ライフサイエンスコーパス: minigenome

1 nscription and replication of a rabies virus minigenome.

2 pression of the reporter gene carried on the minigenome.

3 ailed to direct packaging and passage of the minigenome.

4 individual incorporation into a dicistronic minigenome.

5 , viral RNA, and messenger RNA from the EBOV minigenome.

6 f viral transcription and replication in the minigenome.

7 s virus transcription and replication in the minigenome.

8 ription and/or replication of a rabies virus minigenome.

9 in support of replication of the respective minigenomes.

10 In a dicistronic SH-HN minigenome, a U4-G combination was functionally equivale

11 mutations at T286 and showed defects in both minigenome activity and viral growth.

12 n at K254 to arginine (P-K254R) reduced PIV5 minigenome activity, as well as the sumoylation level of

13 id (T286D), or glutamic acid (T286E) reduced minigenome activity.

14 tein, via coinfection with an engineered VSV minigenome, also restored polR growth.

15 llular RNA replication of a plasmid-encoded "minigenome" analog of viral genomic RNA was directed by

16 A series of copyback defective interfering minigenome analogs were constructed to contain substitut

17 Intracellular coexpression of the LCMV minigenome and LCMV L and NP proteins supplied from cotr

18 mutations affected the expression of an LCMV minigenome and the infectivity of virus-like particles,

19 This system involves an LCMV minigenome and the minimal viral trans-acting factors (N

20 Mutational analysis of bicistronic minigenomes and recombinant EBOVs showed no direct corre

21 ted due to the short length of monocistronic minigenomes and which is due at least partially to a pre

22 Time-of-addition, minigenome, and viral entry studies demonstrated that th

23 n requirements for packaging and passaging a minigenome are N, P, M, and F, although the efficiency i

24 tions in vitro as well as VP35 function in a minigenome assay and EBOV replication.

25 lowed efficient viral RNA transcription in a minigenome assay and that RNP activity played an essenti

26 TRIM6 enhances EBOV polymerase activity in a minigenome assay and TRIM6 knockout cells have reduced r

27 virus genus, functions poorly in the RSVlacZ minigenome assay despite conservation of the Cys(3)-His(

28 We developed the first minigenome assay for pig cells and compared the activiti

29 protein can be examined by using an RSVlacZ minigenome assay in vitro since the expression of the la

30 ype when coexpressed with wild-type L in the minigenome assay system.

31 ain within L remains unknown, but by using a minigenome assay we showed that it might be involved in

32 In a minigenome assay, nucleotide substitutions within the Le

33 n and avian cells for many years by use of a minigenome assay, similar investigations in pig cells ha

34 Using a luciferase minigenome assay, we quantified the polymerase activity

35 Using a minigenome assay, we show that phosphorylation of VP30 i

36 teins from the two viruses, as measured in a minigenome assay.

37 ins were analyzed for their functions with a minigenome assay.

38 tely abolished the P protein function in the minigenome assay.

39 Results of minigenome assays and an EBOV reverse genetic system res

40 g L-mCherry fusion protein was functional in minigenome assays and incorporated into virus-like parti

41 (RT-PCR) measurements of RNAs synthesized in minigenome assays established that each of these NP amin

42 e viral polymerase (L protein), and by using minigenome assays we showed that the mutant polymerases

43 ription and genome replication in cell-based minigenome assays, indicating that it inhibits a step co

44 However, minigenome assays, which assess viral RNA polymerase com

45 ctional T7 polymerase-based M- and S-segment minigenome assays, which revealed errors in the publishe

46 All blocked RSV polymerase activity in minigenome assays.

47 Here we have used minigenome-based approaches to evaluate expression level

48 revent the encapsidation of plasmid supplied minigenome, but it affected both transcription and RNA r

49 ciferase reporter gene expression from HPIV3 minigenomes by viral proteins in a recombinant vaccinia

50 To this end, we constructed an LCMV S minigenome consisting of a negative-sense copy of the ch

51 es (VLPs), which contain an Ebola virus-like minigenome consisting of a negative-sense copy of the gr

52 The monocistronic RSV-CAT minigenome consists of the chloramphenicol acetyltransfe

53 Intracellular minigenome contained only the mutant assignment, indicat

54 Unexpectedly, each recovered minigenome contained the complement of this nonviral ext

55 n complex was supplied from cDNA plasmids, a minigenome containing either the APV leader or trailer w

56 A dicistronic minigenome containing the M-F gene junction was used to

57 In a minigenome containing the NS1 and NS2 genes in their aut

58 nd avian pneumovirus (APV) was studied using minigenomes containing a reporter gene.

