ライフサイエンスコーパス: EBNA-1

1 antigen-diffuse (EA-D) and nuclear antigen (EBNA-1).

2 responses to Epstein-Barr nuclear antigen 1 (EBNA-1).

3 rotein Epstein-Barr virus nuclear antigen-1 (EBNA-1).

4 in the presence of the EBV-encoded protein, EBNA-1.

5 e binding sites for the EBV-encoded protein, EBNA-1.

6 er and/or the BamHI W promoter) are used for EBNA-1.

7 mber that binds to the Q locus and displaces EBNA-1.

8 ngle viral gene product, the nuclear protein EBNA-1.

9 mids introduced into cell lines that contain EBNA-1.

10 etention in cells expressing the EBV protein EBNA-1.

11 cells and with the extremely long t(1/2) of EBNA-1.

12 ngle infecting virus subtype by mutations in EBNA-1.

13 nhibited by a dominant-negative inhibitor of EBNA-1.

14 ort long-term replication in the presence of EBNA-1.

15 express a single viral trans-acting factor, EBNA-1.

16 efficiently in human cells in the absence of EBNA-1.

17 he ability to act as inhibitors of wild-type EBNA-1.

18 expressing the viral transactivator protein EBNA-1.

19 le for strong but nonspecific RNA binding by EBNA-1.

20 We conclude that the EBNA-1/293c18 cell expression model represents a useful

21 The results show that (i) the EBNA-1/293c18 expression system results in a larger incr

22 (EBNA-1) cDNA (293c18 cells) to evaluate the EBNA-1/293c18 expression system.

23 Epstein-Barr virus nuclear antigen 1 (EBNA-1), a functional homologue of LANA, is also require

24 vantage of the transactivating properties of EBNA-1, a latency protein expressed in all EBV-containin

25 urther evidence that this novel mechanism of EBNA-1 action functions during latency.

26 A-1-responsive templates and have shown that EBNA-1 activates transcription from these chromatin-embe

27 moter and therefore asked whether LANA, like EBNA-1, activates transcription by direct binding to DNA

28 EBNA-1 acts post-synthetically through unknown mechanism

29 oncogenic potential, enforced expression of EBNA-1 alone in EBV-negative Akata cells failed to resto

30 EBNA-1 also regulates viral gene expression and is requi

31 equired for genome segregation; in addition, EBNA-1 also supports efficient DNA replication of oriP-c

32 ds 1-90 or histone H1-2 could substitute for EBNA-1 amino acids 1-378 in mediating more efficient acc

33 isome maintenance was evaluated by replacing EBNA-1 amino acids 1-378 with cell proteins that have si

34 ne transcription is largely autoregulated by EBNA 1 and EBNA 2.

35 ndancy in lymphomagenesis between transgenic EBNA-1 and bcl-2.

36 rt-term replication of this plasmid requires EBNA-1 and can be inhibited by a dominant-negative inhib

37 of Qp activity is reciprocally controlled by EBNA-1 and E2F.

38 y antigen, and Epstein-Barr nuclear antigen (EBNA-1 and EBNA-2) in blood samples collected before dia

39 transfected with an oriP plasmid expressing EBNA-1 and hygromycin phosphotransferase give rise to dr

40 ins retain the biological activities of both EBNA-1 and large T-antigen, their constituent proteins d

41 Using fusion proteins of EBNA-1 and large T-antigen, we tested whether tethering

42 and this was associated with somewhat higher EBNA-1 and lower LMP1 expression, consistent with the ne

43 pus arises through molecular mimicry between EBNA-1 and lupus autoantigens and provide further eviden

44 ly, although the parental LCLs express viral EBNA-1 and other Epstein-Barr virus latency-related elem

45 oy newly synthesized plasmids, and that both EBNA-1 and the family of repeats of oriP are required fo

46 rated that the plasmid-retention function of EBNA-1 and the FR did not contribute significantly to th

47 EBNA-1 humoral immune response, fragments of EBNA-1 and the maximally overlapping unique octapeptides

48 e EBNA-1 sites and that interactions between EBNA-1 and this protein(s) are critical for replicator f

49 ck the linking or the retention functions of EBNA-1 and were analyzed for the residual ability to act

50 fidence interval [CI], 1.1-8.7), and an anti-EBNA-1/anti-EBNA-2 antibody ratio </= 1.0 versus > 1.0 (

51 was significantly associated with a low anti-EBNA-1/anti-EBNA-2 antibody ratio.

