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1 ood mononuclear immune cells that respond to Coxsackievirus.
2 for some adenovirus (AdV) types and group B coxsackieviruses.
3 -fold more resistant to in vitro cleavage by Coxsackievirus 2A protease (2A(Pro)) than wild-type eIF4
4 man K562 cells were cleaved with recombinant Coxsackievirus 2A protease and the N- terminal domains p
7 ssay, neutralizing antibodies titers against coxsackievirus A16 (CA16), enterovirus 71 (EV71), PV I-I
8 e two serotypes Enterovirus A71 (EV-A71) and Coxsackievirus A16 (CV-A16) being responsible for the ma
11 causative agents are enterovirus 71 (EV71), coxsackievirus A16 (CVA16), and, most recently, coxsacki
12 interspersed phylogenetically with clades of coxsackievirus A16 and other EV species A serotypes.
13 s most typically caused by enterovirus 71 or coxsackievirus A16 and results in asymptomatic infection
15 poliovirus 2C(ATPase) interacts with VP3 of coxsackievirus A20, in the context of a chimeric virus.
19 ution of variants of the common-cold-causing coxsackievirus A21, an EV with tropism for the human int
22 everal serotypes of human adenovirus (HAdV), coxsackievirus A24, enterovirus 70, and herpes simplex-v
23 ent targets for designing anti-CVA6 vaccines.Coxsackievirus A6 (CVA6) causes hand, foot and mouth dis
28 ar with the severe variant of HFMD caused by coxsackievirus A6, include it in their differential diag
33 -B) in the family Picornaviridae consists of coxsackievirus A9; coxsackieviruses B1 to B6; echoviruse
34 ith different fiber shaft lengths and either coxsackievirus-Ad receptor (CAR)-interacting Ad serotype
36 The knobs remained trimeric and bound the coxsackievirus-Ad receptor, and the phage knob-displayed
37 t HD-RIGIE injections efficiently transduced coxsackievirus adenovirus receptor-expressing keratocyte
43 d5) involves fiber capsid protein binding to coxsackievirus-adenovirus receptor (CAR) at the cell sur
44 majority of adenovirus serotypes utilize the coxsackievirus-adenovirus receptor (CAR) for virus-host
46 We hypothesized that the expression of the coxsackievirus-adenovirus receptor (CAR), a viral recept
48 e variant of the extracellular domain of the coxsackievirus-adenovirus receptor (sCAR-Fc) was express
49 rabasal cells that express the high-affinity coxsackievirus-adenovirus receptor, CAR, whereas the pro
51 Ad) fiber protein mediates Ad binding to the coxsackievirus and Ad receptor (CAR) and is thus a major
52 f the primary cellular receptor for Ads, the coxsackievirus and Ad receptor (CAR), in permitting intr
53 have shown that although Ad2ts1 can bind the coxsackievirus and Ad receptor and undergo internalizati
54 hafted Ad vectors had no impact on knob-CAR (coxsackievirus and Ad receptor) interaction compared to
57 s 259 and 260 in the cytoplasmic tail of the coxsackievirus and adenovirus receptor (CAR) are known t
58 While group B coxsackieviruses (CVB) use the coxsackievirus and adenovirus receptor (CAR) as the rece
59 ruses into target cells is expression of the coxsackievirus and adenovirus receptor (CAR) at the cell
61 associated with the widespread expression of coxsackievirus and adenovirus receptor (CAR) in normal h
68 we demonstrate that in the adult brain, the coxsackievirus and adenovirus receptor (CAR) is located
72 rity of adenovirus serotypes can bind to the coxsackievirus and adenovirus receptor (CAR) on human ce
73 protein serves this purpose, binding to the coxsackievirus and adenovirus receptor (CAR) present on
75 In this study, a zebrafish homologue of the coxsackievirus and adenovirus receptor (CAR) protein was
78 novirus serotype 5 fiber protein engages the coxsackievirus and adenovirus receptor (CAR) to bind cel
80 s many adenoviruses infect cells through the coxsackievirus and adenovirus receptor (CAR), group B ad
90 and reveal a direct interaction between the coxsackievirus and adenovirus receptor and the immune sy
92 presence of varied concentrations of soluble coxsackievirus and adenovirus receptor showed that the o
93 es), cardiac fibrosis, apoptosis, lower CAR (Coxsackievirus and adenovirus receptor) expression and C
94 tudy demonstrates that hiPSC-CMs express the coxsackievirus and adenovirus receptor, are susceptible
97 beta, tumor-derived growth factor beta; CAR, coxsackievirus and adenovirus receptor; MLV, murine leuk
