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1                                          The enteroviral 2A proteinase (2A(pro)) is essential for rep
2                                          The enteroviral 2C protein is a therapeutic target, but the
3 rk presents a model for the structure of the enteroviral 5' UTR.
4 dentified features contribute to a model for enteroviral 5' UTRs with type I IRES elements that links
5      Subsequently, the spectrum of antirhino/enteroviral activity of the more interesting analogues w
6     YAP is thus an important host factor for enteroviral amplification, offering a potential antivira
7 lipid microenvironment is essential for both enteroviral and flaviviral RNA replication; PI4KIIIbeta
8                  It is desirable to localize enteroviral antigens so as to establish a link between t
9 r biology have improved our understanding of enteroviral biology and of potential alternative pathoge
10                              The presence of enteroviral capsid protein 1 (VP1) and the expression of
11        Protease 2A has a significant role in enteroviral cardiomyopathy and alone is sufficient to in
12 However, the direct effect of protease 2A in enteroviral cardiomyopathy is less clear because other v
13 cture represents a conserved architecture of enteroviral cloverleaf-like domains, including the A40 a
14 Respiratory diseases and gastrointestinal or enteroviral diseases declined more than sexually transmi
15               To determine whether low-level enteroviral gene expression similar to that observed wit
16 naturally occurring genomic alteration to an enteroviral genome associated with long-term viral persi
17  site (IRES)-mediated translation of a donor enteroviral genome enhanced recombination instead of imp
18 ngle-stranded region in recruiting PCBP2 for enteroviral genome replication and illuminating the prom
19 ls a novel mode of viral transmission, where enteroviral genomes are transmitted from cell-to-cell en
20  demonstrates that restricted replication of enteroviral genomes in myocytes in a pattern similar to
21 a demonstrate that restricted replication of enteroviral genomes in the heart can induce dilated card
22 gammaglobulinemia were examined to determine enteroviral genotypic variability.
23                                  Adult human enteroviral heart disease is often associated with the d
24 red cells decreased the cytopathic effect of enteroviral infection and the release of virus from the
25 ly true for studies focussing on the role of enteroviral infection as a potential cause of beta-cell
26                                              Enteroviral infection can cause an acquired form of dila
27  suggest a molecular mechanism through which enteroviral infection contributes to the pathogenesis of
28 the development and persistence of a chronic enteroviral infection in human beta-cells.
29 istent with the possibility that a low-grade enteroviral infection in the pancreatic islets contribut
30                                         Both enteroviral infection of the heart and mutations in the
31 e cleavage of initiation factor eIF5B during enteroviral infection, along with the viral internal rib
32               Many cases are attributable to enteroviral infection, and in particular to coxsackievir
33 may have a blunted innate immune response to enteroviral infection, leading to reduced viral clearanc
34 lls have been reported to support persistent enteroviral infection, the hybrid 1.1B4 cells appeared t
35 stance to the acute cardiac injury caused by enteroviral infection.
36 d binding to 2A and complete protection from enteroviral infection.
37 ype 1 diabetes have suggested a link between enteroviral infections and the development of this disea
38 etic autoimmunity to determine whether acute enteroviral infections can promote progression from auto
39                                              Enteroviral infections of the heart are among the most c
40 prospects of developing therapeutics against enteroviral infections targeting this replication platfo
41 ailable antiviral for the treatment of rhino/enteroviral infections, a series of vinylacetylene benzi
42 diabetes (T1D) risk has been associated with enteroviral infections, particularly coxsackieviruses B
43                                       During enteroviral infections, the canonical translation factor
44 al sequelae might be expected after neonatal enteroviral infections, yet antiviral treatment initiate
45 ular methods for the detection and typing of enteroviral infections.
46  nervous system, particularly for herpes and enteroviral infections.
47  interactions between HLA class II genes and enteroviral infections.
48                       The assay detected all enteroviral isolates tested with no cross-reactivity to
49 oles for the endocytic machinery in both the enteroviral life cycle and host cell cholesterol homeost
50 s of two representative sequence variants of enteroviral loop B RNA.
51 ystrophin is critical for viral propagation, enteroviral-mediated cytopathic effects, and the develop
52 he expected August/September/October peak in enteroviral meningitis did not occur in 2020, possibly r
53 he expected August/September/October peak in enteroviral meningitis did not occur in 2020, possibly r
54                                              Enteroviral meningitis is seasonal, typically exhibiting
55 ssay should prove useful in the diagnosis of enteroviral meningitis versus bacterial meningitis, ther
56                    The overall prevalence of enteroviral meningitis was 26.04%.
57                           Clinical truth for enteroviral meningitis was defined as clinical evidence
58 ed as the new gold standard for diagnosis of enteroviral meningitis, and their use can improve the ma
59 d a high degree of accuracy for diagnosis of enteroviral meningitis.