52 Anti-EBNA-1 antibodies are associated with pediatric-onset SL

53 In current constructs, selectable marker and EBNA-1 are not always co-expressed.

54 at the putative E2F binding sites within the EBNA-1 binding domain can exert a positive influence on

55 Third, EBNA-1 binding is required for the site-specific demethy

56 wo thymines occur at unique positions within EBNA-1 binding sites 1 and 4 at the DS and become sensit

57 these experiments also show that the paired EBNA-1 binding sites are not functionally equivalent and

58 t it is negatively autoregulated through two EBNA-1 binding sites downstream of the transcription ini

59 nent (DS) of oriP, which depends on multiple EBNA-1 binding sites for activity.

60 That is, EBNA-1 protein binding prevents the EBNA-1 binding sites from being remethylated after one r

61 Deletion of 11 EBNA-1 binding sites in the FR or replacement of the FR

62 ation of the first DNA strand in oriP at the EBNA-1 binding sites involves a passive (replication-dep

63 In this study, demethylation at the EBNA-1 binding sites of the Epstein-Barr virus latent re

64 The DS contains two pairs of closely spaced EBNA-1 binding sites, and a previous study had shown tha

65 f the DS, including a pair of closely spaced EBNA-1 binding sites, had significant replicator activit

66 halves of the DS share in common, other than EBNA-1 binding sites, is a 9-bp sequence that is present

67 ore appears to be simply two properly spaced EBNA-1 binding sites.

68 oriP contains 24 EBNA-1 binding sites; 20 are located within the family o

69 In investigating the significance of EBNA-1 binding to mitotic chromosomes, we identified the

70 EBV-encoded nuclear antigen-1 (EBNA-1) binding to a cis-acting viral DNA element, oriP,

71 Although EBNA-1 binds multiple sites within oriP, its role in DNA

72 EBNA-1 binds to two clusters of sites at oriP, an 1, 800

73 sensitive to oxidation by permanganate when EBNA-1 binds, but mutation of each to the consensus base

74 es a very useful tool for rapid screening of EBNA-1 blockers in biomedical research.

75 In the two cases that were positive for EBNA-1, both of which occurred in patients of Asian ethn

76 t only a mechanism to constitutively express EBNA-1 but also one which may sustain EBNA-1 expression

77 ther encodes Epstein-Barr nuclear antigen 1 (EBNA-1), but lacks FR.

78 Twelve cases (25%) were positive for EBNA-1 by immunohistochemistry, all but one different fr

79 ealthy matched controls were tested for anti-EBNA-1 by Western blotting and enzyme-linked immunosorbe

80 In contrast, the EBNA-1 C terminus (amino acids 379-641), which includes

81 Previously reported EBNA-1 C-terminal region amino acid sequence variants, b

82 EBNA-1 can also activate transcription on binding to the

83 ion with the Epstein-Barr neutral antigen-1 (EBNA-1) cDNA (293c18 cells) to evaluate the EBNA-1/293c1

84 S plasmid was established efficiently in 293/EBNA-1 cells, being lost at a rate of only 8% per cell g

85 approximately 30% per cell generation in 293/EBNA-1 cells, indicating that the FR inhibits oriP's est

86 establishment of the oriP derivative in 293/EBNA-1 cells.

87 s which maintain the exclusive expression of EBNA-1 characteristic of the tumor.

88 rmore, an altered humoral immune response to EBNA-1, characteristic of SLE, has been found and may be

89 Lipofection of the oriP/EBNA-1-containing version into mouse Hepa1-6 cells resul

90 rly and within the nucleus and to block anti-EBNA-1 cytotoxic T cell responses.