98 ase-control study of the association between coxsackieviruses and cardiac impairment, 24 human immuno
99 is the primary cellular receptor for group B coxsackieviruses and most adenovirus serotypes and plays
100 ves as the cell surface receptor for group B coxsackieviruses and most adenoviruses, but the physiolo
101 molytic streptococci and rheumatic fever; B3 Coxsackieviruses and myocarditis; Trypanosoma cruzi and
102 FP(A20) exhibited up to 50-fold increases in coxsackievirus- and-adenovirus-receptor-independent tran
103 binds with high affinity to the cell surface coxsackievirus-and-adenovirus receptor (CAR), and penton
104 egression to test for an association between coxsackievirus antibody titer and the presence or absenc
106 = .12), human bocavirus (aOR 9.1, P < .01), Coxsackieviruses (aOR 5.1, P = .09), rhinovirus A (aOR 3
108 ous observations suggesting that the group B coxsackieviruses are associated with the risk of type 1
115 al dissemination in released EMVs.IMPORTANCE Coxsackievirus B (CVB) can cause a number of life-threat
119 alized host factor that negatively regulates coxsackievirus B (CVB) replication through its control o
120 ental murine infections and in cell culture, coxsackievirus B (CVB) RNA can persist for weeks in the
121 eptors for poliovirus, human rhinovirus, and coxsackievirus B (CVB) serve to bind the viruses to targ
123 enteroviruses, including echovirus 11 (E11), coxsackievirus B (CVB), and enterovirus 71 (EV71), and t
134 icornaviridae consists of coxsackievirus A9; coxsackieviruses B1 to B6; echoviruses 1 to 7, 9, 11 to
136 fection with a suspected diabetogenic virus, Coxsackievirus B3 (CB3), NOD.Ncf1(m1J) mice remained res
137 of IL-12 and IFN-gamma on the development of Coxsackievirus B3 (CB3)-induced myocarditis, we examined
138 The first-described DAF-binding isolate, coxsackievirus B3 (CB3)-RD, was obtained during passage
140 ngth VP1 genes of poliovirus 1 (Polio 1) and coxsackievirus B3 (Cox B3) were cloned, and the encoded
142 d identified RIP3 as a positive regulator of coxsackievirus B3 (CVB) replication in intestinal epithe
143 ne was effective against poliovirus (PV) and coxsackievirus B3 (CVB3) and exhibited greater activity
147 B infection, we previously demonstrated that coxsackievirus B3 (CVB3) could infect neuronal progenito
148 larized human intestinal epithelial cells by coxsackievirus B3 (CVB3) depends on virus interaction wi
149 ar to humans, male BALB/c mice infected with coxsackievirus B3 (CVB3) develop more severe inflammatio
152 we describe the generation of a recombinant coxsackievirus B3 (CVB3) expressing the enhanced green f
155 eviously described a neonatal mouse model of coxsackievirus B3 (CVB3) infection and determined that p
159 ate immunity can determine susceptibility to coxsackievirus B3 (CVB3) infection, the present study ev
168 esent recent findings on the pathogenesis of coxsackievirus B3 (CVB3) myocarditis based on animal mod
170 l mouse model, we previously determined that coxsackievirus B3 (CVB3) preferentially targets prolifer
172 ed in pancreatic acinar cells, and show that coxsackievirus B3 (CVB3) requires autophagy for optimal
173 Previously, we described the ability of coxsackievirus B3 (CVB3) to infect proliferating neurona
175 We previously demonstrated the ability of coxsackievirus B3 (CVB3) to persist within the neonatal
177 xchanges between poliovirus type 1 (PV1) and coxsackievirus B3 (CVB3) utilizing an in vitro translati
182 The IRESs of poliovirus, the cardiotropic coxsackievirus B3 (CVB3), and the hepatotropic hepatitis
183 mice, IL-13 KO BALB/c mice developed severe coxsackievirus B3 (CVB3)-induced autoimmune myocarditis
184 In this study, we examined the role of CR on coxsackievirus B3 (CVB3)-induced myocarditis using mice
197 oliovirus, foot-and-mouth disease virus, and coxsackievirus B3 and can lead to reduced cell surface e
200 l targeting of key residues, and screens for Coxsackievirus B3 fidelity variants, we isolated nine po
202 iants corresponding to Poliovirus type 1 and Coxsackievirus B3 have virtually the same structure, bas
207 induced after intraperitoneal inoculation of coxsackievirus B3 into C57Bl/6 IRAK4-deficient mice and
209 inistration on the development of autoimmune coxsackievirus B3 myocarditis and dilated cardiomyopathy
