ライフサイエンスコーパス: episome

1 ak repair, and impaired maintenance of an F' episome.

2 required for stable maintenance of the viral episome.

3 me persists as a multicopy, extrachromosomal episome.

4 ells maintained the viral DNA as a monomeric episome.

5 xpression and maintenance of the KSHV latent episome.

6 BNA1 expression and amplification of the EBV episome.

7 roducts facilitates maintenance of the viral episome.

8 nome is established as a double-stranded DNA episome.

9 content in keratinocytes that maintain viral episomes.

10 ence by manipulating levels of viral nuclear episomes.

11 on of mature NCs and increased viral nuclear episomes.

12 ls in a precancer cell line harboring HPV31b episomes.

13 erentiated keratinocytes that maintain viral episomes.

14 el results in the failure to establish viral episomes.

15 ized to concentrated dots in the presence of episomes.

16 endogenous Epstein-Barr virus (EBV) circular episomes.

17 fects the number and integrity of KSHV viral episomes.

18 long-term increases abrogated maintenance of episomes.

19 dels, infected cultures gradually lost viral episomes.

20 ates that directly transition to ds circular episomes.

21 riants of a prophage family as circular cp32 episomes.

22 isomal cDNAs are replaced by M184V-harboring episomes.

23 ing replication and segregation of the viral episomes.

24 sient and long-term maintenance of the viral episomes.

25 f the establishment and maintenance of HPV16 episomes.

26 a since HPV E6 stimulates the integration of episomes.

27 chromatin and the stable maintenance of BPV episomes.

28 ple copies of the KSHV genome in the form of episomes.

29 DNA replication and the persistence of viral episomes.

30 Transposition events into the target episome, accompanied by characteristic target site dupli

31 ls the prophage excises and replicates as an episome, allowing mutL to be expressed.

32 ch the viral genome (i) was maintained as an episome and (ii) expressed latency-associated, but not l

33 h the viral genome persisting as a multicopy episome and expressing only a small subset of viral gene

34 ne regulation through focal assembly of KSHV episomes and a molecular mechanism of late gene expressi

35 ch as B lymphocytes, gammaHVs exist as viral episomes and express few viral genes.

36 ed both for maintenance of the bacteriophage episomes and for transcriptional regulation of the cp32

37 The labile nature of viral episomes and hence their validity as surrogate markers o

38 Deep sequencing of the viral episomes and host chromosomes in iSLK.219 cells revealed

39 dentify genome-wide associations between EBV episomes and host chromosomes.

40 n showed sustained transgene expression from episomes and provided molecular evidence for long-term e

41 t to P. tricornutum centromeres can maintain episomes and recruit the diatom centromeric histone prot

42 The close proximity of EBV episomes and the super enhancers that are enriched for t

43 e broad-spectrum mutagenesis of chromosomes, episomes and viruses in vivo, and are applicable to both

44 e persists as a circular, histone-associated episome, and transcription of viral lytic cycle genes is

45 vities of the identical sequences assayed on episomes, and furthermore are correlated with different

46 romosomes during latency rather than forming episomes, and the integrated viral genome is capable of

47 sly published compound that destabilizes HPV episomes, aphidicolin was also found to markedly decreas

48 erapies via AAV-delivered F8 transgene in an episome are costly and nonpermanent.

49 ies showed that epigenetic marks on the KSHV episome are well organized, exemplified by the absence o

50 posi's sarcoma-associated herpesvirus (KSHV) episomes are coated with viral latency-associated nuclea

51 e molecular details, less is known about how episomes are established after de novo infection.

52 KSHV episomes are known to possess bivalent chromatin domains

53 However, little is known about where EBV episomes are located in interphase cells.

54 bsence of antibiotic selection and show that episomes are maintained as closed circles at copy number

55 These episomes are metabolically stable and support long-term

56 sarcoma-associated herpesvirus (KSHV) latent episomes are poised to be activated by the KSHV replicat

57 How KSHV episomes are prepared such that they maintain latent inf

58 quickly lost by segregation of latent viral episomes as spindle cells divide.

