ライフサイエンスコーパス: LTR

1 LTR retrotransposons are mobile elements that are able,

2 LTR retrotransposons are repetitive DNA elements compris

3 LTR were prospectively enrolled (N = 130) between Januar

4 LTRs mismatched for CMV (donor(+)/recipient(-); D(+)R(-)

5 ssion rate was 30.6% among a total of 25,054 LTRs.

6 to target a 34-bp sequence within the HIV-1 LTR (loxLTR).

7 tment, potentially due to intermittent HIV-1 LTR activation.

8 revealed that HspBP1 was recruited on HIV-1 LTR at NF-kappaB enhancer region (kappaB sites).

9 in U87MG cells stably integrated with HIV-1 LTR luciferase reporter.

10 tions, in this work for the first time HIV-1 LTR model featuring repressed, intermediate, and activat

11 REV-ERB synthetic agonists to inhibit HIV-1 LTR promoter activity and viral replication, supporting

12 leased in order for it to activate the HIV-1 LTR promoter and facilitate HIV-1 viral replication in t

13 n production and enhanced Tat-mediated HIV-1 LTR promoter transactivation, along with stabilization o

14 nduced depletion of HDAC1 and 3 on the HIV-1 LTR that was associated with hyperacetylation of histone

15 dolysosome pH, as well as Tat-mediated HIV-1 LTR transactivation in U87MG cells stably integrated wit

16 the effects of ML-SA1 on Tat-mediated HIV-1 LTR transactivation were blocked using pharmacological i

17 olysosomes and restricted Tat-mediated HIV-1 LTR transactivation.

18 he amount of Tat available to activate HIV-1 LTR, we hypothesize that acidifying endolysosomes may en

19 d that the host protein Naf1 inhibited HIV-1 LTR-driven transcription of HIV genes and contributed to

20 at histone H3K27 and H3R26 orchestrate HIV-1 LTR-mediated transcription, and potentially opens a new

21 th hyperacetylation of histones on the HIV-1 LTR.

22 d not to YY1 DNA-binding sites in the HTLV-1 LTR but to the R region.

23 effective at cleaving patient-derived HIV-1 LTRs from five patients.

24 ccurately predicted TOL vs. non-TOL in 12/14 LTR.

25 rately predicted TOL versus non-TOL in 12/14 LTRs before weaning.

26 orilla-specific integrations, including 31 2-LTR proviruses.

27 of additional control conditions, such as 2-LTR quantification and the addition of reverse transcrip

28 levels of episomal HIV DNA (as measured by 2-LTR circles) and decreases the levels of HIV transcripti

29 Total and integrated HIV DNA, 2-LTR circles, and cell-associated unspliced HIV RNA were

30 ci that include approximately full-length (2-LTR) and solo-LTR alleles in addition to the unoccupied

31 1 nuclear entry evidenced by inhibition of 2-LTR but not linear forms of viral DNA.

32 An increase in 2-long-terminal-repeat (2-LTR) circles in the depleted FACT complex cell line indi

33 Several 2-LTR insertions have intact reading frames in some or all

34 and circular DNA fragments containing the 2-LTR palindrome junction can be efficiently cleaved in vi

35 dividual loci identified three new unfixed 2-LTR proviruses within our set, including an intact provi

36 ere with antisense transcription from the 3' LTR and vice versa, even with strong transcription emana

37 By combining 5'LTR-to-3'LTR single-genome amplification and direct amplicon sequ

38 g the DNA sequence of nucleosome A of the 3'-LTR of the mouse mammary tumor virus (147 bp MMTV-A).

39 We saw active 5' LTR use in tumorigenic cells only, suggesting that the c

40 o oscillate, than the constitutive MoMuLV 5' LTR (MMLV) promoter (0/25).

41 no evidence to suggest that these active 5' LTRs were influencing nearby host gene expression.