91 Inhibition of EBNA-1 decreases survival of these tumor cells by induci

92 An EBNA-1-deficient mutant of EBV was isolated and found to

93 orter activity, including that driven by the EBNA-1-dependent enhancer in the origin of plasmid repli

94 ted plasmids, and the DS supported efficient EBNA-1-dependent replication in the absence of the FR.

95 In conclusion, the DS of oriP is an EBNA-1-dependent replicator, and its minimal active core

96 Our results revealed that EBNA-1 does not inhibit transcription from Qp, as previo

97 ugh fulfilling functions similar to those of EBNA-1, does so by very different mechanisms.

98 r Qp, which mediates exclusive expression of EBNA-1 during the restricted programs of EBV latency ass

99 d antigen (RR, 1.58; 95% CI, 0.79-3.14), and EBNA-1/EBNA-2 ratio </= 1.0 (RR, 1.52; 95% CI, 0.91-2.55

100 tween EBV serostatus, elevated titers, or an EBNA-1/EBNA-2 ratio </= 1.0 and NHL risk overall.

101 The virus-encoded EBNA-1 (EBV nuclear antigen 1) and latent replication or

102 was further retrofitted with either the oriP/EBNA-1 elements from Epstein-Barr virus, which allow epi

103 e, expressed pluripotency markers, lost oriP/EBNA-1 episomal vectors, generated teratomas, retained d

104 t epitope of 60 kDa Ro or the cross-reactive EBNA-1 epitope progressively develop autoantibodies bind

105 8+ T-cell responses was confirmed by mapping EBNA-1 epitopes and demonstrating HLA class I presentati

106 8+ T cells in 6 of 6 donors, including 2 new EBNA-1 epitopes presented by HLA A0206 and A6802.

107 , this clearly has no impact on the level of EBNA-1 expressed in proliferating cells.

108 d 2 are induced in pre-neoplastic samples of EBNA-1 expressing mice.

109 ered by recombinant adenoviruses to suppress EBNA-1 expression and to block virus-induced B cell prol

110 ity is cell cycle regulated, Qp activity and EBNA-1 expression are predicted to be regulated in a cel

111 tained the EBV-derived family of repeats, an EBNA-1 expression cassette, and 19 kb of human DNA that

112 e an efficient means to monitor and regulate EBNA-1 expression from Qp, ensuring levels adequate for

113 liferative disorders and from the restricted EBNA-1 expression in Burkitt's lymphoma tissues.

114 However, the kinetics of LANA/EBNA-1 expression in individual B-cell subsets throughou

115 xpress EBNA-1 but also one which may sustain EBNA-1 expression in the face of the antiviral effects o

116 We found that EBV EBNA-1 expression is downregulated in PEL cells at both

117 ing cell and to coordinate the activation of EBNA-1 expression necessary for EBV genome replication a

118 mple but efficient mechanism of ensuring the EBNA-1 expression necessary to sustain long-term latency

119 scriptional regulatory proteins that mediate EBNA-1 expression via the viral promoter Qp, which is ac

120 is to direct the pRb-mediated suppression of EBNA-1 expression within resting B cells, the principal

121 ncy, the BamHI Q promoter (Qp) gives rise to EBNA-1 expression.

122 of selected cellular genes as a response to EBNA-1 expression.

123 in certain cell lines, the essential role of EBNA-1 for infection of these cell lines is likely to be

124 We have made and screened derivatives of EBNA-1 for the ability to act as inhibitors of wild-type

125 ral proteins Epstein-Barr nuclear antigen 1 (EBNA-1) for Epstein-Barr virus and latency-associated nu

126 ing, however, necessitates the expression of EBNA-1 from the EBNA-1-specific promoter Qp to ensure ag

127 persistent LCV infection and the role of the EBNA-1 GAR for immune evasion in vivo.

128 we introduced a frameshift mutation into the EBNA-1 gene of EBV by recombination along with a flankin

129 This is a significant problem since the EBNA-1 gene product can be toxic in some cell types and

130 o-vector system limited host exposure to the EBNA-1 gene product.

