ライフサイエンスコーパス: encephalomyocarditis virus

1 mediated by the prototypical IRES element of encephalomyocarditis virus.

2 cation of poliovirus, coxsackievirus B3, and encephalomyocarditis virus.

3 ade up of two viral species, Theilovirus and Encephalomyocarditis virus.

4 g fibroblast cell line (104C1) infected with encephalomyocarditis virus.

5 mulation of viral proteins of poliovirus and encephalomyocarditis virus.

6 ters of vesicular stomatitis virus (VSV) and encephalomyocarditis virus.

7 siae, Pseudomonas aeruginosa, adenovirus, or encephalomyocarditis virus.

8 ival postinfection with either HSV type 1 or encephalomyocarditis virus.

9 ubiquitin-protein ligases that recognize the encephalomyocarditis virus 3C protease as a substrate we

10 Our measurements show that the encephalomyocarditis virus 3C protease is ubiquitinated

11 Replacing specific encephalomyocarditis virus 3C protease lysine residues w

12 n destruction signal in the rapidly degraded encephalomyocarditis virus 3C protease.

13 cloned under the control of T7 promoter and encephalomyocarditis virus 5'-untranslated region (EMCV-

14 The encephalomyocarditis virus 5'-untranslated region, which

15 and a human coronavirus, HCoV-OC43, but not encephalomyocarditis virus, a picornavirus.

16 y, a pathway well correlative with the anti- encephalomyocarditis virus action of IFN-alpha.

17 l diarrhea virus; and two unrelated viruses, encephalomyocarditis virus and cricket paralysis virus.

18 ast, ribozymes were inactive against IRES of encephalomyocarditis virus and human rhinovirus.

19 t that prevented antiviral host responses to encephalomyocarditis virus and influenza A virus.

20 mice and cells are resistant to infection by encephalomyocarditis virus and SARS-CoV-2 because of enh

21 The 3C proteases of the encephalomyocarditis virus and the hepatitis A virus are

22 icornaviridae includes two distinct species, Encephalomyocarditis virus and Theilovirus.

23 of foot-and-mouth disease virus, rhinovirus, encephalomyocarditis virus, and hepatitis A virus) are m

24 h after infection with rhinovirus type 1a or encephalomyocarditis virus, but the protein was stable i

25 x virus type 1 by about 48 h and that of the encephalomyocarditis virus by about 20 h.

26 rimary polyprotein cleavage, were created in encephalomyocarditis virus cDNA, expressed, and characte

27 IRES elements of Sabin type 1 poliovirus or encephalomyocarditis virus, confirming the low activity

28 Unlike TMEV and encephalomyocarditis virus, each of which is monotypic,

29 se fibroblasts in response to infection with encephalomyocarditis virus (ECMV), a picornavirus that r

30 viroporin activity of influenza virus M2 or encephalomyocarditis virus (EMCV) 2B protein triggers tr

31 Encephalomyocarditis virus (EMCV) and hepatitis C virus

32 factors or IFNs blocks cell death induced by encephalomyocarditis virus (EMCV) and HSV.

33 at different nononcogenic viruses, including encephalomyocarditis virus (EMCV) and human parainfluenz

34 y induced by herpes simplex virus 1 (HSV-1), encephalomyocarditis virus (EMCV) and influenza A virus

35 Previous studies using wild-type Encephalomyocarditis virus (EMCV) and Mengo virus, which

36 at QC suppresses translation directed by the encephalomyocarditis virus (EMCV) and poliovirus IRESs i

37 th no apparent role in cell-free systems for encephalomyocarditis virus (EMCV) and Theiler's murine e

38 We show here that two other RNA viruses, encephalomyocarditis virus (EMCV) and vesicular stomatit

39 We have shown that L from encephalomyocarditis virus (EMCV) binds and inhibits the

40 In contrast, replication of a PV-encephalomyocarditis virus (EMCV) chimera containing the

41 e internal ribosome entry site (IRES) of the encephalomyocarditis virus (EMCV) genomic RNA.

