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1                                              HTNV causes the most severe form of HFRS (5 to 15% case-
2                                              HTNV Gn is structurally conserved with the Gn of a genet
3                                              HTNV-infected cells treated with ribavirin showed a slig
4                        In contrast to NY-1V, HTNV uniquely induced a variety of chemokines and cell a
5     We found that VEGF addition to ANDV- and HTNV-infected endothelial cells results in the hyperphos
6 ted hamsters against infection with SEOV and HTNV.
7 ed trend for the peptides to inhibit SNV and HTNV to a greater extent than they inhibited PHV, a find
8 ng that supports the contention that SNV and HTNV use beta(3) integrins and PHV uses a different rece
9 novel peptides that inhibit entry by SNV and HTNV via beta(3) integrins and that can be used as lead
10 e were able to detect an interaction between HTNV N protein and importin alpha, a nuclear import mole
11 assays to define the ability of each to bind HTNV N protein.
12 ly time compared with three genes altered by HTNV or NY-1V.
13  induce most cellular chemokines directed by HTNV (3/14) or genes primarily activated by NF-kappaB.
14 imes p.i., 13 genes were commonly induced by HTNV and NY-1V that were not induced by PHV.
15  staining demonstrated that cells expressing HTNV N protein and a green fluorescent protein-p65 fusio
16 N protein showed an enhanced specificity for HTNV vRNA as compared with the S segment open reading fr
17                          The K(d) values for HTNV and Sin Nombre virus N proteins were nearly identic
18 ER-Golgi intermediate compartment (ERGIC) in HTNV-infected Vero E6 cells, not with the ER, Golgi comp
19 alteration in the level of p65 expression in HTNV N-expressing cells.
20 ssociated elevation in mutation frequency in HTNV vRNA similar to that previously reported in vitro.
21 virin-treated mice, the amount of infectious HTNV was significantly decreased relative to that in unt
22                               Interestingly, HTNV Gn crystallized at acidic pH, in a compact tetramer
23 alyses demonstrated geographic clustering of HTNV strains from clinical specimens with the HTNV strai
24 e genome, although we observed extinction of HTNV.
25 tment in the lethal, suckling mouse model of HTNV infection would act similarly.
26 es were measured for 3 days posttreatment of HTNV-infected Vero E6 cells.
27 rt here that the nucleocapsid (N) protein of HTNV was able to inhibit TNF-alpha-induced activation of
28   Here, we describe the crystal structure of HTNV envelope glycoprotein Gn, an integral component of
29 terize the inhibitory effect of ribavirin on HTNV, the levels of viral RNAs, proteins, and infectious
30 d protein synthesis by PHV, but not NY-1V or HTNV, is inhibited at 2 to 4 days postinfection.
31 ed to intracellular vesicles within ANDV- or HTNV-, but not TULV-, infected endothelial cells.
32 or sphingosine-1-phosphate (S1P) to ANDV- or HTNV-infected cells blocked VE-cadherin internalization
33 (3) Fab fragment, c7E3, or specific ANDV- or HTNV-neutralizing antibodies.
34 on of rhesus monkeys with either the SEOV or HTNV M gene elicited high levels of neutralizing antibod
35 , the assembly of Sin Nombre virus N protein-HTNV vRNA complexes was inhibited by the presence of Mg(
36          Collectively, our data suggest that HTNV N protein can sequester NF-kappaB in the cytoplasm,
37                                          The HTNV genomic RNA (vRNA) copy number and infectious virus
38 ein was examined for its ability to bind the HTNV S segment vRNA with filter binding and gel electrop
39 specific recognition of the HTNV vRNA by the HTNV N protein resides in the noncoding regions of the H
40 95-217 retained 94% of the vRNA bound by the HTNV N protein, while peptides 175-186 and 205-217 bound
41 aluation of a DNA vaccine that expresses the HTNV M gene products, G1 and G2.
42                                 However, the HTNV N protein showed an enhanced specificity for HTNV v
43 ization compatible with recombination of the HTNV S segment.
44 a model in which specific recognition of the HTNV vRNA by the HTNV N protein resides in the noncoding
45 tein resides in the noncoding regions of the HTNV vRNA.
46 cells transfected with cDNA representing the HTNV N gene, were confirmed using HTNV-infected cells.
47 Structural overlay analysis reveals that the HTNV Gn fold is highly similar to the Gn of Puumala viru
48         DNA vaccination of hamsters with the HTNV M gene conferred sterile protection against infecti
49 TNV strains from clinical specimens with the HTNV strains circulating in rodents, suggesting the most
50 e studies mapped a minimal region within the HTNV N protein (amino acids 175 to 217) that bound vRNA.
51 d a positive selection for codons within the HTNV N protein gene in the ribavirin-treated vRNA popula
52          Surprisingly, in ribavirin-treated, HTNV-infected mice, vRNA levels were similar to those in
53 RNA increased to that observed for untreated HTNV-infected cells on day 2, whereas mRNA levels were m
54  contrast, the vRNA population in untreated, HTNV-infected mice showed a lower level of diversity, re
55                                In untreated, HTNV-infected mice, the vRNA copy number increased for 1
56 enting the HTNV N gene, were confirmed using HTNV-infected cells.
57          Hantaviruses such as Hantaan virus (HTNV) and Andes virus cause two human diseases, hemorrha
58 tivity and GTP repression for Hantaan virus (HTNV) and evidence for RBV's ability to promote error-pr
59 ogenic Andes virus (ANDV) and Hantaan virus (HTNV) and nonpathogenic Tula virus (TULV) hantaviruses.
60 virus (ANDV) and HFRS causing Hantaan virus (HTNV) are inhibited by alpha(v)beta(3) integrin antibodi
61 her whole genome sequences of Hantaan virus (HTNV) from HFRS patients and rodent hosts in endemic are
62 ), for the interaction of the Hantaan virus (HTNV) N protein and its genomic S segment (vRNA) was mea
63  acids 175 to 217) within the Hantaan virus (HTNV) N protein that interacts with a high affinity with
64  define the domain within the Hantaan virus (HTNV) N protein that mediates these interactions, 14 N-
65 ted from the S segment of the Hantaan virus (HTNV) vRNA.
66 eir abilities to inhibit SNV, Hantaan virus (HTNV), and Prospect Hill virus (PHV) infection.
67 ogenic NY-1 virus (NY-1V) and Hantaan virus (HTNV), nonpathogenic Prospect Hill virus (PHV) elicits e
68             Four hantaviruses-Hantaan virus (HTNV), Seoul virus (SEOV), Dobrava virus (DOBV) and Puum
69 n ectodomain from the Asiatic Hantaan virus (HTNV), the most prevalent pathogenic hantavirus.
70 ey were found to be caused by Hantaan virus (HTNV), the most prevalent pathogenic hantavirus.
71 e that Andes virus (ANDV)- or Hantaan virus (HTNV)-infected endothelial cells specifically direct the
72 n acts as a lethal mutagen in Hantaan virus (HTNV)-infected Vero E6 cells, resulting in an increased
73 ototype Old World hantavirus, Hantaan virus (HTNV).
74  the production of infectious Hantaan virus (HTNV); however, its mechanism of action is unknown.
75 [New York-1 virus (NY-1V) and Hantaan virus (HTNV)] bind immobilized beta3 polypeptides containing th
76  York-1 virus (NY-1V)], HFRS [Hantaan virus (HTNV)], or by a hantavirus not associated with human dis
77 ed sterile protection against infection with HTNV, SEOV, and DOBV.

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