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

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

2 mediated by the prototypical IRES element of 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 ubiquitin-protein ligases that recognize the encephalomyocarditis virus 3C protease as a substrate we

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

10 Replacing specific encephalomyocarditis virus 3C protease lysine residues w

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

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

13 The encephalomyocarditis virus 5'-untranslated region, which

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

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

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

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

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

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

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

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

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

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

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

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

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

27 Encephalomyocarditis virus (EMCV) and hepatitis C virus

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Encephalomyocarditis virus (EMCV) infection of macrophag

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

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

44 Highly cytolytic encephalomyocarditis virus (EMCV) infection was shifted

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

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

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

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

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

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

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

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

53 Encephalomyocarditis virus (EMCV) is a picornavirus that

54 Encephalomyocarditis virus (EMCV) is capable of stimulat

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

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

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

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

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

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

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

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

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

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

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

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

67 2 internal ribosomal entry sites (IRESs) of encephalomyocarditis virus (EMCV), foot-and-mouth diseas

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 3C-dependent P3 region cleavage sequences of encephalomyocarditis virus have been constructed.

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

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

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

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

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

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

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

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

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

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

94 By contrast, encephalomyocarditis virus internal ribosome entry site-

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

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

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

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

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

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

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

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

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

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

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

106 Accordingly, infections with encephalomyocarditis virus or vesicular stomatitis virus

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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