59 cell lines that stably maintain HPV 31 or 16 episomes, as well as cervical cancer lines that contain

60 To facilitate this, we have developed an episome-based assay to detect products of RAG-mediated t

61 NCL-K429 to support EBNA1 and oriP-mediated episome binding and maintenance, whereas the NCL C-termi

62 hort hairpin RNAs in cells that maintain HPV episomes blocked ATM induction and differentiation-depen

63 underwent significant reductions in the KSHV episome burden, LANA RNA and protein expression over tim

64 Transmitted Bogota probes formed episomes but did not integrate into the cellular genome.

65 , maintenance, and segregation of the latent episome, but the structural features of EBNA1 that confe

66 mutant E2(Y131A) genomes were established as episomes, but at a markedly lower copy number than that

67 apsidated into virions and transmitted as an episome by whiteflies.

68 The KSHV episome carries multiple reiterated copies of the termin

69 long the KSHV episome were examined by whole-episome ChIP analysis.

70 in endless configuration, consistent with an episome configuration.

71 Total cellular HIV-1 DNA and episomes containing two copies of the viral long termina

72 n boundary function, DNA loop formation, and episome copy number control during EBV latency.

73 We also observed that the EBV episome copy number was elevated in EBVDeltaCTCF166 and

74 knockdown of H2AX resulted in decreased KSHV episome copy number.

75 ction conditions was unable to maintain high episome copy numbers in epithelial cell lines.IMPORTANCE

76 protein (GFP) expression from TR-containing episomes deficient in DNA replication, consistent with a

77 edominantly as double-stranded (ds) circular episomes derived from input linear single-stranded virio

78 We report that PAN RNA promotes LANA-episome disassociation through an interaction with LANA

79 and it formed minichromosomes as HBV cccDNA episome DNA does when it was transfected into human hepa

80 ntrast, maintenance of previously methylated episomes does not require Lsh, implying a functional rol

81 n and maintenance of the human herpesvirus-8 episome during latency can be disrupted by glycyrrhizic

82 viral protein required to maintain the viral episome during latency.

83 posi's sarcoma-associated herpesvirus (KSHV) episome during latent infection and found a striking col

84 genome is maintained as an extrachromosomal episome during latent infection of B lymphocytes.

85 centromeric proteins for persistence of KSHV episomes during cell division.

86 enance, replication, and segregation of KSHV episomes during mitosis, which makes LANA an ideal targe

87 In contrast, LANA rapidly disassociates from episomes during reactivation.

88 acilitates LANA sequestration away from KSHV episomes during reactivation.

89 also important for the maintenance of viral episomes during the differentiation-dependent productive

90 s as most maintain their genomes as circular episomes during the quiescent stage of infection.

91 Escherichia coli OmpP is an F episome-encoded outer membrane protease that exhibits 71

92 CLs) that carry EBV DNA as extra-chromosomal episomes, express 9 latency-associated EBV proteins, and

93 These episomes expressed transgenes, were stable, and became p

94 hanges in the physical distribution of these episomes following stimulation.

95 These episomes form the molecular basis for viral latency and

96 HCF1 depletion resulted in the loss of EBV episomes from Burkitt's lymphoma cells with type I laten

97 DNA replication and caused the loss of KSHV episomes from latently infected PEL cells.

98 Analysis of episomes from productive cells indicates a propensity to

99 ytic transcription, which only a fraction of episomes had.

100 f a 3,008,626-bp chromosome and an 18,019-bp episome, has been determined and exhibits considerable d

101 Together, our results also indicate that HPV episomes have a stability profile that is remarkably sim

102 s to form a minichromosome also known as an "episome." Histones, which are core components of chromat

103 pesvirus (KSHV) persists as a latent nuclear episome in dividing host cells.