42 By combining 5'LTR-to-3'LTR single-genome amplification and direct ampl

43 d by ELISA in BALF and serum samples from 60 LTRs.

44 8 BALF levels were significantly higher in 8 LTRs who additionally developed HCMV disease, as compare

45 In mouse, we identified more than 800 LTRs from ORR1, MT, MT2, and MLT families, which resembl

46 ed in cis to stabilize assembly of the ERV-9 LTR enhancer complex and facilitate long-range LTR enhan

47 a single copy of the primate-specific ERV-9 LTR in the 100 kb human beta-globin gene locus.

48 cribed from many of the 4000 copies of ERV-9 LTR retrotransposons acted by a similar cis mechanism to

49 rying approximately 4000 copies of the ERV-9 LTRs and in transgenic mouse erythroblasts carrying a si

50 uring repressed, intermediate, and activated LTR states is integrated with generation of long (env) a

51 ) revealed a comprehensive catalog of active LTR retrotransposons without the need for mapping transp

52 We included all LTRs who survived beyond the first year and followed the

53 A retrospective study including all LTRs at Duke Hospital during January 2013-May 2017 with

54 The other is an LTR/Gypsy transposable element family member, which gene

55 TA-AM attenuated Tat endolysosome escape and LTR transactivation.

56 TPCs) attenuated Tat endolysosome escape and LTR transactivation.

57 corresponding to integrated viral genes and LTR retrotransposons, but not to DNA transposons, are de

58 polyadenylation revealed that LTR/Gypsy and LTR/Copia were two major transposable elements within th

59 Together, endogenous retroviruses and LTR retrotransposons represent major components of anima

60 n, which is conserved among retroviruses and LTR-retrotransposons.

61 oss-reactions between lentiviral vectors and LTR genomes targeted in the HIV-1 NAAT caused the HIV-1

62 non-essential protein coding genes, rDNA and LTRs.

63 In Arabidopsis, LTR retrotransposons are activated by mutations in the c

64 by ten-eleven translocation (TET) enzymes at LTR regions of ERVs, because vitamin C acts as a cofacto

65 lso increases the local level of H3K36me3 at LTR.

66 The amplification of athila LTR-retrotransposons, members of the gypsy superfamily,

67 n miniature (TRIMs) are small non-autonomous LTR retrotransposons consisting of two terminal direct r

68 ature assembled capsids is conserved between LTR retrotransposons and retroviruses.

69 IN removes two 3'-nucleotides from both LTR ends and catalyses strand transfer of the recessed 3

70 We found that both LTR retrotransposons and endogenous viral elements are s

71 py numbers of NLRs were greatly increased by LTR-retrotransposon-mediated retroduplication.

72 In addition to canonical LTR-RTs with 5'-TG...CA-3' termini, LTR_retriever also i

73 During the study period, 350 consecutive LTRs underwent 1078 bronchoscopies.

74 psis (Arabidopsis thaliana), the constructed LTR library showed excellent sensitivity and specificity

75 gans and related Caenorhabditis spp. contain LTR retrotransposons and, as described here, numerous in

76 by retroviruses such as HIV-1, and controls LTR/non-LTR retrotransposition in marsupials.

77 In silico, D-LTR-P4-227913 (package of the top 4 gRNAs) accounted for

78 Furthermore, the D-LTR-P4-227913 was predicted to cleave a median of 96.1%

79 are produced by transposition of a defective LTR retrotransposon that we have termed dRemp (defective

80 of two or more parental genes, demonstrating LTR-retroposition as a novel mechanism of exon shuffling

81 and CD4(+)T-bet(+) induction differentiated LTR controllers from early viremic relapsers, correlatin

82 is even higher, because we show that dormant LTR promoter activity can rescue loss of an essential up

83 3K9me3 levels and derepression of endogenous LTR- and LINE-repetitive DNA elements during differentia

84 Our work indicates that enFeLV-LTR elements negatively correlate with exogenous FeLV re

85 eLV restriction was highly related to enFeLV-LTR copy number.

