ライフサイエンスコーパス: viral binding

1 d cells via its signaling activity following viral binding.

2 eservation of lectin activity and detectable viral binding.

3 thesis and is also associated with increased viral binding.

4 2 internalization and gene delivery, but not viral binding.

5 1-98K/145Q/164E mutant potentially increases viral binding ability and that surveillance studies shou

6 and healthy adults and greatly increased the viral binding ability to cells.

7 e of MBL and conglutinin conferred increased viral binding activity, it did not favorably affect bact

8 points, an early time point consistent with viral binding and a later sustained activation consisten

9 argeting the proteoglycan syndecan-2 blocked viral binding and abrogated any calcium response.

10 Viral binding and entry activate STAT3 in the first 2 h

11 447) in the RRV VP4 protein is required for viral binding and entry into biliary epithelial cells.

12 we reevaluated the role of P antigen in the viral binding and entry into cells.

13 is not complete, in that the early stages of viral binding and entry into hepatocytes and production

14 demonstrate that in UV-inactivated viruses, viral binding and entry were not sufficient to induce ap

15 tor and coreceptor, CD4 and CXCR4, enhancing viral binding and entry.

16 -residue, acidic, cysteine-rich sequence for viral binding and entry.

17 wo residues result in the loss of or reduced viral binding and hemagglutination and in the inability

18 Finally, viral binding and internalization studies indicate that

19 Viral binding and transduction assays on mutant Chinese

20 PCZ can block DENV infection by targeting viral binding and viral entry through D2R- and clathrin-

21 The knockout cells were permissive for viral binding, and virus triggered an intracellular calc

22 ific mutation of selected pit amino acids on viral binding as well as other replicative functions of

23 ce of the region of Tva that encompasses the viral binding domain.

24 UD-UCMSCs, although permissive to viral binding, had a very limited uptake capacity, where

25 , despite P antigen positivity and efficient viral binding, HEL, K562, and HL-60 cells could not be t

26 gh the inhibition of these molecules reduced viral binding, HTLV-1 transmission from DCs to T cells w

27 on does not correlate with the efficiency of viral binding, (iii) P antigen is necessary but not suff

28 First, we showed that viral binding induced a number of immunoregulatory genes

29 interactions-were identified within host and viral binding interfaces predicted by our models.

30 8 mRNA and protein levels, consistent with a viral binding-mediated mechanism.

31 cholesterol depletion, however, was seen on viral binding; moreover, there was no reduction in the s

32 he augmented transduction was due to neither viral binding nor promoter activity, affected multiple r

33 Taken together, our findings show that viral binding of the gH/gL/UL128-131 complex to integrin

34 ic studies showed that Ifitm3 did not affect viral binding or entry but inhibited pH-dependent fusion

35 aB was translocated to the nucleus following viral binding or purified viral ligand binding.

36 nteraction of this tegument protein with its viral binding partners but also its interactions with mi

37 the difficulties associated with identifying viral binding partners where the basis of motor recruitm

38 secretors." FUT2 polymorphisms may influence viral binding patterns and, therefore, may influence hos

39 this well defined nanopatterning and role in viral binding remain enigmatic.

40 Viral particles will bind to this viral binding sequence (VBS) with high affinity in vitro

41 Although Bcl-2 was upregulated following viral binding/signaling through cellular integrins (comp

42 , we present structural data that reveal the viral binding site of one of the first HIV-1-neutralizin

43 the sensitivity of unprotected virus and the viral binding site on the cell surface to trypsin, viral

44 hin the SU variable region A which increases viral binding through an independent mechanism.

45 erally harbor amino acid changes that affect viral binding to a single class of carbohydrate receptor

46 virus with HA P194S mutation that decreased viral binding to alpha2,6 receptor.

47 HCMV-induced angiogenic response depended on viral binding to and signaling through the beta(1) and b

48 entry studied included the method of initial viral binding to cells, pH dependency, and expression an

49 on can be curbed by competitively preventing viral binding to cells.

50 This escape decreases viral binding to cellular receptors, which must be compe

51 s in disease pathogenesis, the mechanisms of viral binding to DCs have not been fully delineated.

52 s and cultured epithelial cells, even though viral binding to epithelial cells was inhibited by both

53 regulation of cellular activation following viral binding to human monocytes.

54 Blocking viral binding to integrins inhibits Ang-2 release.

55 receptor ligand-mediated signaling following viral binding to integrins on monocytes could trigger th

56 inimize collateral damage to normal tissues: viral binding to its natural receptors must be ablated a

57 n is thought to cause atherosclerosis, while viral binding to LDL has been suggested to facilitate he

58 n efficiency did not directly correlate with viral binding to muscle cells but rather appeared to inv

59 o identify sequences in sigma1 important for viral binding to sialic acid, a component of the recepto

60 Utilizing a modified ELISA to evaluate viral binding to target cells, we observed a significant

61 e interaction between MBL and SARS-S blocked viral binding to the C-type lectin, DC-SIGN.

62 lent capsomeres and its inability to prevent viral binding to the cell surface suggest that receptor

63 of neutralizing antibodies that can inhibit viral binding to the cell surface, while mAb 5B6 is repr

64 lomaviruses without significantly inhibiting viral binding to the cell surface.

65 nd fusion (F) envelope glycoproteins mediate viral binding to the ephrinB2/ephrinB3 cell receptors an

66 , which is necessary and sufficient for both viral binding to the target cell and fusion between the

67 er HTLV-1 attachment factors was analyzed in viral binding, transmission, and productive infection us

68 the epidermal growth factor receptor during viral binding triggered the upregulation of Mcl-1.

69 hanges in cellular activation initiates with viral binding via envelope glycoproteins to the cognate