104 herpesvirus (KSHV) is maintained as a stable episome in latently infected pleural effusion lymphoma (

105 mTR-associated DNA persisted as an episome in latently MHV68-infected tumor cells, demonstr

106 g both mLANA and mTRs in cis persisted as an episome in murine A20 or MEF cells.

107 on, authentic LANA binding sites on the KSHV episome in naturally infected cells were identified usin

108 lished, due to failure to maintain the viral episome in proliferating B cells.

109 Persistence of the viral episome in proliferating tumor cells requires the intera

110 rovide considerable genetic stability to the episome in replicating cells while avoiding insertional

111 uclear antigen-1 (EBNA1) maintains the viral episome in replicating infected human B cells, and EBNA1

112 In contrast, mTR DNA never persisted as an episome in the absence of mLANA.

113 ection by persisting as an extra-chromosomal episome in the infected cells and by maintaining its gen

114 h stable latent infection as a chromatinized episome in the nucleus of infected cells.

115 /or maintenance of an extrachromosomal viral episome in vivo, which is likely required for the reacti

116 We find that EBV episomes in Burkitt's lymphoma cells preferentially asso

117 NuMA is required for persistence of the KSHV episomes in daughter cells.

118 positional enhancer blocker on chromatinized episomes in human cells, blocking the HS2 enhancer of th

119 DNA regions by using patch-methylated stable episomes in human cells.

120 ent infections that maintain low-copy-number episomes in infected basal cells.

121 ma-associated herpesvirus (KSHV) persists as episomes in infected cells by circularizing at the termi

122 his mutation were unable to establish stable episomes in keratinocytes.

123 lete loss of the closed-circular form of EBV episomes in latently infected B lymphocytes.

124 posi's sarcoma-associated herpesvirus (KSHV) episomes in latently infected cells is dependent on the

125 antigen (LANA) mediates persistence of viral episomes in latently infected cells.

126 ve splenocytes revealed the absence of viral episomes in mLANA-null infected mice, suggesting that th

127 well as Y102E were not maintained as stable episomes in murine C127 cells.

128 4 interaction fails to efficiently establish episomes in primary human keratinocytes.

129 essential for efficient maintenance of KSHV episomes in the host.

130 reatment with PhenDC3 showed a loss of viral episomes in the infected cells.

131 e common property of persisting as multicopy episomes in the nuclei of rapidly dividing host cells.

132 e assembly of RNA polymerase II around viral episomes in the nucleus may be a previously unexplored a

133 shes latent infection as chromatin-assembled episomes in which all but a few viral genes are transcri

134 This episome includes two elements from EBV: an EBV nuclear a

135 depletion in cell lines that maintain HPV-31 episomes increased viral copy number.

136 Herpesvirus genomes exist and replicate as episomes inside the host cell nucleus during latent infe

137 An assay to detect transposition from an episome into the human genome failed to detect bona fide

138 Transfection of the episome into unstimulated white blood cells showed that

139 on and is responsible for partitioning viral episomes into daughter cells during cell division.

140 To segregate the episomes into daughter cells during mitosis, they are te

141 After removal of the episome, iPS cells completely free of vector and transge

142 Moreover, the HVS episome is able to persist and provide prolonged transge

143 The Epstein-Barr virus (EBV) episome is known to interact with the three-dimensional

144 This episome is tethered to host chromatin to ensure proper s

145 inhibition of ATM proteins had no effect on episome levels, but ATM knockdown by siRNA significantly

146 idicolin was also found to markedly decrease episome levels, but via a different pathway from that of

147 ATM knockdown by siRNA significantly reduced episome levels, suggesting that ATM proteins are playing

148 hibitors of Chk2 and DNA-PK had no effect on episome levels.

149 se results outline two pathways that trigger episome loss from cells and suggest the existence of a l

150 1 (EBNA1) binds to FR and DS to promote EBV episome maintenance and DNA replication during latent in

151 have demonstrated that LANA is important for episome maintenance and replication of the TR-containing

152 repeat sequences that is important for viral episome maintenance and the regulation of cellular and v

153 risingly critical role for NCL K429 in EBNA1 episome maintenance and transcription, which may be a ta

154 Overall, the reductions in episome maintenance closely correlated with DNA replicat

155 rotein required for viral origin binding and episome maintenance during latency.

