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1 tly reduces levels of apoptosis triggered by reovirus infection.
2 al entry into these cells is dispensable for reovirus infection.
3  for antibody in the clearance of intestinal reovirus infection.
4 nity, inflammation, and cell death following reovirus infection.
5 s is diminished in ATXN2L-KO cells following reovirus infection.
6  of necroptosis also requires late stages of reovirus infection.
7                            5-NT also blocked reovirus infection.
8  cells or primary cortical neurons abrogates reovirus infection.
9 for Daxx in Fas-mediated apoptosis following reovirus infection.
10  indicating that endogenous IFITM3 restricts reovirus infection.
11 y prodeath function for this molecule during reovirus infection.
12 Slc35a1 as potential host genes required for reovirus infection.
13 ion uncoating is an essential early event in reovirus infection.
14  these inflammatory mediators and ISG during reovirus infection.
15 nce and prevent tissue injury in response to reovirus infection.
16 ibitor of cathepsin L led to amelioration of reovirus infection.
17 eovirus, and 112 were induced in response to reovirus infection.
18 ndently or in combination, in the absence of reovirus infection.
19 bryo fibroblasts conferred susceptibility to reovirus infection.
20 nished in the CNS of p50-null mice following reovirus infection.
21 ovary cells, which are poorly permissive for reovirus infection.
22 encephalitis and myocarditis associated with reovirus infection.
23 ly activate host cell apoptotic responses to reovirus infection.
24 s involved in apoptosis and DNA repair after reovirus infection.
25  sigma 3 form protein-RNA complexes early in reovirus infection.
26 IgA(+) and IgG2a(+) B cells after intranasal reovirus infection.
27 ivated in a strain-specific manner following reovirus infection.
28  establishment and maintenance of persistent reovirus infections.
29 ere clinical manifestations of rotavirus and reovirus infections.
30                               In particular, reovirus infection accentuated Warburg-like metabolic pe
31                                              Reovirus infection activates NF-kappaB, which leads to p
32                             We now show that reovirus infection activates transforming growth factor
33 diate this response, we investigated whether reovirus infection alters the activation state of the tr
34  that render microglial cells susceptible to reovirus infection and expands current understanding of
35 that p53 is activated in the brain following reovirus infection and may provide a therapeutic target
36              Importantly, the combination of reovirus infection and proteasomal inhibition significan
37 or flexibility of sigma1 resulted in delayed reovirus infection and reduced viral titers.
38 factor kappaB (NF-kappaB) is activated after reovirus infection and that this activation is required
39 ation was accelerated in the early phases of reovirus infection, and yields of reovirus were increase
40                  These findings suggest that reovirus infections are common during early childhood.
41                                              Reovirus infections are initiated by the binding of vira
42                                     Although reovirus infections are thought to be common in adults,
43                             Moreover, during reovirus infection, association with sigma3 may regulate
44               We found that, while vgRNA and reovirus infection both induce a similar IRF-dependent g
45                                       During reovirus infection, both sigma NS and mu NS are detectab
46 und that 5-nonyloxytryptamine (5-NT) impairs reovirus infection by altering viral transport during ce
47 ength of time between primary and subsequent reovirus infection can alter reassortment frequency.
48                                 Furthermore, reovirus infection can be used as a promising approach t
49 any cells which otherwise support productive reovirus infection cannot efficiently mediate this essen
50         Inhibition of JNK activity following reovirus infection delays the release of proapoptotic mi
51                                   Similar to reovirus infection, ectopic expression of mu1 caused rel
52                                              Reovirus infection elicits production of type I interfer
53 laboratory previously demonstrated that oral reovirus infection elicits specific serum immunoglobulin
54 immunoglobulin G2a (IgG2a), while parenteral reovirus infection elicits the mixed production of speci
55 s infection in vivo Upon murine norovirus or reovirus infection, Ifnlr1 depletion in IECs largely rec
56 induced at late times (36 to 48 h) following reovirus infection in a manner dependent on IRF-3 and NF
57 ponses and viral clearance following enteric reovirus infection in C57BL/6, B6129F2, and beta2-microg
58 nse to 5'pp-RNA is essential for controlling reovirus infection in cultured cells and in mice.
59  genes activated by NF-kappaB in response to reovirus infection in the central nervous system.
