ライフサイエンスコーパス: reovirus infection

1 of necroptosis also requires late stages of reovirus infection.

2 for antibody in the clearance of intestinal reovirus infection.

3 for Daxx in Fas-mediated apoptosis following reovirus infection.

4 indicating that endogenous IFITM3 restricts reovirus infection.

5 y prodeath function for this molecule during reovirus infection.

6 ion uncoating is an essential early event in reovirus infection.

7 these inflammatory mediators and ISG during reovirus infection.

8 nce and prevent tissue injury in response to reovirus infection.

9 ibitor of cathepsin L led to amelioration of reovirus infection.

10 eovirus, and 112 were induced in response to reovirus infection.

11 ndently or in combination, in the absence of reovirus infection.

12 bryo fibroblasts conferred susceptibility to reovirus infection.

13 5-NT also blocked reovirus infection.

14 nished in the CNS of p50-null mice following reovirus infection.

15 ovary cells, which are poorly permissive for reovirus infection.

16 encephalitis and myocarditis associated with reovirus infection.

17 ly activate host cell apoptotic responses to reovirus infection.

18 s involved in apoptosis and DNA repair after reovirus infection.

19 sigma 3 form protein-RNA complexes early in reovirus infection.

20 cells or primary cortical neurons abrogates reovirus infection.

21 IgA(+) and IgG2a(+) B cells after intranasal reovirus infection.

22 ivated in a strain-specific manner following reovirus infection.

23 tly reduces levels of apoptosis triggered by reovirus infection.

24 al entry into these cells is dispensable for reovirus infection.

25 establishment and maintenance of persistent reovirus infections.

26 Reovirus infection activates NF-kappaB, which leads to p

27 We now show that reovirus infection activates transforming growth factor

28 diate this response, we investigated whether reovirus infection alters the activation state of the tr

29 that p53 is activated in the brain following reovirus infection and may provide a therapeutic target

30 Importantly, the combination of reovirus infection and proteasomal inhibition significan

31 or flexibility of sigma1 resulted in delayed reovirus infection and reduced viral titers.

32 factor kappaB (NF-kappaB) is activated after reovirus infection and that this activation is required

33 These findings suggest that reovirus infections are common during early childhood.

34 Reovirus infections are initiated by the binding of vira

35 Although reovirus infections are thought to be common in adults,

36 Moreover, during reovirus infection, association with sigma3 may regulate

37 During reovirus infection, both sigma NS and mu NS are detectab

38 und that 5-nonyloxytryptamine (5-NT) impairs reovirus infection by altering viral transport during ce

39 Furthermore, reovirus infection can be used as a promising approach t

40 any cells which otherwise support productive reovirus infection cannot efficiently mediate this essen

41 Inhibition of JNK activity following reovirus infection delays the release of proapoptotic mi

42 Similar to reovirus infection, ectopic expression of mu1 caused rel

43 Reovirus infection elicits production of type I interfer

44 laboratory previously demonstrated that oral reovirus infection elicits specific serum immunoglobulin

45 immunoglobulin G2a (IgG2a), while parenteral reovirus infection elicits the mixed production of speci

46 s infection in vivo Upon murine norovirus or reovirus infection, Ifnlr1 depletion in IECs largely rec

47 induced at late times (36 to 48 h) following reovirus infection in a manner dependent on IRF-3 and NF

48 ponses and viral clearance following enteric reovirus infection in C57BL/6, B6129F2, and beta2-microg

49 nse to 5'pp-RNA is essential for controlling reovirus infection in cultured cells and in mice.