86 ent and identifies an integral role for ERVK LTR repetitive elements.

87 Transcribed ERVK LTRs are CpG-rich and located in close proximity to gene

88 ERVL LTRs thus offer means for a comprehensive survey of the

89 Altogether, ERVL LTRs provide molecular mechanisms for stochastically sca

90 gesting that this effect is specific to FeLV-LTR elements.

91 steady, and long-term amplification of a few LTR retrotransposon families.

92 One hundred five LTRs (75% of survivors) were assessed (M = 3.9 years pos

93 mmediately cotranscribed with their flanking LTR retrotransposons.

94 As expected, the greatest improvement is for LTR retroelements.

95 le progression into mitosis are required for LTR-mediated viral expression, suggesting that the evolu

96 Here, we uncover an unusual family of giant LTR retrotransposons from the Solanum clade, named MESSI

97 o large loci (>50 kbp) characterized by high LTR density.

98 anism encompassing NFkappaB/SP1-mediated HIV LTR activation.

99 e transfected with different variants of HIV LTR promoters and then exposed to METH.

100 NFkappaB/SP1-dependent activation of the HIV LTR and with the subsequent alterations of NPC neurogene

101 induced transcriptional activity of the HIV LTR promotor, an effect that required both NFkappaB and

102 a repressive chromatin structure at the HIV LTR.

103 omes suggested that developed NF reduced HIV-LTR expression significantly in comparison to unbound Ca

104 However, LTR sequences are disproportionately present in human lo

105 Many of these proviruses have identical LTRs, and are insertionally polymorphic, consistent with

106 mulation of mutations in initially identical LTRs.

107 ading-empowered Perl program that identifies LTR-RTs and generates high-quality LTR libraries from ge

108 e successfully used programs for identifying LTRs and non-LTR retrotransposons in eukaryotic genome s

109 Importantly, LTR-driven transcription was restricted to tumorigenic c

110 predictor of future cardiovascular events in LTR, which can be incorporated in clinical practice to a

111 f operational tolerance could be observed in LTR withdrawn from SRL and if blood/graft tolerance biom

112 CMV promoter, suggesting a role of SSRP1 in LTR-driven gene expression but not in viral DNA integrat

113 S withdrawal directly from mTOR-I therapy in LTR and achieved >50% operational tolerance.

114 and assessed CMV-specific T-cell immunity in LTRs at high risk for CMV events, using flow cytometry a

115 cant predictor of calendar year mortality in LTRs.

116 f operational tolerance could be observed in LTRs withdrawn from SRL and if blood/graft tolerance bio

117 s a safe alternative to inhaled ribavirin in LTRs.

118 S withdrawal directly from mTOR-I therapy in LTRs and achieved > 50% operational tolerance.

119 d inhaled RBV appear to be well tolerated in LTRs, and our data support the use of oral RBV as a safe

120 in (RBV) has been used to treat RSV-infected LTRs with limited data.

121 fers a unique target to specifically inhibit LTR-retrotransposons, and tRF-targeting is a potentially

122 e maintenance of HIV-1 latency by inhibiting LTR-driven HIV-1 gene transcription in a nuclear factor

123 us estimate, and revealed a high Solo:Intact LTR ratio of 8.2.

124 ogeny population of chromosomally integrated LTR retrotransposons consisting of pairwise recombinatio

125 em dRemp repeats containing several internal LTRs, suggestive of extensive recombination during retro

126 Here, we investigated LTRs with intrapulmonary HCMV replication for the chemok

127 h prevalence of relapsing CMV viremia in IPF-LTRs compared with non-IPF-LTRs (69% vs. 31%; odds ratio

128 The short telomere defect in IPF-LTRs was associated with significantly impaired CMV-spec

129 MV viremia in IPF-LTRs compared with non-IPF-LTRs (69% vs. 31%; odds ratio, 4.98; 95% confidence inte

130 ed IPF-LTRs (n = 42) and age-matched non-IPF-LTRs (n = 42) and assessed CMV outcomes.

