ライフサイエンスコーパス: episome

1 ells maintained the viral DNA as a monomeric episome.

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

3 xpression and maintenance of the KSHV latent episome.

4 BNA1 expression and amplification of the EBV episome.

5 roducts facilitates maintenance of the viral episome.

6 replace those that have segregated the viral episome.

7 ions, or by complementation with an arginase episome.

8 missive chromatin domain in the HSV-1 latent episome.

9 ecessary and sufficient to maintain the KSHV episome.

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

11 required for stable maintenance of the viral episome.

12 erentiated keratinocytes that maintain viral episomes.

13 el results in the failure to establish viral episomes.

14 ized to concentrated dots in the presence of episomes.

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

16 long-term increases abrogated maintenance of episomes.

17 a since HPV E6 stimulates the integration of episomes.

18 dels, infected cultures gradually lost viral episomes.

19 ates that directly transition to ds circular episomes.

20 riants of a prophage family as circular cp32 episomes.

21 chromatin and the stable maintenance of BPV episomes.

22 isomal cDNAs are replaced by M184V-harboring episomes.

23 nction with cells that stably maintain HPV31 episomes.

24 cle by facilitating the maintenance of viral episomes.

25 nd expresses genes from high copy number DNA episomes.

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

27 f the establishment and maintenance of HPV16 episomes.

28 DNA replication and the persistence of viral episomes.

29 ence by manipulating levels of viral nuclear episomes.

30 on of mature NCs and increased viral nuclear episomes.

31 ls in a precancer cell line harboring HPV31b episomes.

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

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

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

35 into B cells, the virus is maintained as an episome and can establish and maintain latency over the

36 mutant LacZ reporter gene, residing in both episome and chromosome.

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

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

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

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

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

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

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

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

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

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

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

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

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

54 These episomes are metabolically stable and support long-term

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

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

57 Epstein-Barr virus (EBV) episomes are stably maintained in permissive proliferati

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 g the E4M9 mutant genomes were maintained as episomes at copy numbers similar to those in keratinocyt

61 thelial cells, HPV genomes are maintained as episomes at low copy number.

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

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

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

65 ation was targeted specifically to the phage episome but not the phage provirus or the host chromosom

66 nsfection, mutant genomes were maintained as episomes but at significantly reduced levels than in cel

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

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

69 through tissue culture, along with the viral episome, but was not retained through meiosis.

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

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

72 omologous DNA sequences localized in nuclear episomes can modulate the expression of active chromosom

73 The KSHV episome carries multiple reiterated copies of the termin

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

75 in endless configuration, consistent with an episome configuration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 acilitates LANA sequestration away from KSHV episomes during reactivation.

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

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

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

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

96 The resulting circular EBV episomes expressed a transgene and contained the EBV-der

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

98 at contains all of the sequences for the EBV episome flanked by loxP sites.

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

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

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

102 Analysis of episomes from productive cells indicates a propensity to

103 Cells with a high numbers of viral episomes (>20/cell) were predominantly Ig null, and cell

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

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

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

107 s, the cis and trans elements encoded by the episomes have been effectively defined but the chromosom

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

109 arly necessary for the stable maintenance of episomes, HPV type 11 (HPV-11) genomes that contained tr

110 HPV16 genome replicated and persisted as an episome in cervical keratinocytes.

111 n, and persistence of the viral genome as an episome in differentiated epithelial cells.

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

113 species, and the viral genome persists as an episome in infected cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 tion, AAV DNA can persist mainly as circular episomes in human tissues.

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

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

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

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

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

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

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

136 AAV DNA existed as circular double-stranded episomes in our tissues.

137 4 interaction fails to efficiently establish episomes in primary human keratinocytes.

138 mitotic chromosomes for persistence of viral episomes in PV-infected cells.

139 -based model system to study the role of DNA episomes in reduction of yeast life span.

140 s and is critical for the maintenance of EBV episomes in the infected cells.

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

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

143 To achieve quantitative delivery of EBV episomes in vitro and in vivo, we developed a binary hel

144 Successful delivery of EBV episomes in vivo was demonstrated in the liver of transg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 Episome maintenance is conferred by the binding of the K

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

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

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

172 be important for the establishment of latent episome maintenance through tethering of the viral genom

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

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

175 n that plays roles in viral DNA replication, episome maintenance, and transcriptional regulation.

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

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

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

179 l LANA sequences results in highly deficient episome maintenance.

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

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

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

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

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

185 small subpopulation being capable of stable episome maintenance.

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

187 al transcription, histone modifications, and episome maintenance.

188 modification, transcription regulation, and episome maintenance.

189 were deficient for LANA DNA replication and episome maintenance.

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

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

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

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

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

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

196 of wild-type episomes with M184V-containing episomes occurred while proviruses remained wild type.

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

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

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

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

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

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

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

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

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

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

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

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

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

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 KSHV terminal repeat DNA mediates multicopy episome persistence.

223 ciation, LANA1-mediated DNA replication, and episome persistence.

224 s partially deficient in DNA replication and episome persistence.

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

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

227 replication defects account for the reduced episome persistence.

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

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

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

231 rpesvirus genome is maintained as a circular episome, replicating in synchrony with host chromosomes.

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

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

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

235 s of replication per cell cycle and prevents episome replication.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 irst 22 amino acids, which are necessary for episome tethering, does not affect nuclear localization

253 features of the translocation process on an episome that propagates in human cells.

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

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

256 However, those episomes that were being transcribed would spontaneously

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

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

259 LANA tethers the viral episome to the host chromosome, thus ensuring efficient

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

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

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

263 Previous studies showed the ability of EBV episomes to confer long-term transgene expression and co

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

288 In the absence of selection, EBV episomes were lost at a rate of 8 to 10% per cell divisi

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

290 antly Ig null, and cells with low numbers of episomes were predominantly sIgM positive.

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

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

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

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

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

296 romosomes, to block association of the viral episomes with Brd4, and to inhibit BPV-1 DNA-mediated ce

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

298 rtantly, a complete replacement of wild-type episomes with M184V-containing episomes occurred while p

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