50 e pathogenesis of the pathologic response to reovirus infection in the lungs and further understand t

51 We propose that experimental reovirus infection in the lungs can serve as a model for

52 atory and inflammatory proteases can promote reovirus infection in vitro and that preexisting inflamm

53 The relevance of these results to reovirus infection in vivo was assessed by treating viri

54 y shown that serotype 3, but not serotype 1, reovirus infection induces a G(2)-to-M transition arrest

55 Here we show that reovirus infection induces apoptosis in cancer cell line

56 Reovirus infection induces apoptosis in cultured cells a

57 colocalizes with Src during cell entry, and reovirus infection induces phosphorylation of Src at the

58 To determine whether reovirus infection initiated in the absence of JAM-A and

59 Reovirus infection is a well-characterized experimental

60 Concordantly, reovirus infection is ablated in primary cortical neuron

61 Reovirus infection is also associated with the activatio

62 Reovirus infection is associated with selective down-reg

63 In an effort to determine whether reovirus infection is associated with these disorders, w

64 inhibition of cellular translation following reovirus infection is complex and involves multiple inte

65 Reovirus infection is initiated by interactions between

66 Since reovirus infection is known to activate cellular transcr

67 dicate that the apoptotic response following reovirus infection is mediated directly by genes respons

68 We found that reovirus infection leads initially to nuclear translocat

69 Reovirus infection leads to apoptosis in cultured cells

70 hought to be required for two early steps in reovirus infection: membrane penetration and activation

71 To determine whether sigma1s is required for reovirus infection of cultured cells, we compared the gr

72 We have previously shown that reovirus infection of epithelial cell lines activates JN

73 the formation of p53/Bak complexes following reovirus infection of ex vivo brain slice cultures and r

74 We now show that reovirus infection of HEK cells is associated with selec

75 ed in electrophoretic mobility shift assays, reovirus infection of HeLa cells leads to nuclear transl

76 cific for other integrin subunits, inhibited reovirus infection of HeLa cells.

77 itecture of sigma1 is required for efficient reovirus infection of host cells.

78 Reovirus infection of human airway epithelia was more ef

79 ng are responsible for strain differences in reovirus infection of macrophage-like P388D cells and ot

80 Further, reovirus infection of mice deficient in the expression o

81 omponents required for intestinal clearance, reovirus infection of mice with null mutations in the im

82 JAM binds directly to sigma1 and permits reovirus infection of nonpermissive cells.

83 To investigate the mechanisms of reovirus infection of polarized epithelial cells, we ass

84 Reovirus infection of target cells can perturb cell cycl

85 Reovirus infection of the mouse SC was also associated w

86 A requisite step in reovirus infection of the murine intestine is proteolysi

87 Reovirus infection of the murine spinal cord (SC) was us

88 s is important for maintenance of persistent reovirus infections of cultured cells.

89 Establishment of persistent reovirus infections of MEL cells was not associated with

90 our data suggest that the acid dependence of reovirus infections of most other cell types may reflect

91 Persistent reovirus infections of murine L929 cells select cellular

92 We propose that reovirus infection promotes apoptosis via the expression

93 In natural enteric reovirus infections, proteolytic uncoating takes place e

94 As reovirus infection requires disassembly in the endocytic

95 We now show that reovirus infection resulted in activation of JNK and cas

96 Serotype 3 reovirus infection results in differential expression of

97 Serotype 1 reovirus infection results in differential expression of

98 Mammalian reovirus infection results in perturbation of host cell

99 We now show that reovirus infection results in the selective activation o

100 These findings indicate that persistent reovirus infections select cellular mutations that affec

101 e required for efficient apoptosis following reovirus infection, suggesting a common mechanism of ant

102 ssive cells conferred full susceptibility to reovirus infection, suggesting that cell surface molecul

103 Reovirus infection synergistically and specifically sens

104 sigma1s is required for apoptosis induced by reovirus infection, T3C84-MA and T3C84 were tested for t

105 ant HEK293 cells and prevents the ability of reovirus infection to sensitize TRAIL-resistant cells to

106 Despite differences in cell tropism, reovirus infection was also reduced in M cell-depleted m

107 tations in sigma3 selected during persistent reovirus infection, we determined the S4 gene nucleotide

108 olecule screen to identify host mediators of reovirus infection, we found that treatment of cells wit

109 ength and flexibility at different stages of reovirus infection, we generated viruses with mutant sig

110 host genes activated by NF-kappaB following reovirus infection, we used HeLa cells engineered to exp

111 beta 2-/- mice cleared reovirus infection with normal kinetics, while MuMT mice

112 atresia, but previous attempts to correlate reovirus infection with this disease have yielded confli