131 Our results suggest that any variation in EBNA-1 gene sequence is caused by a polymorphism present

132 ollowed by DNA sequencing, we found a single EBNA-1 gene sequence variant in each tissue, whether rea

133 Variant EBNA-1 gene sequences were more common in both neoplasti

134 ect to type and previously defined LMP-1 and EBNA-1 gene variations, from virus detected in the perip

135 in reaction (PCR) to amplify portions of the EBNA-1 gene, followed by DNA sequencing, we found a sing

136 ct integration, as well as expression of the EBNA-1 gene, which, in turn, increases transfection freq

137 circular molecule carrying both oriP and the EBNA-1 gene.

138 ein-Barr virus-associated nuclear antigen-1 (EBNA-1) gene carboxy (C)-terminal mutations occurring in

139 transcription of the EBV nuclear antigen 1 (EBNA-1) gene is mediated by the promoter Qp.

140 levations were significant for antibodies to EBNA-1 (GMT, 515 vs 203; P =.03), EBNA-2 (GMT, 91 vs 40;

141 EBNA-1 has also been reported to have oncogenic potentia

142 e, and a recent study has questioned whether EBNA-1 has any direct role in replication.

143 and a potential immune evasion mechanism for EBNA-1 has been conserved in rhLCV.

144 A mutational analysis of EBNA-1 has identified a domain required for transcriptio

145 Epstein-Barr nuclear antigen 1 (EBNA-1) has been shown to activate transcription from tr

146 p5170 and transfected the constructs into an EBNA-1(+) human cell line.

147 To define the fine specificity of their anti-EBNA-1 humoral immune response, fragments of EBNA-1 and

148 ed and potentially deleterious expression of EBNA-1 in a nonproliferating cell and to coordinate the

149 zed to mimic the palindromic target sites of EBNA-1 in the EBV genome.

150 Expression of EBNA-1 in uninfected cells also can inhibit apoptosis in

151 nt with the generation of variant species of EBNA-1 in vivo.

152 Epstein-Barr virus (EBV) nuclear antigen-1 (EBNA-1) in B-cells which show a predisposition to lympho

153 xpression of Epstein-Barr nuclear antigen 1 (EBNA-1) in common.

154 on from oriP requires EBV nuclear antigen 1 (EBNA-1) in trans; however, its contributions to this rep

155 to express essential viral proteins, such as EBNA-1, in the face of cell-mediated repression of EBV g

156 can exert a positive influence on Qp that is EBNA-1 independent, suggesting that these regulatory ele

157 plasmids, including the mutant form with the EBNA-1 internal deletion, correlated directly with their

158 Latent EBNA-1 is a promising target for a therapeutic vaccine,

159 test whether the humoral immune response to EBNA-1 is a risk factor for pediatric SLE.

160 EBNA-1 is an EBV protein consistently expressed in all E

161 Our findings demonstrate that EBNA-1 is critical for the continued survival of EBV-ass

162 selected cell clones when the viral protein EBNA-1 is provided, being lost at a rate of 2 to 4% per

163 The data indicate that EBNA-1 is required for efficient and stable latent infec

164 EBNA-1 is required for episome maintenance, binds to ori

165 In contrast, EBNA-1 is the only EBV nuclear antigen expressed in Burk

166 intenance (segregation) function of oriP and EBNA-1 is what is required.

167 The Epstein-Barr nuclear antigen 1 (EBNA-1) is an important target for vaccination because i

168 se diseases, Epstein-Barr nuclear antigen 1 (EBNA-1) is constitutively expressed.

169 EBV nuclear antigen 1 (EBNA-1) is expressed in all EBV-infected cells and plays

170 Epstein-Barr virus (EBV) nuclear antigen-1 (EBNA-1) is potentially a universal target for immune rec

171 Epstein-Barr viral nuclear antigen-1 (EBNA-1) is required for the stable replication of plasmi

172 Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA-1) is required in trans to support replication of t

173 Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA-1) is the essential protein for maintenance of the

174 Epstein-Barr nuclear antigen 1 (EBNA-1) is the only viral protein consistently expressed

175 alignancies, Epstein-Barr nuclear antigen 1 (EBNA-1), is required for survival of one of these cancer

176 iation of replication at the DS, mediated by EBNA-1, is important for the natural life cycle of EBV,

177 emplates can be inhibited by a derivative of EBNA-1 lacking the amino acids required for activation f

178 EBNA-1 lacks enzymatic activities that are present in th

179 onal EBV and expressed the EBV latency genes EBNA-1, LMP-1, and LMP-2.