42 The infection of RAW264.7 cells with encephalomyocarditis virus (EMCV) induces iNOS expressio

43 e of this pathway in vivo, we studied murine encephalomyocarditis virus (EMCV) infection in mice and

44 tibody-independent protection against lethal encephalomyocarditis virus (EMCV) infection in the natur

45 ntiviral activity was investigated following encephalomyocarditis virus (EMCV) infection of cell line

46 Encephalomyocarditis virus (EMCV) infection of macrophag

47 Similar to dsRNA, encephalomyocarditis virus (EMCV) infection of RAW 264.7

48 ritical for their replication, the impact of encephalomyocarditis virus (EMCV) infection on the host

49 Highly cytolytic encephalomyocarditis virus (EMCV) infection was shifted

50 In response to encephalomyocarditis virus (EMCV) infection, resident is

51 entire PV 5' noncoding region (NCR) with the encephalomyocarditis virus (EMCV) internal ribosomal ent

52 [aa] 613 to 1090) binds eIF3, eIF4A, and the encephalomyocarditis virus (EMCV) internal ribosomal ent

53 replication of chimeric RNAs containing the encephalomyocarditis virus (EMCV) internal ribosome entr

54 since Vhs cuts circular mRNAs containing an encephalomyocarditis virus (EMCV) internal ribosome entr

55 lete separation of E2 and p7 by inserting an encephalomyocarditis virus (EMCV) internal ribosome entr

56 S2/C113S mutant was restored by inserting an encephalomyocarditis virus (EMCV) internal ribosome entr

57 These data suggest that insertion of the encephalomyocarditis virus (EMCV) IRES element between t

58 inhibition of a cap-dependent luciferase or encephalomyocarditis virus (EMCV) IRES luciferase report

59 (HRV2) IRES and 5-fold more active than the encephalomyocarditis virus (EMCV) IRES.

60 The encephalomyocarditis virus (EMCV) is a mouse-tropic memb

61 Encephalomyocarditis virus (EMCV) is a picornavirus that

62 Encephalomyocarditis virus (EMCV) is capable of stimulat

63 which the internal ribosome entry (IRES) for encephalomyocarditis virus (EMCV) is positioned between

64 Recently, we showed that -1 PRF in encephalomyocarditis virus (EMCV) is trans-activated by

65 tudy, potential cellular enzymes involved in encephalomyocarditis virus (EMCV) L-directed Nup phospho

66 investigated the suitability of the porcine encephalomyocarditis virus (EMCV) model for such studies

67 triphosphate RNA, or MDA5 activators such as encephalomyocarditis virus (EMCV) or poly(I . C).

68 Viral infection with Encephalomyocarditis virus (EMCV) or Sendai virus led to

69 A5 RNA-agonist stimulation or infection with encephalomyocarditis virus (EMCV) or West Nile virus.

70 Here, we show that infection with encephalomyocarditis virus (EMCV) rapidly reduces platel

71 The leader (L) protein of encephalomyocarditis virus (EMCV) shuts off host cell nu

72 the internal ribosomal entry site (IRES) of encephalomyocarditis virus (EMCV) which mediates initiat

73 ional components in HeLa cells infected with encephalomyocarditis virus (EMCV), a cardiovirus.

74 LGP2/RNA complexes from cells infected with encephalomyocarditis virus (EMCV), a picornavirus detect

75 sicular stomatitis virus, a Rhabdovirus, and encephalomyocarditis virus (EMCV), a picornavirus of the

76 ficient mice exposed to extracellular dsRNA, encephalomyocarditis virus (EMCV), and herpes simplex vi

77 ffect from Vesicular stomatitis virus (VSV), Encephalomyocarditis virus (EMCV), and Reovirus-3 virus

78 ISPR deletion of TNK2, WASL, or NCK1 reduced encephalomyocarditis virus (EMCV), coxsackievirus B3 (CV

79 2 internal ribosomal entry sites (IRESs) of encephalomyocarditis virus (EMCV), foot-and-mouth diseas

80 Using a chimeric recombinant encephalomyocarditis virus (EMCV), in which we functiona

81 Picornaviruses, such as encephalomyocarditis virus (EMCV), induce a pro-inflamma

82 viruses (D(T)), such as adenovirus (Adeno), encephalomyocarditis virus (EMCV), influenza virus (H1N1

83 iruses, vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMCV), may also activate the

84 For encephalomyocarditis virus (EMCV), the prototype of the

85 ice and show that upon lethal challenge with encephalomyocarditis virus (EMCV), which is sensed by MD

86 we have shown that NF-kappaB is required for encephalomyocarditis virus (EMCV)- and dsRNA-stimulated

87 t mice lacking ADAM9 are more susceptible to encephalomyocarditis virus (EMCV)-induced death and fail

88 hat the iPLA2beta-selective (S)-BEL inhibits encephalomyocarditis virus (EMCV)-induced iNOS expressio

89 Internal Ribosome Entry Site (IRES) from the Encephalomyocarditis Virus (EMCV).

90 human coronavirus virus (HCoV) OC43 but not encephalomyocarditis virus (EMCV).