131 We studied IPF-LTRs (n = 42) and age-matched non-IPF-LTRs (n = 42) and

132 Within this subset, IPF-LTRs who had short telomeres had the highest risk of CMV

133 ry young (~530,000 years) cis-acting 2.25-kb LTR retrotransposon insertion reducing expression of the

134 e insulator was inserted into the lentiviral LTR.

135 Exemplified in melanoma, LTR-overlapping transcripts were highly predictable, dis

136 ruits LSD1/HDAC corepressor complex to MERVL LTR for transcriptional repression.

137 mmary tumor virus long terminal repeat (MMTV-LTR).

138 acted by a similar cis mechanism to modulate LTR enhancer function in activating transcription of dow

139 ing gene evolution-D6Ertd527e-in which an MT LTR provided a promoter and the 5' exon with a functiona

140 Surprisingly, the mutagenic LTR retrotransposons differed in the active lines, sugge

141 Unlike the mutagenic LTR retrotransposons identified previously, dRemp is pre

142 y used programs for identifying LTRs and non-LTR retrotransposons in eukaryotic genome sequences.

143 minal repeat (LTR) retrotransposons, and non-LTR retrotransposons, including long interspersed nuclea

144 rspersed Elements (LINEs), also known as non-LTR retrotransposons, encode a multifunctional protein t

145 rspersed element 1 (L1) is an autonomous non-LTR retroelement that is active in mammalian genomes.

146 LINE-1 (or L1) is an autonomous non-LTR retrotransposon in the human genome, comprising 17%

147 or many related bacterial and eukaryotic non-LTR retroelement RTs.

148 oviruses such as HIV-1, and controls LTR/non-LTR retrotransposition in marsupials.

149 s type 1 (HIV-1) and the mobility of LTR/non-LTR retrotransposons.

150 n-long terminal repeat (LTR) and MGEScan-non-LTR are successfully used programs for identifying LTRs

151 , and harbors features characteristic of non-LTR retrotransposons.

152 g activity of group II intron- and other non-LTR retroelement-encoded RTs, as well as the optimizatio

153 ded by mobile group II introns and other non-LTR retroelements differ from retroviral RTs in being ab

154 , LTR_retriever also identifies noncanonical LTR-RTs (non-TGCA), which have been largely ignored in g

155 The majority of noncanonical LTRs are Copia elements, with which the LTR is four time

156 We identified seven types of noncanonical LTRs from 42 out of 50 plant genomes.

157 otherapy withdrawal in nonimmune, nonviremic LTRs > 3 years post-LT.

158 Notably, LTRs nearby ISGs are derepressed likely rendering these

159 pression in NF-kappaB mediated activation of LTR-driven gene-expression.

160 models have been explored in the context of LTR-protein interactions, in this work for the first tim

161 The identification of LTR-RTs is critical for achieving high-quality gene anno

162 developed for the de novo identification of LTR-RTs; however, these programs are associated with low

163 ell is a critical component for induction of LTR promoter activity.

164 NA-seq provides a comprehensive landscape of LTR retrotransposons and their control at transcriptiona

165 h the positions and the degradation level of LTR retrotransposons copies.

166 ncy virus type 1 (HIV-1) and the mobility of LTR/non-LTR retrotransposons.

167 g HIV to STAT3 sequences supports a model of LTR-driven STAT3 overexpression as a driver of preferent

168 luding viral envelope genes that are part of LTR retrotransposons.

169 nching model for studying the propagation of LTR retrotransposons in these genomes.

170 ck from Tat shifts and expands the regime of LTR bimodality.

171 cterized mainly by a reversible silencing of LTR promoter-driven transcription of an integrated provi

172 Silencing of LTR retrotransposons is dependent on downstream RNAi fac

173 This extended view of LTR elements provides the framework for functional valid

174 us cultures was reported for 15% (52/350) of LTRs between 2 and 4 years after transplantation.

