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1 eservation of lectin activity and detectable viral binding.
2 thesis and is also associated with increased viral binding.
3 d cells via its signaling activity following viral binding.
4 2 internalization and gene delivery, but not viral binding.
5 uch as fetal bovine serum (FBS), can have on viral binding.
6 1-98K/145Q/164E mutant potentially increases viral binding ability and that surveillance studies shou
7 and healthy adults and greatly increased the viral binding ability to cells.
8 e of MBL and conglutinin conferred increased viral binding activity, it did not favorably affect bact
9 amino acid substitution at E367 enhanced the viral binding affinity for glycosaminoglycans (GAGs) and
10  points, an early time point consistent with viral binding and a later sustained activation consisten
11 argeting the proteoglycan syndecan-2 blocked viral binding and abrogated any calcium response.
12                                              Viral binding and entry activate STAT3 in the first 2 h
13  447) in the RRV VP4 protein is required for viral binding and entry into biliary epithelial cells.
14  we reevaluated the role of P antigen in the viral binding and entry into cells.
15 is not complete, in that the early stages of viral binding and entry into hepatocytes and production
16 (ACE-2), the SARS-CoV-2 receptor, to mediate viral binding and entry into T cells.
17  demonstrate that in UV-inactivated viruses, viral binding and entry were not sufficient to induce ap
18 tor and coreceptor, CD4 and CXCR4, enhancing viral binding and entry.
19 -residue, acidic, cysteine-rich sequence for viral binding and entry.
20  has not been clear how modified Sias affect viral binding and entry.
21 wo residues result in the loss of or reduced viral binding and hemagglutination and in the inability
22                                     Finally, viral binding and internalization studies indicate that
23 , we determined key residues responsible for viral binding and internalization, respectively and iden
24 olecular dynamics simulations to investigate viral binding and S2 core exposure.
25                                              Viral binding and transduction assays on mutant Chinese
26    PCZ can block DENV infection by targeting viral binding and viral entry through D2R- and clathrin-
27       The knockout cells were permissive for viral binding, and virus triggered an intracellular calc
28 ific mutation of selected pit amino acids on viral binding as well as other replicative functions of
29 s on the viral particle, providing very high viral binding avidity.
30 In the present study, for the first time the viral binding behavior at virus-imprinted polymers (VIPs
31  by novel viral exposures due to their broad viral binding breadth.
32 ants into either human or dog ACE2 abolishes viral binding, diminishing cellular infection.
33 ce of the region of Tva that encompasses the viral binding domain.
34 may contain a common region(s) for mediating viral binding during infection.
35 ation efficiency of lipid nanoparticles, the viral binding efficiencies of different nanobodies, and
36 lycosylation plays key roles in altering the viral binding/function and infectivity.
37            UD-UCMSCs, although permissive to viral binding, had a very limited uptake capacity, where
38 , despite P antigen positivity and efficient viral binding, HEL, K562, and HL-60 cells could not be t
39 gh the inhibition of these molecules reduced viral binding, HTLV-1 transmission from DCs to T cells w
40 on does not correlate with the efficiency of viral binding, (iii) P antigen is necessary but not suff
41 e we identified a strong association between viral binding in high serum and the expression of chondr
42                        First, we showed that viral binding induced a number of immunoregulatory genes
43 thetic glycomimetics to act as inhibitors of viral binding/infection.
44 interactions-were identified within host and viral binding interfaces predicted by our models.
45 8 mRNA and protein levels, consistent with a viral binding-mediated mechanism.
46  cholesterol depletion, however, was seen on viral binding; moreover, there was no reduction in the s
47 he augmented transduction was due to neither viral binding nor promoter activity, affected multiple r
48       Taken together, our findings show that viral binding of the gH/gL/UL128-131 complex to integrin
49 ic studies showed that Ifitm3 did not affect viral binding or entry but inhibited pH-dependent fusion
50 8 genomic RNA replication but did not impact viral binding or entry into host cells.
51 aB was translocated to the nucleus following viral binding or purified viral ligand binding.
52 nteraction of this tegument protein with its viral binding partners but also its interactions with mi
53 the difficulties associated with identifying viral binding partners where the basis of motor recruitm
54 secretors." FUT2 polymorphisms may influence viral binding patterns and, therefore, may influence hos
55 DNA polymerase subunit, as the most abundant viral binding protein of the L1 ribonucleoprotein (RNP)
56 this well defined nanopatterning and role in viral binding remain enigmatic.
57            Viral particles will bind to this viral binding sequence (VBS) with high affinity in vitro
58     Although Bcl-2 was upregulated following viral binding/signaling through cellular integrins (comp
59 , we present structural data that reveal the viral binding site of one of the first HIV-1-neutralizin
60 the sensitivity of unprotected virus and the viral binding site on the cell surface to trypsin, viral
61                 Polyreactivity augmented mAb viral binding strength by increasing antibody flexibilit
62 hin the SU variable region A which increases viral binding through an independent mechanism.
63  the sole viral protein responsible for both viral binding to a host cell and the membrane fusion eve
64 erally harbor amino acid changes that affect viral binding to a single class of carbohydrate receptor
65  virus with HA P194S mutation that decreased viral binding to alpha2,6 receptor.
66 HCMV-induced angiogenic response depended on viral binding to and signaling through the beta(1) and b
67 entry studied included the method of initial viral binding to cells, pH dependency, and expression an
68 on can be curbed by competitively preventing viral binding to cells.
69                        This escape decreases viral binding to cellular receptors, which must be compe
70 s in disease pathogenesis, the mechanisms of viral binding to DCs have not been fully delineated.
71 s and cultured epithelial cells, even though viral binding to epithelial cells was inhibited by both
72  regulation of cellular activation following viral binding to human monocytes.
73                                     Blocking viral binding to integrins inhibits Ang-2 release.
74 receptor ligand-mediated signaling following viral binding to integrins on monocytes could trigger th
75 inimize collateral damage to normal tissues: viral binding to its natural receptors must be ablated a
76 n is thought to cause atherosclerosis, while viral binding to LDL has been suggested to facilitate he
77 n efficiency did not directly correlate with viral binding to muscle cells but rather appeared to inv
78 o identify sequences in sigma1 important for viral binding to sialic acid, a component of the recepto
79       Utilizing a modified ELISA to evaluate viral binding to target cells, we observed a significant
80 e interaction between MBL and SARS-S blocked viral binding to the C-type lectin, DC-SIGN.
81 lent capsomeres and its inability to prevent viral binding to the cell surface suggest that receptor
82  of neutralizing antibodies that can inhibit viral binding to the cell surface, while mAb 5B6 is repr
83 lomaviruses without significantly inhibiting viral binding to the cell surface.
84 nd fusion (F) envelope glycoproteins mediate viral binding to the ephrinB2/ephrinB3 cell receptors an
85 , which is necessary and sufficient for both viral binding to the target cell and fusion between the
86 er HTLV-1 attachment factors was analyzed in viral binding, transmission, and productive infection us
87  the epidermal growth factor receptor during viral binding triggered the upregulation of Mcl-1.
88 hanges in cellular activation initiates with viral binding via envelope glycoproteins to the cognate
89                         LYS353 also promotes viral binding via several mechanisms including dispersio
90       Across the 25 ACE2 sites implicated in viral binding, we identify 6 amino acid substitutions un