91 infection with some viral pathogens such as encephalomyocarditis virus (EMCV).

92 embers of the Picornaviridae family, such as encephalomyocarditis virus (EMCV).

93 control IRESs from both human rhinovirus and encephalomyocarditis virus exhibited strong IRES activit

94 However, sunitinib had no effect on encephalomyocarditis virus growth in cells lacking both

95 Nlrp6(-/-) mice orally infected with encephalomyocarditis virus had increased mortality and v

96 nd control mice systemically challenged with encephalomyocarditis virus had similar mortality; howeve

97 e amino terminus of the required element for encephalomyocarditis virus has now been mapped to includ

98 3C-dependent P3 region cleavage sequences of encephalomyocarditis virus have been constructed.

99 were resistant to viral pathogens, including encephalomyocarditis virus, human rhinovirus, and respir

100 ibited the replication of vaccinia virus and encephalomyocarditis virus in cell culture, suggesting t

101 mpaired IFNalpha-mediated protection against encephalomyocarditis virus infection and reversal of IFN

102 and induces in vivo protection of mice from encephalomyocarditis virus infection.

103 ) protected mice against lethal vaccinia and encephalomyocarditis virus infection.

104 in two different contexts, cap-mediated and encephalomyocarditis virus internal ribosomal entry site

105 n in several bicistronic messages having the encephalomyocarditis virus internal ribosome entry site

106 resistance gene, MDR1 linked together by the encephalomyocarditis virus internal ribosome entry site

107 ame of the reporter gene was preceded by the encephalomyocarditis virus internal ribosome entry site,

108 re inhibited by interferon treatment, but an encephalomyocarditis virus internal ribosome entry site-

109 By contrast, encephalomyocarditis virus internal ribosome entry site-

110 ural proteins (NS3 to NS5B) was driven by an encephalomyocarditis virus internal ribosome entry site.

111 ivity comparable to that of a variant of the encephalomyocarditis virus IRES element in a context-ind

112 cifically to a structural element within the encephalomyocarditis virus IRES upstream of the initiati

113 hat obtained by using the well characterized encephalomyocarditis virus IRES when tested in the same

114 etion mutations into the J-K elements of the encephalomyocarditis virus IRES, translationally defecti

115 ated from the 5' cap, and the other from the encephalomyocarditis virus IRES.

116 n directed hydroxyl radical probing with the encephalomyocarditis virus IRES.

117 valent or higher than that observed from the encephalomyocarditis virus IRES.

118 al resistance to infection with picornavirus encephalomyocarditis virus is known to require CD1d-depe

119 how that frameshifting in a model RNA virus, encephalomyocarditis virus, is trans-activated by viral

120 similarity to a circularly permuted form of encephalomyocarditis virus J-K domain, suggesting a cons

121 Initiation of translation of encephalomyocarditis virus mRNA is mediated by an intern

122 transcription in vivo during infection with encephalomyocarditis virus or transfection with poly(I:C

123 Accordingly, infections with encephalomyocarditis virus or vesicular stomatitis virus

124 Furthermore, RNA from cells infected with encephalomyocarditis virus or with vaccinia virus and pr

125 ternal ribosome entry site (IRES) element of encephalomyocarditis virus picornavirus have been invest

126 ve reconstituted IRES-mediated initiation on encephalomyocarditis virus RNA from purified components

127 ranslation from another unrelated IRES (from encephalomyocarditis virus RNA), but did not affect the

128 ed to prevent diabetes in mice infected with encephalomyocarditis virus strain D (EMCV-D), which has

129 lpha and was protective against infection by encephalomyocarditis virus, suggesting an alternative in

130 N production in response to infection by the encephalomyocarditis virus, the replication of which act

131 asts resulted in about a 12-fold increase in encephalomyocarditis virus titers.

132 ion and identified putative IRES elements in encephalomyocarditis virus, vascular endothelial growth

133 alpha against several RNA viruses, including encephalomyocarditis virus, vesicular stomatitis virus,

134 ey mesangial cells, as opposed to podocytes, encephalomyocarditis virus, vesicular stomatitis virus,

135 ruses such as vesicular stomatitis virus and encephalomyocarditis virus was not inhibited by IFN-beta

136 ibosome entry site (IRES) of a picornavirus, encephalomyocarditis virus, was used instead of the seco

137 of responses to dsRNA [poly(I).poly(C)] and encephalomyocarditis virus were greatly enhanced by IFN-

138 type 1 (e.g., poliovirus) and type 2 (e.g., encephalomyocarditis virus), which are dissimilar except