175 This is a retrospective cohort of LTRs from January 2010 to December 2014.

176 report an extraordinary impact of a group of LTRs from the mammalian endogenous retrovirus-related ER

177 Next generation sequencing (NGS) of LTRs from 269 HIV-1-infected samples in the Drexel CARES

178 n and detecting hypomethylation hot spots of LTRs and LINEs.

179 Identifying this high-risk subset of LTRs has implications for risk assessment, management, a

180 contrast, the absence of structural data on LTR retrotransposon capsids hinders our understanding of

181 Twenty-one LTR were consented; 6 were excluded due to subclinical A

182 Twenty-one LTRs consented; 6 were excluded due to subclinical acute

183 ses and should be widely applicable to other LTR retrotransposons, endogenous retroviruses (ERVs), an

184 The genomic positions of 1048 polymorphic LTRs were strongly associated with a range of stress res

185 dentifies LTR-RTs and generates high-quality LTR libraries from genomic sequences.

186 We prospectively studied 27 D(+)R(-) LTRs during primary CMV infection to determine whether a

187 In R+ LTRs, significantly higher gB-specific AB levels develop

188 the ADCC response in HCMV-seropositive (R+) LTRs and in seronegative recipients of positive organs (

189 mples were collected from 35 R+ and 28 D+/R- LTRs for 1 (R+) or 2 (D+/R-) years posttransplantation a

190 R enhancer complex and facilitate long-range LTR enhancer function in activating transcription of dow

191 antifies specific HIV provirus reactivation (LTR promoter) relative to nonspecific host cell gene exp

192 evaluate this relationship in LT recipients (LTR).

193 ory profiles in liver transplant recipients (LTR), mTOR-I therapy might allow for increased success w

194 rofiles in liver transplant (LT) recipients (LTRs), mTOR-I therapy might allow for increased success

195 SV) infection in lung transplant recipients (LTRs) causes mortality rates of 10%-20% despite antivira

196 ontrolled trial, lung transplant recipients (LTRs) using a mobile health intervention, Pocket Persona

197 In lung transplant recipients (LTRs), human cytomegalovirus (HCMV) DNA detection in the

198 and mortality in lung transplant recipients (LTRs).

199 porary cohort of lung transplant recipients (LTRs).

200 particularly in lung transplant recipients (LTRs).

201 re infections in lung transplant recipients (LTRs).

202 s predictors in liver transplant recipients (LTRs).

203 Cellular and viral factors regulating LTR activity contribute to HIV-1 latency, and certain re

204 Cellular and viral proteins regulating LTR activity contribute to the modulation of HIV-1 laten

205 : MGEScan-long terminal repeat (LTR) and MGEScan-non-LTR are successfully used programs

206 usceptibility and FeLV long terminal repeat (LTR) copy number, similar to observations in natural FeL

207 tic cat enFeLV env and long terminal repeat (LTR) copy numbers were determined for each individual an

208 ripts overlapping with long-terminal repeat (LTR) elements, several thousand of which were expressed

209 ex with the viral cDNA long terminal repeat (LTR) ends termed an intasome.

210 activity of the viral long terminal repeat (LTR) from Vpr-deficient proviruses was significantly red

211 ffect of ZL0580 on HIV long terminal repeat (LTR) in microglia.

212 ral targets within the long terminal repeat (LTR) of HIV.

213 HspBP1 inhibits HIV-1 long terminal repeat (LTR) promoter activity.

214 cription driven by the long terminal repeat (LTR) promoter of HIV-1.

215 ed Tat-dependent HIV-1 long-terminal repeat (LTR) promoter transactivation as well as HIV-1 virion pr

216 proximal region of the long terminal repeat (LTR) promoter was associated with the absence of RNAPII

217 proteins is flanked by long terminal repeat (LTR) regions from the retrovirus.