59 A panel of minigenomes containing additional sequence at the 3' end

60 Minigenomes containing heterologous extensions of 6 nucl

61 s studies indicated that a 719-nt subgenomic minigenome (DENV-MINI) is an efficient template for tran

62 Deletion of the cre(2C) RNA sequences from minigenomes eliminates their ability to serve as templat

63 (L), nucleocapsid protein (N) and a reporter minigenome expressed in human HuH-7 cells resulted in fo

64 roteins not related to Z did not affect LCMV minigenome expression.

65 ely 10-fold lower inhibitory activity on ARM minigenome expression.

66 ection of the Z cDNA strongly inhibited LCMV minigenome expression.

67 ion of overlapping genes in EBOV bicistronic minigenomes followed the stop-start mechanism, similar t

68 due to reduced availability of encapsidated minigenomes for packaging.

69 y (NJ) serotype of VSV was inserted into the minigenome gene junction.

70 anscripts produced from di- and tricistronic minigenomes indicated that a significant proportion of a

71 immunoprecipitation analysis of the mutated minigenomes indicated that the first three nucleotides o

72 nations together with a plasmid containing a minigenome into cells infected with a vaccinia virus rec

73 The dicistronic RSV-CAT-LUC minigenome is a derivative of RSV-CAT into which the ORF

74 We therefore adapted a reverse-genetics minigenome (MG) rescue system based on Junin virus, the

75 studied the role of the LCMV IGR by using a minigenome (MG) rescue system based on RNA analogues of

76 pothesis, we established a helper-virus-free minigenome (MG) system where intracellular synthesis of

77 ning the 3'-terminal 20-nt region of an LCMV minigenome (MG) was generated, and the mutant MGs were a

78 ransfected with a plasmid containing an LCMV minigenome (MG).

79 protein with N and L proteins also enhanced minigenome mRNA transcription in the cells expressing vi

80 d a transcription- and replication-competent minigenome of VSV to generate a series of deletions span

81 Progeny minigenomes of six different mutants were recovered post

82 Genome analogs ("minigenomes") of Sendai and measles viruses replicate ef

83 were analyzed with cDNA-encoded RNA analogs (minigenomes) of nonsegmented negative-sense RSV genomic

84 )-tagged L, and viral minigenome resulted in minigenome replication and transcription, a finding that

85 acid residue changes (Vcpi-) still inhibits minigenome replication as does the wild-type V protein.

86 deleted P with wild-type P had no effect on minigenome replication in vivo, notwithstanding the form

87 nd in vivo chloramphenicol acetyltransferase minigenome replication were studied under conditions tha

88 The in vivo system takes advantage of minigenome replication, which measures luciferase report

89 relevant doses of ribavirin inhibited CCHFV minigenome replication.

90 that this interaction is essential for EBOV minigenome replication.

91 uses equally affected mRNA transcription and minigenome replication.

92 the replication and transcription of an RSV minigenome replicon at 37 and 39 degrees C.

93 When tested in an RSV minigenome replicon system using beta-galactosidase as a

94 ncreased translation of nonreplicating viral minigenome reporter RNAs during infection and also delay

95 y, replication and transcription of the RVFV minigenome required expression of viral N and L proteins

96 n and gene expression were exchangeable in a minigenome rescue assay.

97 oriomeningitis virus (LCMV), in vivo using a minigenome rescue assay.

98 of N, hemagglutinin (HA)-tagged L, and viral minigenome resulted in minigenome replication and transc

99 Consistent with the minigenome results, cells transiently expressing Z exhib

100 hable from previously studied negative-sense minigenome RNA in its ability to participate in transcri

101 were sufficient for packaging an Ebola virus minigenome RNA into VLPs.

102 Since the minigenome RNA needs to be encapsidated before transcrip

103 Minigenome RNA replication was not affected by changes i

104 indicating that the effect of NSs protein on minigenome RNA replication was unrelated to a putative N

105 ins resulted in a significant enhancement of minigenome RNA replication.