180 t has not been entirely clear to what extent EBNA-1 might be required for replication from oriP per s

181 CV-1/EBNA-1 monkey kidney epithelial cells expressing Epstein

182 Z1) to lymphoblastoid cell lines, suppressed EBNA-1 mRNA and protein expression, significantly reduce

183 Furthermore, LMP-1 reduced EBNA-1 mRNA derived from Qp only in type I cells in whic

184 omoter (Qp) is used for the transcription of EBNA-1 mRNA in type I and type II latency, which are EBV

185 omoter (Qp) is used for the transcription of EBNA-1 mRNA in type I latency, which is an EBV infection

186 the endogenous Qp but marginally reduced the EBNA-1 mRNA level.

187 Following release from G2/M block, EBNA-1 mRNA levels declined as the synchronized cells en

188 As cells proceeded into S phase, EBNA-1 mRNA levels increased parallel to the peak in cel

189 ithin G(0)/G(1) in growth-arrested BL cells, EBNA-1 mRNA levels were twofold lower than in S phase, s

190 cycle variation in the expression of either EBNA-1 mRNA or protein in exponentially growing BL cells

191 ion of Epstein-Barr virus nuclear antigen 1 (EBNA-1) mRNA in cells in the most restricted (type I) la

192 ts identical in structure to EBV Qp-specific EBNA-1 mRNAs are present in nonhuman LCV-infected cells,

193 biochemical approaches demonstrated that an EBNA-1 mutant lacking residues 16 to 372 bound to oriP p

194 genic B-cell lines using either Cp/Wp or Qp, EBNA-1 occupancy of Qp is equivalent, suggesting that au

195 ults were obtained with vaccines that target EBNA-1 of rhLCV, a virus closely related to EBV.

196 racteristic lysine patch, which is absent in EBNA-1 of the Epstein-Barr virus.

197 uch as Epstein-Barr virus nuclear antigen 1 (EBNA-1) of the related gamma-herpesvirus Epstein-Barr vi

198 ntenance functions of EBV nuclear antigen 1 (EBNA-1), one of six EBNAs expressed from a common promot

199 laced with the dimeric DNA binding domain of EBNA-1 or Gal4 bound efficiently to the Brd4 protein, bu

200 We show that deleting EBNA-1 or oriP disrupts mitotic chromosome tethering but

201 ion reactions in the presence of full-length EBNA-1 or proteins with various deletions to assess the

202 cause the prey plasmid was maintained by the EBNA-1/Ori-P system.

203 of 36 matched EBV-positive controls targeted EBNA-1 (P < 0.005).

204 CD8+ T-cell responses to a complete panel of EBNA-1 peptides in an HLA-characterized population.

205 ence-specific DNA-binding protein that, like EBNA-1, plays an important role in DNA replication and g

206 sitive cases showed rare EBER-1-, ZEBRA-, or EBNA-1- positive cells (<0.1%); in none of these cases w

207 In EBNA-1-positive 143B and H1299 cells, plasmids containin

208 iP replicons are not intrinsically stable in EBNA-1-positive cell lines.

209 d in Escherichia coli, and reintroduced into EBNA-1-positive cells are likewise established inefficie

210 uction of oriP plasmids into a population of EBNA-1-positive cells, oriP plasmids replicate but are l

211 as less than 1% as efficient as an isogenic, EBNA-1-positive strain in this assay.

212 homologs are indeed utilized as alternative EBNA-1 promoters.