218 discovery of complete long terminal repeat (LTR) retroelements, which are widespread in eukaryotic g

219 tingly, we find that a long terminal repeat (LTR) retrotransposon insertion upstream of MdMYB1, a cor

220 th specific classes of long terminal repeat (LTR) retrotransposons and organize into large loci (>50

221 rms appeared to target long terminal repeat (LTR) retrotransposons and other unrelated genes.

222 enous retroviruses and long terminal repeat (LTR) retrotransposons are mobile genetic elements that a

223 roviruses evolved from long terminal repeat (LTR) retrotransposons by acquisition of envelope functio

224 ernal A particle (IAP) long terminal repeat (LTR) retrotransposons in cultivated cells.

225 ons of low-copy number long terminal repeat (LTR) retrotransposons or deletions, the same two classes

226 able elements (MITEs), long terminal repeat (LTR) retrotransposons, and non-LTR retrotransposons, inc

227 es (ERVs), also called long terminal repeat (LTR) retrotransposons, begins with transcription by RNA

228 of methods annotating long terminal repeat (LTR) retrotransposons, terminal inverted repeat (TIR) tr

229 ecific low-copy number long-terminal repeat (LTR) retrotransposons, which differ among lines.

230 y resembles endogenous long terminal repeat (LTR) sequences, pointing to a select role of BRD4S-BRG1

231 ted in the foamy virus long terminal repeat (LTR) that has high-affinity binding to the CCCTC-binding

232 ecies the CMTs silence long terminal repeat (LTR) transposons in the distal chromatin that are younge

233 ng P-TEFb to the HIV-1 long terminal repeat (LTR), and we show that inhibition of HSF1 attenuates the

234 of HIV's promoter, the long terminal repeat (LTR), to generate bimodal ON-OFF expression and that tra

235 n A1 (HMGA1) and viral long terminal repeat (LTR), which led to higher levels of HIV-1 genomic integr

236 found two instances of long terminal repeat (LTR)-driven provirus transcription but no evidence to su

237 ex essential for HIV-1 long terminal repeat (LTR)-mediated and general cellular transcription.

238 In the mouse, long terminal repeat (LTR)-retrotransposons, or endogenous retroviruses (ERV),

239 U3 region of the viral long terminal repeat (LTR).

240 'Copy-and-paste' long-terminal-repeat (LTR) retrotransposons have been particularly successful

241 (targeting gag and the long terminal repeat [LTR]).

242 endogenous retroviral long terminal repeats (LTR), short and long interspersed nuclear elements (SINE

243 5' and 3' peripheral long terminal repeats (LTRs) containing bidirectional promoters.

244 ansposons often carry long terminal repeats (LTRs) for retrovirus-like reverse transcription and inte

245 ransposons containing long terminal repeats (LTRs) form a substantial fraction of eukaryotic genomes.

246 ive versus restricted long terminal repeats (LTRs) revealed that the gene expression patterns were si

247 e prediction of 20.5% long terminal repeats (LTRs) that doubled the previous estimate, and revealed a

248 A sequences, known as long terminal repeats (LTRs), at its 5' and 3' ends.

249 s retrovirus-K (ERVK) long terminal repeats (LTRs), which act as imprinted promoters specifically in

250 ents (TEs), including Long-Terminal-Repeats (LTRs) and SINE-VNTR-Alus (SVAs), that significantly affe

251 at degradation in endolysosomes and restrict LTR transactivation.

252 ng the long terminal repeat-retrotransposon (LTR-RT) type of TE, we estimated their death rates by co

253 Long terminal repeat retrotransposons (LTR-RTs) are prevalent in plant genomes.

254 pG-rich promoter not related to a retroviral LTR, with sites of expression including the placenta as

255 in differentiating the capacity of high-risk LTRs to establish durable immune control during early ch

256 areas was evaluated at follow-up in separate LTR and family caregiver (collateral) assessments.

