heir original infectivity due to cleavage of viral attachment protein sigma1.
92 ed genetically to the S1 gene, which encodes viral attachment protein sigma1.
93 ervous system (CNS) that are dictated by the viral attachment protein sigma1.
94 ystem (CNS) attributable to polymorphisms in viral attachment protein sigma1.
95 respiratory avian coronaviruses based on the viral attachment protein spike (S1).
96 een the receptor-binding domain (RBD) of the viral attachment protein spike from two IBV strains with
97 n AF15561, we identified a residue in the E2 viral attachment protein that is a critical determinant
98 ractions and, along with GP2a, serves as the viral attachment protein that is responsible for mediati
99 tion of an amino acid polymorphism in the E2 viral attachment protein using a mouse model of CHIKV mu
100 , using discrete receptor-binding domains in viral attachment protein, final sigma1.
101 membrane fusion requires the presence of the viral attachment protein, G.
102  E2 glycoprotein, which is thought to be the viral attachment protein, interfered with virus attachme
103 he T3C/96 S1 gene segment, which encodes the viral attachment protein, sigma 1, confirmed the serotyp
104    Using structural homology modeling of the viral attachment protein, we infer that three of the fiv
105 virus (RSV) was identified previously as the viral attachment protein.
106 e globular domain of hemagglutinin (HA), the viral attachment protein.
107                            Many functions of viral attachment proteins are established, but less is k
108                                              Viral attachment proteins can serve multiple functions d
109 s using representative crystal structures of viral attachment proteins in complex with glycans.
110 ts provide new insights into the function of viral attachment proteins in the initiation of infection
111 g properties underlying the nanomechanics of viral attachment proteins offers perspectives in the dev
112 ly high affinity that all available receptor-viral attachment proteins were destined to bind at stead
113 e, both before and after they are ligated by viral attachment proteins.
114 f binding is dictated by the availability of viral attachment proteins.
115 f the large HBV surface protein is the major viral attachment site on hepatocytes and thus offers a t
116 yofibers is not a consequence of the loss of viral attachment sites on the surfaces of mature muscle
117                                    Three GP1 viral attachment subunits assemble to form a chalice, cr
118 surface of the protein and new insights into viral attachment through binding to membrane protein rec
119 annot infect rhesus macaques by proving that viral attachment through gp350 is not the mechanism for
120 tion of viral particles and/or inhibition of viral attachment, thus reducing viral entry.
121 f the SARS-CoV-2 spike glycoprotein mediates viral attachment to ACE2 receptor and is a major determi
122  Initiation of infection is mediated through viral attachment to alpha2,6-sialic acid-containing lact
123 S2, and other proteases that are involved in viral attachment to and entry into target cells.
124  was due to the ability of b12 to block both viral attachment to and uptake by epithelial cells.
125 lement receptor type 2 (CR2) is critical for viral attachment to B lymphocytes.
126          Reovirus cell entry is initiated by viral attachment to cell surface glycans and junctional
127 gs suggest that HHV-7 gp65 may contribute to viral attachment to cell surface proteoglycans.
128              The RSV G glycoprotein mediates viral attachment to cells and contributes to pathogenesi
129 nated mosPTP-1, recruits mosGCTL-1 to enable viral attachment to cells and to enhance viral entry.
130                 HD5 treatment of BKV reduced viral attachment to cells, whereas cellular treatment wi
131  major determinant of cell tropism, mediates viral attachment to cellular receptors.
132  did not, suggesting a direct role for E2 in viral attachment to chromosomes.
133 cells indicating therefore that IgM inhibits viral attachment to core-receptors.
134 C), infected cell binding, and inhibition of viral attachment to epithelial cells.
135 d bound RSV with high affinity and inhibited viral attachment to HEp2 cells.
136 cellular matrix proteins, thereby increasing viral attachment to heparan sulfate proteoglycans and in
137 nhibitor that binds to HIV-1 gp120, blocking viral attachment to host CD4 cells.
138  is the viral envelope protein that mediates viral attachment to host cells and elicits membrane fusi
139           The RSV G glycoprotein is used for viral attachment to host cells and impairment of host im
140  spike (S) glycoprotein is required for both viral attachment to permissive cells and for fusion of t
141  T antigen into ts13 cells, and thus neither viral attachment to receptors, viral tegument proteins,
142 the importance of antibodies that neutralize viral attachment to susceptible cells.
143 viruses solve the conflict between optimized viral attachment to target cells and efficient egress of
144 ct, aggregation of viruses, or inhibition of viral attachment to target cells and the subsequent endo
145  protection is associated with a decrease of viral attachment to target cells and viral entry due to
146 CP and HBV internalization without affecting viral attachment to the cell surface.
147 f defensin exposure to the virus relative to viral attachment to the cell.
148 unodeficiency virus (HIV) as they facilitate viral attachment to the host receptor cell.
149 ts directly inhibit extracellular virions or viral attachment to the human host cell as well as inhib
150  of HuNoV B cell infection and for measuring viral attachment to the surface of B cells.
151 ell-surface proteoglycans is involved in the viral attachment to these CD4-negative epithelial cells.
152 stems from the compound's potential to block viral attachment, virus-cell fusion, or virus entry into
153                                     Although viral attachment was not altered for the passaged viruse

 
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