213 That is, EBNA-1 protein binding prevents the EBNA-1 binding sites

214 in part, to the documented abilities of the EBNA-1 protein both to retain FR-containing DNA intracel

215 This new homogeneous assay for active EBNA-1 protein detection and quantification provides a v

216 smid replication ( oriP ) and expressing the EBNA-1 protein from the Epstein-Barr virus replicate and

217 ported an innovative system to detect active EBNA-1 protein in a homogeneous assay.

218 Although the EBV EBNA-1 protein is expressed in all EBV-associated tumors

219 nd many Burkitt lymphoma cell lines, the EBV EBNA-1 protein is one of six viral nuclear antigens expr

220 Expression of EBNA-1 protein is required for the establishment and mai

221 However, EBNA-1 protein levels showed no detectable change during

222 We have examined sequence variations in the EBNA-1 protein of EBV in normal peripheral blood lymphoc

223 functional similarities between LANA and the EBNA-1 protein of Epstein-Barr virus.

224 dence indicating that phosphorylation of the EBNA-1 protein or EBNA-1-truncated derivatives is not es

225 A-1 proteins to determine the portion of the EBNA-1 protein that is responsible for pausing of forks

226 The presence of EBNA-1 protein was reflected by a large increase in tran

227 mit of detection of 3.75 ng mL(-1) of active EBNA-1 protein with a dynamic detection range from 3.75

228 Expression of the Epstein-Barr virus (EBV) EBNA-1 protein within EBV-positive tumor cells and subpo

229 chromosome tethering are linked through the EBNA-1 protein.

230 ds in mammalian cells in the presence of the EBNA-1 protein.

231 ently infected cells is dependent on the EBV EBNA-1 protein.

232 ing cell lines due to EBV nuclear antigen 1 (EBNA-1) protein-mediated replication and segregation.

233 , we have investigated a series of truncated EBNA-1 proteins to determine the portion of the EBNA-1 p

234 These data lead us to propose that EBNA-1 recruits oriP-containing plasmids into chromatin

235 Here we addressed the mechanism by which EBNA-1 represses Qp through binding downstream of the tr

236 itope mapping revealed that the humoral anti-EBNA-1 response in pediatric SLE was distinct from and l

237 We have established cells with integrated EBNA-1-responsive templates and have shown that EBNA-1 a

238 RhLCV EBNA-1 (rhEBNA-1) was the most frequently targeted laten

239 e, and cytokine production profiles of rhLCV EBNA-1 (rhEBNA-1)-specific T cells in 15 rhesus macaques

240 EBV infections, we examined the capacity of EBNA-1 ribozymes delivered by recombinant adenoviruses t

241 NA-1 that can inhibit up to 98% of wild-type EBNA-1's activities.

242 Efficient inhibitors of EBNA-1's functions would likely prove useful in the ther

243 EBNA-1's mode of activating transfected templates is the

244 Because of EBNA-1's role in stabilizing plasmids through the FR, it

245 ed one derivative of EBNA-1 with only two of EBNA-1's three linking domains which can support transcr

246 n both countries, there were similar variant EBNA-1 sequences present in normal tissues and HD cases.

247 tein-Barr virus (EBV) based on variations in EBNA-1 sequences.

248 dy we characterized the contribution of each EBNA-1 site within the replicator and flanking sequences

249 EBNA-1 sites 1 and 2, together with an element(s) within

250 t the minimal replicator of oriP consists of EBNA-1 sites 3 and 4 and two copies of a 14-bp repeat th

251 cell protein(s) binds sequences flanking the EBNA-1 sites and that interactions between EBNA-1 and th

252 We present evidence that shows that all four EBNA-1 sites are required for an oriP plasmid to be repl

253 ingly, CpG sites adjacent to and between the EBNA-1 sites do not become demethylated.

254 We showed previously that these EBNA-1 sites function in pairs and that mutational inact

255 resent in inverse orientation flanking these EBNA-1 sites.

256 We detected EBNA-1-specific CD8+ T cells in 10 of 14 healthy donors

257 al blood mononuclear cells, suggesting these EBNA-1-specific CD8+ T cells were functionally defective

258 Importantly, EBNA-1-specific CD8+ T cells were significantly less fre

259 ate that humans normally mount a significant EBNA-1-specific CD8+ T-cell response to EBV infection, b

260 EBNA-1-specific CD8+ T-cell responses have been assessed

261 EBNA-1-specific CD8+ T-cell responses were rescued in ap

262 cted cells may be at risk for elimination by EBNA-1-specific cytotoxic T cells.