156 ontribute to the epigenetic control of viral episome maintenance during latency.

157 s in BET protein binding were independent of episome maintenance function.

158 ted herpesvirus (KSHV) is required for viral episome maintenance in host cells during latent infectio

159 Episome maintenance is conferred by the binding of the K

160 ted origin of plasmid replication (oriP) DNA episome maintenance is essential for EBV-mediated tumori

161 intenance requires a dedicated virus-encoded episome maintenance protein (EMP), namely LANA (KSHV), E

162 It is believed that the expression of episome maintenance proteins is turned off in the predom

163 For these viruses, episome maintenance requires a dedicated virus-encoded e

164 Episome maintenance requires epigenetic programming to e

165 We propose that KSHV episome maintenance requires Tim-assisted replication fo

166 was expressed from its native promoters, and episome maintenance was more efficient with higher mLANA

167 fects on EBNA1-dependent DNA replication and episome maintenance with OriP.

168 dynamic genetic element that confers stable episome maintenance, DNA replication initiation, and chr

169 clear antigen 1 (EBNA1) is essential for EBV episome maintenance, replication, and transcription.

170 sed numbers of mTRs conferred more efficient episome maintenance, since DNA containing mLANA and eigh

171 were deficient for LANA DNA replication and episome maintenance.

172 nd provided molecular evidence for long-term episome maintenance.

173 l LANA sequences results in highly deficient episome maintenance.

174 erminal repeat (TR) elements to mediate KSHV episome maintenance.

175 can serve as a cis-acting element for MHV68 episome maintenance.

176 raction of E2 with Brd4 contributes to viral episome maintenance.

177 A sequence renders LANA highly deficient for episome maintenance.

178 egation of TR DNA to daughter cells, but not episome maintenance.

179 ion of this upstream sequence did not reduce episome maintenance.

180 irus-host interaction is essential for viral episome maintenance.

181 n DNA replication, and pronounced defects in episome maintenance.

182 iption, as well as viral DNA replication and episome maintenance.

183 al transcription, histone modifications, and episome maintenance.

184 modification, transcription regulation, and episome maintenance.

185 HPV-16 E2 expressed from intact episomes may act in trans to regulate integrated genome

186 Our data thus suggest that episome-mediated reprogramming is not inherently mutagen

187 DNA regions by using patch-methylated stable episomes (minichromosomes) in human cells.

188 ously reported that RacPyV exists only as an episome (nonintegrated) in neuroglial tumors.

189 t to B cells, where amplification of the EBV episome occurred even with a replication-defective BZLF1

190 Third, mutation at a second locus on the episome occurs even when the lac allele under selection

191 The 2-micron circle broadly resembles the episomes of certain mammalian viruses in its chromosome-

192 vity, we isolated single-cell clones bearing episomes of distinct TR numbers (6TR to 12TR) from epith

193 strong colocalization with LANA and the KSHV episomes on host mitotic chromosomes.

194 ed an Spn1(+) mutant that does not become an episome or express phage genes.

195 enetic element, pLP45, which can exist as an episome or integrated in the bacterial chromosome.

196 mutagenized sequences introduced in trans on episomes or via random or "safe-harbour" integration fai

197 ey role in LANA-mediated DNA replication and episome persistence and may act through a host cell part

198 The two essential components of episome persistence are DNA replication prior to cell di

199 The two central components of episome persistence are DNA replication with each cell d

200 t (TR) DNA to mitotic chromosomes to mediate episome persistence in dividing cells.

201 is a 1,162-amino-acid protein that mediates episome persistence of viral genomes.