60 e pathogenesis of the pathologic response to reovirus infection in the lungs and further understand t
61                 We propose that experimental reovirus infection in the lungs can serve as a model for
62 atory and inflammatory proteases can promote reovirus infection in vitro and that preexisting inflamm
63            The relevance of these results to reovirus infection in vivo was assessed by treating viri
64 y shown that serotype 3, but not serotype 1, reovirus infection induces a G(2)-to-M transition arrest
65                                              Reovirus infection induces an increase in the number and
66                            Here we show that reovirus infection induces apoptosis in cancer cell line
67                                              Reovirus infection induces apoptosis in cultured cells a
68  colocalizes with Src during cell entry, and reovirus infection induces phosphorylation of Src at the
69  activates DNA damage response pathways, and reovirus infection induces robust production of type III
70                         To determine whether reovirus infection initiated in the absence of JAM-A and
71                                              Reovirus infection is a well-characterized experimental
72                                Concordantly, reovirus infection is ablated in primary cortical neuron
73                                              Reovirus infection is also associated with the activatio
74                                              Reovirus infection is associated with selective down-reg
75            In an effort to determine whether reovirus infection is associated with these disorders, w
76 inhibition of cellular translation following reovirus infection is complex and involves multiple inte
77                                              Reovirus infection is initiated by interactions between
78                                        Since reovirus infection is known to activate cellular transcr
79 dicate that the apoptotic response following reovirus infection is mediated directly by genes respons
80                                We found that reovirus infection leads initially to nuclear translocat
81                                              Reovirus infection leads to apoptosis in cultured cells
82 hought to be required for two early steps in reovirus infection: membrane penetration and activation
83 To determine whether sigma1s is required for reovirus infection of cultured cells, we compared the gr
84                We have previously shown that reovirus infection of epithelial cell lines activates JN
85         Astrogliosis also occurred following reovirus infection of ex vivo brain slice cultures (BSCs
86 the formation of p53/Bak complexes following reovirus infection of ex vivo brain slice cultures and r
87                             We now show that reovirus infection of HEK cells is associated with selec
88 ed in electrophoretic mobility shift assays, reovirus infection of HeLa cells leads to nuclear transl
89 cific for other integrin subunits, inhibited reovirus infection of HeLa cells.
90 itecture of sigma1 is required for efficient reovirus infection of host cells.
91                                              Reovirus infection of human airway epithelia was more ef
92 ng are responsible for strain differences in reovirus infection of macrophage-like P388D cells and ot
93                                     Further, reovirus infection of mice deficient in the expression o
94 omponents required for intestinal clearance, reovirus infection of mice with null mutations in the im
95 d expression on the cell surface and mediate reovirus infection of microglial cells.
96     JAM binds directly to sigma1 and permits reovirus infection of nonpermissive cells.
97             To investigate the mechanisms of reovirus infection of polarized epithelial cells, we ass
98                                              Reovirus infection of target cells can perturb cell cycl
99                           Here, we show that reovirus infection of the brain results in the activatio
100                                              Reovirus infection of the mouse SC was also associated w
101                          A requisite step in reovirus infection of the murine intestine is proteolysi
102                                              Reovirus infection of the murine spinal cord (SC) was us
103 s is important for maintenance of persistent reovirus infections of cultured cells.
104                  Establishment of persistent reovirus infections of MEL cells was not associated with
105 our data suggest that the acid dependence of reovirus infections of most other cell types may reflect
106                                   Persistent reovirus infections of murine L929 cells select cellular
107                              We propose that reovirus infection promotes apoptosis via the expression
108                           In natural enteric reovirus infections, proteolytic uncoating takes place e
109                                           As reovirus infection requires disassembly in the endocytic
110                                              Reovirus infection requires the concerted action of vira
111                             We now show that reovirus infection resulted in activation of JNK and cas
112                                              Reovirus infection resulted in astrogliosis, as evidence
113                                              Reovirus infection results in cell death of a variety of
114                                   Serotype 3 reovirus infection results in differential expression of
115                                   Serotype 1 reovirus infection results in differential expression of
116                       One mechanism by which reovirus infection results in inhibition of NF-kappaB is
117                                    Mammalian reovirus infection results in perturbation of host cell
118                             We now show that reovirus infection results in the selective activation o
119      These findings indicate that persistent reovirus infections select cellular mutations that affec
120                  Our study demonstrates that reovirus infection selectively blocks NF-kappaB, likely
121 e required for efficient apoptosis following reovirus infection, suggesting a common mechanism of ant
122 ssive cells conferred full susceptibility to reovirus infection, suggesting that cell surface molecul
123                                              Reovirus infection synergistically and specifically sens
124 sigma1s is required for apoptosis induced by reovirus infection, T3C84-MA and T3C84 were tested for t
125 es function in the innate immune response to reovirus infection that blocks immunological tolerance t
126 ant HEK293 cells and prevents the ability of reovirus infection to sensitize TRAIL-resistant cells to
127                                              Reovirus infection triggers an antiviral response in hos
128         Despite differences in cell tropism, reovirus infection was also reduced in M cell-depleted m
129                       Encephalitis following reovirus infection was dampened in mice lacking neural c
130 evious evidence that active NF-kappaB limits reovirus infection, we conclude that inactivating NF-kap
131 tations in sigma3 selected during persistent reovirus infection, we determined the S4 gene nucleotide
132 by transfected viral genomic RNA (vgRNA) and reovirus infection, we discovered that mammalian reoviru
133 olecule screen to identify host mediators of reovirus infection, we found that treatment of cells wit
134 ength and flexibility at different stages of reovirus infection, we generated viruses with mutant sig
135  host genes activated by NF-kappaB following reovirus infection, we used HeLa cells engineered to exp
136                       beta 2-/- mice cleared reovirus infection with normal kinetics, while MuMT mice
137  atresia, but previous attempts to correlate reovirus infection with this disease have yielded confli

 
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