257 sing on Helitrons, Pack-MULEs, and Sirevirus LTR retrotransposons in the maize genome.

258 6 carefully annotated, full-length Sirevirus LTR retrotransposons in maize, we show that their silenc

259 in an array of structures, ranging from solo LTRs to tandem dRemp repeats containing several internal

260 recombination resulting in a solitary (solo) LTR, although members of one group of human ERVs (HERVs)

261 e approximately full-length (2-LTR) and solo-LTR alleles in addition to the unoccupied site.

262 ic framework to study ERV insertion and solo-LTR formation.

263 th proviral form, and the more numerous solo-LTR form, thought to result from homologous recombinatio

264 We find that the rate of solo-LTR formation decreases rapidly as a function of ERV age

265 age and that an age dependent model of solo-LTR formation describes the history of ERVs more accurat

266 ship between full-length proviruses and solo-LTRs to help identify large scale co-options in distant

267 estimated their death rates by counting solo-LTRs and truncated elements.

268 H loci are markedly less likely to form solo-LTRs than ERVs from other families.

269 and rapid bursts of the three Hevea-specific LTR-retrotransposon families during the last 10 million

270 The functional potential of the studied LTRs is even higher, because we show that dormant LTR pr

271 ed in Tat endolysosome escape and subsequent LTR transactivation.

272 um in Tat endolysosome escape and subsequent LTR transactivation.

273 In Schizosaccharomyces pombe the Tf2 LTR retrotransposons are transcriptionally silenced and

274 better adherence to the medical regimen than LTRs receiving usual care during the first year posttran

275 Interestingly, we find that LTR-driven HIV-1 gene expression is also enhanced by LY6

276 Finally, we found that LTR-mediated retrocopies are immediately cotranscribed w

277 is of intronic polyadenylation revealed that LTR/Gypsy and LTR/Copia were two major transposable elem

278 Overall, our data show that LTR-mediated retroposition is highly conserved across a

279 Our findings suggested that LTR lncRNAs transcribed from many of the 4000 copies of

280 ricted to tumorigenic cells, suggesting that LTR promoter activity is dependent upon the transcriptio

281 The LTR-mediated gene remodeling also extends to hamster, hu

282 the fusion points between the mRNAs and the LTR retrotransposons, we identified shared short similar

283 active histone marks H3K4me3 and H3ac at the LTR.

284 erythroblasts, lncRNAs transcribed from the LTR retrotransposons of ERV-9 human endogenous retroviru

285 Whether and how the LTR lncRNAs serve biological functions are largely unkno

286 ical LTRs are Copia elements, with which the LTR is four times shorter than that of other Copia eleme

287 kness and were primarily associated with the LTR/Gypsy retrotransposons in the heterochromatin flanki

288 nrichment in active histone marks within the LTR.

289 The LTRs function in a stage-specific manner during the oocy

290 The LTRs modulate transcription in both forward (sense) and

291 -containing element that is conserved in the LTRs of HERV-K-10, -K-11, and -K-20, and validated the f

292 Within the cis-regulatory portion of the LTRs, a complex palindrome-rich region acts as a hotspot

293 During the posttransplant follow-up, these LTRs displayed HCMV DNA detection in the BALF by PCR, wh

294 We demonstrate that they exhibit unique LTR dynamics, which ultimately results in differences in

295 Transfection of eight upregulated LTRs into recipient human cells in culture showed robust

296 ed viruses that express genes from the viral LTR but not from an internal immediate-early CMV promote

297 ion by inducing transcription from the viral LTR.

298 herapy withdrawal in non-immune, non-viremic LTR > 3 years post-LT.

299 on in SMYD5 cancer cells was associated with LTR and endogenous retrovirus elements and decreased H4K

300 ucity of young elements; the rarity of young LTR-RTs is a consequence of fewer births rather than acc