202 diately downstream were highly deficient for episome persistence yet maintained the ability to replic

203 All mutants were deficient in episome persistence, and the deficiencies ranged from mi

204 A-mediated DNA replication, segregation, and episome persistence, likely through interactions with ke

205 gate TR DNA, the two principal components of episome persistence, suggesting another role for the res

206 and carboxy-terminal LANA are essential for episome persistence, they are not sufficient, since dele

207 role of the positive patch in LANA-mediated episome persistence.

208 replication defects account for the reduced episome persistence.

209 nuclear antigen (LANA), which mediates viral episome persistence.

210 C-terminal regions of LANA are essential for episome persistence.

211 pendent internal LANA regions for effects on episome persistence.

212 oles of mLANA and MHV68 TR (mTR) elements in episome persistence.

213 ent with the possibility that mLANA mediates episome persistence.

214 mLANA acts on mTR elements to mediate MHV68 episome persistence.

215 ability to mediate both short- and long-term episome persistence.

216 ral terminal repeat (TR) DNA to mediate KSHV episome persistence.

217 importance of the internal LANA sequence for episome persistence.

218 romosomes, and this binding is essential for episome persistence.

219 id not reduce LANA chromosome association or episome persistence.

220 reduced both LANA chromosome association and episome persistence.

221 t (TR) DNA to mitotic chromosomes to mediate episome persistence.

222 tely downstream resulted in highly deficient episome persistence.

223 s did not disrupt mLANA's ability to mediate episome persistence.

224 a critical effect on its ability to maintain episomes, possibly through effects on TR DNA replication

225 ular anchors for non-integrating lentivector episomes, providing sustained gene expression through su

226 n of Deltahgprt/Deltaxprt cells with an APRT episome recapitulated the suppressor phenotype in vitro

227 plication stress, the integrity of the viral episomes remained unaltered.IMPORTANCE DNA viruses have

228 alysis of cis elements within TR that confer episome replication and partitioning revealed that these

229 a yeast-derived sequence that enables stable episome replication in these diatoms even in the absence

230 error prone repair does not render the viral episome replication incompetent: our model predicts that

231 into keratinocytes that stably maintain HPV episomes resulted in short-term elevation of HPV genome

232 ordingly, we show that the presence of an F' episome results in increased resistance to the antimicro

233 o persist in the nucleus as extrachromosomal episomes, revealing a potential mechanism for organellar

234 r analysis supports interactions between EBV episome(s) and active regions of the human genome in lym

235 ied 15,000 reproducible contacts between EBV episome(s) and the human genome.

236 o precisely map the contacts between the EBV episome(s) and the human host genome.

237 the internal repeat elements contributes to episome segregation and persistence.

238 internal repeat elements that contributes to episome segregation and persistence.

239 djacent LANA sequence with distinct roles in episome segregation and persistence.

240 adjacent LANA regions with distinct roles in episome segregation and persistence.IMPORTANCE KSHV LANA

241 e DNA replication prior to cell division and episome segregation to daughter nuclei.

242 n DNA replication, consistent with a role in episome segregation; this region did not independently a

243 ) treatment, which is known to eliminate EBV episomes, shifted EBV replication to earlier times in th

244 long mitotic chromosomes in cells containing episomes, similar to LANA.

245 ffusion lymphoma (PEL) cells disrupted viral episome stability and abrogated sub-G1/G1 arrest of the

246 pose that the TRF2-HDAC complex enhances EBV episome stability by providing a checkpoint that delays

247 f plasmid replication (OriP) is required for episome stability during latent infection.

248 roteins are playing an important role in HPV episome stability that does not require kinase activity.

249 hese pathways play a role in maintaining HPV episome stability.

250 , and furthermore, both events contribute to episome stability.

251 for genome amplification and maintenance of episomes, suggesting an important role for this activity

252 d (ATR) pathways significantly reduced viral episomes, suggesting that these pathways play a role in

253 ocalization between Bub1, LANA, and the KSHV episome tethered to the host chromosome using fluorescen

254 latently infected cells as extrachromosomal episomes that attach to host chromosomes through the tet

255 uli within a single reactivating cell; those episomes that did respond to stimulation, aggregated wit

256 as high-copy-number, circular, nonintegrated episomes that segregate to progeny cells upon division.