106 Enhancement of minigenome RNA synthesis by NSs protein occurred in cell

107 Our finding that RVFV NSs protein augmented minigenome RNA synthesis was in sharp contrast to report

108 genus Bunyavirus) NSs protein inhibits viral minigenome RNA synthesis, suggesting that RVFV NSs prote

109 on of RNA transcripts for viral proteins and minigenome RNA transcripts carrying a reporter gene betw

110 cription in the cells expressing viral-sense minigenome RNA transcripts.

111 in LCMV-infected cells transfected with the minigenome RNA.

112 ength mRNA and, in the case of a dicistronic minigenome, sequential transcription.

113 A previous study, using an RSV minigenome, suggested that the leader (Le) promoter regi

114 within these domains were identified using a minigenome system able to recapitulate CCHFV-specific RN

115 Here we describe a Junin virus functional minigenome system and a reverse genetics system for prod

116 To address this question, we used a minigenome system and recombinant viruses to study the e

117 Interpretation of the data from the minigenome system and the full-length infectious virus i

118 hese results demonstrated the utility of the minigenome system for use in BSL-2 laboratory settings t

119 established an RVFV T7 RNA polymerase-driven minigenome system in which T7 RNA polymerase from an exp

120 Studies with the minigenome system showed that the 530 and 1009 mutations

121 In this work, we established a novel minigenome system that allows the domains of P to be com

122 Using mutational analysis and a minigenome system, we identified regions in the N and C

123 Using an RSV minigenome system, we individually mutated each of the l

124 of a set of PB1 mutants in a model reporter minigenome system.

125 the 1009 mutation also was observed with the minigenome system.

126 NA synthesis using mutational analysis and a minigenome system.

127 (T101A) significantly enhanced activity in a minigenome system.

128 ed effects on virus polymerase activity in a minigenome system.

129 reduced M2-2 activity as measured by the RSV minigenome system.

130 Life cycle modeling systems, including minigenome systems and transcription- and replication-co

131 helper virus-independent S, M, and L segment minigenome systems for analysis of virus RNA and protein

132 region with nonviral sequences resulted in a minigenome template (Rep 22) that was defective in termi

133 tion, it had no effect on replication of any minigenome tested, suggesting that it is not an active p

134 eight times more reporter protein from an MV minigenome than the three wild-type L proteins.

135 nfectious trVLPs containing a tetracistronic minigenome that encodes a reporter and the viral protein

136 Use of a minigenome that incorporated two nucleotide changes foun

137 expression increased the RNA replication of minigenomes that originated from S and L RNA segments.

138 e previously shown, using an SV5 dicistronic minigenome, that replacement of the 22-base M-F intergen

139 dicistronic vesicular stomatitis virus (VSV) minigenome to investigate the effects of either single o

140 dicistronic vesicular stomatitis virus (VSV) minigenomes to dissect the functional importance of the

141 Minigenome transcription also yielded a CAT-LUC readthro

142 t Z has a strong inhibitory activity on LCMV minigenome transcription and RNA replication.

143 With an in vivo VSV minigenome transcription system, we further show that a

144 owever, the same mutant protein complemented minigenome transcription when expressed together with a

145 the N(0)-P complex was unable to support VSV minigenome transcription, although it efficiently suppor

146 In two different dicistronic minigenomes, transcription of each gene was equally sens

147 Four of the minigenome variants containing naturally occurring inter

148 ency of encapsidation of the plasmid-derived minigenome was not altered by coexpression of NS1, indic

149 The RSV-CAT-LUC minigenome was synthesized in vitro and transfected into

150 Each minigenome was synthesized in vitro and transfected into

151 cription and replication of the rabies virus minigenome were significantly lower with the unphosphory

152 The termini of the recovered minigenomes were examined for five mutants by RNA circul

153 The minigenomes were generated entirely from cDNA and contai

154 Two minigenomes were used.

155 activities on the expression of the LCMV ARM minigenome, whereas the Z protein of the genetically mor

156 uential transcription were investigated with minigenomes which contained one to five genes which were

157 However, the activity of a minigenome with a 56-nucleotide extension could be resto

158 A series of minigenomes with mutant Le sequences was generated, and