263 Here, we studied the EBNA-1-specific immune response using the EBV-homologous

264 cessitates the expression of EBNA-1 from the EBNA-1-specific promoter Qp to ensure against genome los

265 Herein, EBNA-1-specific T cell epitopes were evaluated after AdC

266 important proof of principle that functional EBNA-1-specific T cells can be expanded by vaccination.

267 This study demonstrated that EBNA-1-specific T cells can be expanded by vaccination.

268 We report on the use of adoptive transfer of EBNA-1-specific T cells in 10 pediatric and adult patien

269 Adoptive ex vivo transfer of EBNA-1-specific T cells is a feasible and well-tolerated

270 In vivo expansion of transferred EBNA-1-specific T cells was observed in eight of 10 pati

271 However, in 11 of 12 American tumors, the EBNA-1 subtype was V-leu.

272 hromosomal maintenance of DNA with the oriP /EBNA-1 system is not compatible with linear molecules ca

273 We have identified derivatives of EBNA-1 that can inhibit up to 98% of wild-type EBNA-1's

274 es for Epstein-Barr virus nuclear antigen 1 (EBNA-1), the sole viral protein required for the replica

275 The ability of EBNA-1 to activate transcription from both integrated an

276 d versus normal titers and the ratio of anti-EBNA-1 to anti-EBNA-2 titers (</= 1.0 vs > 1.0).

277 hat the mutant lost the ability of wild-type EBNA-1 to associate with interphase chromatin.

278 rget the rhesus (rh) lymphocryptovirus (LCV) EBNA-1 to determine if ongoing T cell responses during p

279 d new light on the potential contribution of EBNA-1 to EBV associated tumorigenicity as well as to th

280 To investigate the importance of EBNA-1 to latent infection by EBV, we introduced a frame

281 oriP, while the FR acts in conjunction with EBNA-1 to prevent the loss of plasmids from proliferatin

282 e found that plasmids carrying oriP required EBNA-1 to replicate efficiently even when assayed only 2

283 Binding of EBNA-1 to the Q locus represses Qp constitutive activity

284 regulatory factor (IRF) family may regulate EBNA-1 transcription by targeting an essential cis-regul

285 attern of EBV gene expression, consisting of EBNA-1 transcription from the Qp promoter, in the absenc

286 We previously identified a promoter of EBNA-1 transcription, designated Fp, in early-passage Mu

287 vations of transcription from Fp to generate EBNA-1 transcripts can be attributed to lytic-cycle gene

288 lly indistinguishable from EBV Qp, and (iii) EBNA-1 transcripts identical in structure to EBV Qp-spec

289 EBNA-1 transgenic mice were generated with transgene exp

290 hat phosphorylation of the EBNA-1 protein or EBNA-1-truncated derivatives is not essential for pausin

291 maximally overlapping unique octapeptides of EBNA-1 were tested by modified ELISAs.

292 essing Epstein-Barr virus nuclear antigen 1 (EBNA-1) were stably transfected with a reporter plasmid

293 e a repetitive glycine and alanine domain of EBNA-1, were generated in the same way and found to immo

294 We found that EBNA-1, when bound to the FR, inhibits DNA unwinding in

295 Unlike EBNA-1, which activates transcription through binding of

296 omoters (C/Wp) are used for transcription of EBNA-1, which raises the question of how usage of these

297 pediatric SLE patient sera tested recognized EBNA-1, while sera from only 25 of 36 matched EBV-positi

298 The replacement of 60% of EBNA-1 with cell protein is a significant step toward el

299 We have also identified one derivative of EBNA-1 with only two of EBNA-1's three linking domains w

300 strategy to analyze the interactions of both EBNA-1 with viral episomes and viral episomes with host

301 omosomes, we identified the basic domains of EBNA-1 within amino acids 1-89 and 323-386 as critical f