257 However, those episomes that were being transcribed would spontaneously

258 for segregation and maintenance of the KSHV episomes through a temporally controlled mechanism of bi

259 to persistent circular and concatemeric DNA episomes through intramolecular and intermolecular recom

260 acts via replicating and tethering the virus episome to the host chromatin and exerts other functions

261 LANA is required for tethering of the KSHV episome to the host chromosomes and efficiently segregat

262 spots in the nucleus, where it tethers viral episomes to cellular chromatin and interacts with nuclea

263 Additionally, LANA tethers episomes to chromosomes via interactions with histones H

264 binding functions necessary for segregating episomes to daughter nuclei, the mutants were highly def

265 ic chromosomes to mediate the segregation of episomes to daughter nuclei.

266 rminal repeat (TR) DNA and tethers the viral episomes to host chromosomes through the association of

267 This process tethers the viral episomes to host chromosomes.

268 data and our 4C-seq experiments position EBV episomes to host genomes with active epigenetic marks.

269 ociated nuclear antigen (LANA) tethers viral episomes to host heterochromatin and displays a punctate

270 omavirus E2 protein, which tethers the viral episomes to host mitotic chromosomes, we examined whethe

271 on, N- and C-terminal regions of LANA tether episomes to mitotic chromosomes to segregate episomes to

272 these functions by tethering papillomavirus episomes to mitotic chromosomes; however, the mechanism

273 he term "stability" refers to the ability of episomes to persist with little copy number variation in

274 episomes to mitotic chromosomes to segregate episomes to progeny cell nuclei.

275 (KSHV) is critical for segregation of viral episomes to progeny nuclei and allows for maintenance of

276 mediates KSHV DNA replication and segregates episomes to progeny nuclei.

277 ogeneity in the responses of individual KSHV episomes to stimuli within a single reactivating cell; t

278 proach is highly efficient at delivering EBV episomes to target cells in vivo.

279 s are maintained by EBNA1, which tethers EBV episomes to the host chromosomes during mitosis.

280 have been implicated in tethering LANA/viral episomes to the host mitotic chromosomes, and LANA chrom

281 tical for the perpetual segregation of viral episomes to the progeny nuclei of newly divided cells.

282 mRNA transfer (RMT), and retrovirus-mediated episome transfer (RET) represent powerful methodologies

283 ulation for regulatory sequences residing in episomes versus chromosomes remain almost completely unk

284 the terminal repeat (TR) region of the viral episome via adjacent LANA binding sites (LBS), but the m

285 NA persists in latently infected cells as an episome via tethering to the host chromosomes.

286 titative PCR analysis confirmed that the EBV episome was stable at approximately 30 copies per cell f

287 erences of H2AX and gammaH2AX along the KSHV episome were examined by whole-episome ChIP analysis.

288 introduced into human cells on an SV40-based episome were invariably repaired, this process induced m

289 SEGS-2 episomes were also found in virions and whiteflies.

290 me, two endothelial cell lines in which KSHV episomes were maintained indefinitely in the absence of

291 the single-cell level, we found that not all episomes were uniformly transcribed following reactivati

292 ntly infected cells carry a circularized EBV episome where the origin of replication (oriP) is compri

293 leus to maintain the viral genome as nuclear episomes, which are the basis for virus persistence.

294 at reporter assays are mainly implemented on episomes, which are thought to lack physiological chroma

295 MB infection as an integrated copy and/or an episome, while SEGS-2 was originally from the cassava ge

296 that stably maintain complete HPV genomes as episomes, while low levels are seen in cells that expres

297 colonies, and the genomes were maintained as episomes, while those infected with Y138E quasiviruses d

298 ) establishes latent infections as multicopy episomes with complex patterns of viral gene transcripti

299 was not disrupted, but parasites containing episomes with the tgdhfr selection cassette were retriev

300 l genome is maintained as an extrachomosomal episome, with stable maintenance in dividing cells media