60 rease the costs for caring for children with enteroviral meningitis.
61  (95% CI, 94.6 to 100%) for the diagnosis of enteroviral meningitis.
62 T-PCR results were used to classify cases of enteroviral meningitis.
63 ly useful treatments, such as pleconaril for enteroviral meningoencephalitis are under clinical evalu
64 d cardiomyopathy seen in humans with chronic enteroviral myocarditis.
65  We screened TLR3 in patients diagnosed with enteroviral myocarditis/cardiomyopathy and identified a
66                                     Although enteroviral nucleic acids have been detected in selected
67        Here, we demonstrate that clusters of enteroviral particles are packaged within phosphatidylse
68              Specificity testing against non-enteroviral pathogens confirmed no cross-reactivity.
69                                              Enteroviral persistence has been implicated in the patho
70 d Pro(357), which is absolutely conserved in enteroviral polymerases, was found to be critical for pr
71                           Upon CV infection, enteroviral protease 2A cleaves a small number of host p
72          We previously demonstrated that the enteroviral protease 2A cleaves dystrophin; therefore, w
73              We previously demonstrated that enteroviral protease 2A directly cleaves the cytoskeleta
74 ophin is the first cellular substrate of the enteroviral protease 2A that was identified using by a b
75 h inducible cardiac-restricted expression of enteroviral protease 2A was generated.
76  and which has been shown previously to bind enteroviral protein 3A and to be required for viral RNA
77 vels are correlated with the presence of the enteroviral protein VP1.
78 y also highlight the importance of targeting enteroviral proteinases to inhibit viral replication whi
79                                      The two enteroviral proteinases, 2A proteinase (2A(pro)) and 3C
80                                              Enteroviral proteins were radiolabeled with [35S]methion
81                        Until now, all of the enteroviral proteins were thought to derive from the pro
82 te cholesterol as a critical determinant for enteroviral replication and outline roles for the endocy
83 o The mechanisms by which polyamines enhance enteroviral replication are unknown.
84 ution structural framework for understanding enteroviral replication mechanisms, which will aid in de
85                                              Enteroviral replication-linked cloverleaf RNAs recruit t
86 ed us to predict the models of several other enteroviral REPLRs using homology modeling, which genera
87 inding site, abrogated its interactions with enteroviral REPLRs, suggesting the critical roles of thi
88 zyme immunoassay (DEIA) kit for detection of enteroviral reverse transcription-PCR (RT-PCR) products
89                                              Enteroviral ribonucleic acids have been identified in he
90                                  We detected enteroviral RNA and cultured infectious virus from a ser
91 ated CSF protein levels and the detection of enteroviral RNA by reverse transcription (RT)-PCR.
92                                          All enteroviral RNA genomes have a long and highly structure
93                                              Enteroviral RNA genomes share a long, highly structured
94 se is often associated with the detection of enteroviral RNA in cardiac muscle tissue in the absence
95 replicative recombination and persistence of enteroviral RNA lacking an IRES.
96 inhibition interferes with this process; and enteroviral RNA polymerases specifically bind PI4P.
97                                              Enteroviral RNA was detected in 6 of 11 myocarditis samp
98 opose that such studies use assays to detect enteroviral RNA, in addition to IgM serology.
99  reproducibly quantify down to 510 copies of enteroviral RNA/ml of cerebrospinal fluid.
100  presence of West Nile virus during the 2002 enteroviral season contributed to a change in these corr
101 ) samples submitted during the 2007 and 2008 enteroviral seasons were included in a study to determin
102                                              Enteroviral sequences were detected in seven patients an
103  prototype strains belonging to 20 different enteroviral serotypes.
104 racts with the viral 2A protease of multiple enteroviral species, and we map the residues in 2A that
105 nd 3CD with cloverleafs from seven different enteroviral species, we demonstrate that while the 3D do
106 mong children < or =7 years of age, elevated enteroviral titers were more frequent in those with juve
107 onset date, and young patients have elevated enteroviral titers, as do young geographic controls.
108 ion for the development of new nonpoliovirus enteroviral vectors.
109 d islets have shown significant variation in enteroviral virulence to beta cells between serotypes an
110                                  A consensus enteroviral VPg protein had the same distinctive high pK

 
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