211 have previously engineered more than a dozen coxsackievirus B3 polymerase mutations that significantl
216 BL/6 endothelial cells with a nonmyocarditic coxsackievirus B3 variant, H310A1, which is a poor induc
217 ated that infection by another picornavirus (coxsackievirus B3) causes SRp20 to relocalize from the n
219 f Aichi virus, bovine kobuvirus, poliovirus, coxsackievirus B3, and human rhinovirus 14 all copurify
220 on is enhanced in cells infected with the EV coxsackievirus B3, but the related poliovirus has no sig
221 om the binding site of DAF on the surface of coxsackievirus B3, indicating that there are independent
222 this study, we analyzed the role of PAR-1 in coxsackievirus B3-induced (CVB3-induced) myocarditis and
223 re profiled in both human myocarditis and in Coxsackievirus B3-injected mice, comparing myocarditis-s
229 A59, Theiler's encephalomyelitis virus, and Coxsackievirus B3] in mice with autoantibodies to a cent
233 acteristics of the T-cell response to the EV Coxsackievirus B4 (CVB4) in patients with type 1 diabete
234 tion in nonobese diabetic (NOD) mice through coxsackievirus B4 (CVB4) infection requires a preexistin
235 This study of the pancreatropic enterovirus Coxsackievirus B4 (CVB4) shows that although infection a
240 ve analysis of global gene expression during coxsackievirus B4-induced acute and chronic pancreatitis
241 -cell biology, we investigated the impact of coxsackievirus B5 (CVB5) infection on the cellular expre
242 beacons (MBs) for the real-time detection of coxsackievirus B6 replication in living Buffalo green mo
243 uced into BGMK cell monolayers infected with coxsackievirus B6, a discernible fluorescence was observ
245 CAR residues interacting deep within the coxsackievirus canyon are highly conserved in zCAR and h
246 Newborn pups were extremely vulnerable to coxsackievirus CNS infection, and this susceptibility de
247 ovirus (E) 6 (7.6%), E14 (7.6%), E11 (7.4%), coxsackievirus (CV) B3 (7.4%), E25 (5.6%), CVB5 (4.9%),
257 type-specific antibodies against the group B coxsackieviruses (CVBs), which have been linked to diabe
258 rrelia burgdorfii and Lyme arthritis; and B4 Coxsackievirus, cytomegalovirus or rubella and type 1 di
259 Despite replicating to very high titers, coxsackieviruses do not elicit strong CD8 T-cell respons
263 se results do not identify a causal role for coxsackieviruses for cardiomyopathy in HIV-1-infected ch
269 espect, IKK-induced cardiomyopathy resembled Coxsackievirus-induced myocarditis, during which the NF-
270 be used to model the pathogenic processes of coxsackievirus-induced viral myocarditis and to screen a
273 extreme susceptibility of newborn infants to coxsackievirus infection and viral tropism for the CNS,
275 and adenovirus receptor, are susceptible to coxsackievirus infection, and can be used to predict ant
279 hermore, a sex bias for severe sequelae from coxsackievirus infections has been observed in humans.
280 Neonates are particularly susceptible to coxsackievirus infections of the central nervous system
282 s as an antiviral factor during infection by coxsackievirus or human rhinovirus, suggesting a common
283 he RNA template sequence, the origin of VPg (coxsackievirus or poliovirus), the origin of 3D polymera
284 or poliovirus), the origin of 3D polymerase (coxsackievirus or poliovirus), the presence and origin o
287 dystrophin is proteolytically cleaved by the Coxsackievirus protease 2A leading to functional impairm
293 ally important pathogens such as poliovirus, coxsackievirus, rhinovirus, enterovirus 71 and foot-and-
294 ypes of cardiomyocytes, we demonstrated that coxsackievirus RNAs harboring 5' deletions ranging from
296 experiments use intraperitoneal injection of coxsackievirus to infect mice, bypassing the intestine.
297 pro) proteins from diverse enteroviruses and coxsackieviruses to interfere with type I IFN induction
298 ribe an "Open sesame!" strategy developed by coxsackieviruses to invade the organism through the inte
299 Chemicon) with 10 poliovirus, echovirus, and coxsackievirus type A and B stock isolates and College o
300 encapsidation of poliovirus and of C-cluster coxsackieviruses, which are prototypes of enteroviruses,
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