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1                                              LTR relapsers demonstrated reduced CD8(+)Ki67(+) cells e
2                                              LTR retrotransposons are mobile elements that are able,
3                                              LTR retrotransposons are repetitive DNA elements compris
4                                              LTRs may be infected in PCP outbreaks simultaneously wit
5                                              LTRs mismatched for CMV (donor(+)/recipient(-); D(+)R(-)
6                                              LTRs mismatched for CMV (donor+/recipient-; D+R-) are at
7 or SSRP1 protein enhances Tat-mediated HIV-1 LTR (long terminal repeat) promoter activity.
8  to target a 34-bp sequence within the HIV-1 LTR (loxLTR).
9 s to activate gene expression from the HIV-1 LTR and found that KSHV ORF45 is the most potent activat
10 dulate the activation of an integrated HIV-1 LTR and revealed that the most potent individual activat
11  revealed that HspBP1 was recruited on HIV-1 LTR at NF-kappaB enhancer region (kappaB sites).
12 ific and regulated activity toward the HIV-1 LTR promoter, which is mediated by G-quadruplexes.
13 nduced depletion of HDAC1 and 3 on the HIV-1 LTR that was associated with hyperacetylation of histone
14 n RNA polymerase II recruitment to the HIV-1 LTR, leading to enhanced transcriptional output.
15 d that the host protein Naf1 inhibited HIV-1 LTR-driven transcription of HIV genes and contributed to
16 at histone H3K27 and H3R26 orchestrate HIV-1 LTR-mediated transcription, and potentially opens a new
17 th hyperacetylation of histones on the HIV-1 LTR.
18                                            2-LTR circles decreased with cART but remained detectable
19                                            2-LTR circles were analyzed by droplet digital polymerase
20                                            2-LTR circles were detected pre-ART in 20/29 and in 8/30 p
21 ure total HIV DNA, integrated HIV DNA, and 2-LTR circles in CD4(+) T cells from HIV-infected subjects
22         Higher levels of total HIV DNA and 2-LTR circles were detected in untreated subjects than ind
23     Total HIV DNA, integrated HIV DNA, and 2-LTR circles were detected in, respectively, 100%, 94%, a
24  of additional control conditions, such as 2-LTR quantification and the addition of reverse transcrip
25 levels of episomal HIV DNA (as measured by 2-LTR circles) and decreases the levels of HIV transcripti
26              Total and integrated HIV DNA, 2-LTR circles, and cell-associated unspliced HIV RNA were
27 ci that include approximately full-length (2-LTR) and solo-LTR alleles in addition to the unoccupied
28     An increase in 2-long-terminal-repeat (2-LTR) circles in the depleted FACT complex cell line indi
29 V-1 DNA, including 2-long terminal repeat (2-LTR) circles, and multiply spliced (ms-) and unspliced (
30 ted HIV DNA, and two long terminal repeat (2-LTR) circles.
31 se in the level of 2-long terminal repeat (2-LTR) circles.
32  0.04), detectable 2-long terminal repeat (2-LTR), and lower nadir CD4(+) (P < 0.01) were independent
33                                    Several 2-LTR insertions have intact reading frames in some or all
34 dividual loci identified three new unfixed 2-LTR proviruses within our set, including an intact provi
35 etermined by 2 independent reviewers) in 250 LTRs in a single university transplantation program.
36 ere with antisense transcription from the 3' LTR and vice versa, even with strong transcription emana
37          Antisense transcription from the 3' LTR regulates expression of a single gene, hbz, while se
38 ere with antisense transcription from the 3' LTR, allowing viral genes encoded on opposite DNA strand
39 long terminal repeat (LTR) but not on the 3' LTR.
40 tire HIV-1 genome spanning between 5' and 3' LTRs of integrated HIV-1 proviral DNA copies from latent
41  between the gag-pol coding region and the 3'LTR.
42                      By combining 5'LTR-to-3'LTR single-genome amplification and direct amplicon sequ
43 g the DNA sequence of nucleosome A of the 3'-LTR of the mouse mammary tumor virus (147 bp MMTV-A).
44 7 LTR at time point of CLAD diagnosis and 37 LTR without any complication at routinely performed BAL.
45               The BALF was collected from 37 LTR at time point of CLAD diagnosis and 37 LTR without a
46                             We saw active 5' LTR use in tumorigenic cells only, suggesting that the c
47 o oscillate, than the constitutive MoMuLV 5' LTR (MMLV) promoter (0/25).
48 , hbz, while sense transcription from the 5' LTR controls expression of all other viral genes, includ
49 e found that sense transcription from the 5' LTR does not interfere with antisense transcription from
50  no evidence to suggest that these active 5' LTRs were influencing nearby host gene expression.
51                               By combining 5'LTR-to-3'LTR single-genome amplification and direct ampl
52 d by ELISA in BALF and serum samples from 60 LTRs.
53 8 BALF levels were significantly higher in 8 LTRs who additionally developed HCMV disease, as compare
54        In mouse, we identified more than 800 LTRs from ORR1, MT, MT2, and MLT families, which resembl
55                 In a prospective study of 85 LTRs, expression of cytokines (tumor necrosis factor, in
56 ed in cis to stabilize assembly of the ERV-9 LTR enhancer complex and facilitate long-range LTR enhan
57  a single copy of the primate-specific ERV-9 LTR in the 100 kb human beta-globin gene locus.
58 cribed from many of the 4000 copies of ERV-9 LTR retrotransposons acted by a similar cis mechanism to
59 rying approximately 4000 copies of the ERV-9 LTRs and in transgenic mouse erythroblasts carrying a si
60   In contrast, substitution of both FeLV-945 LTR and SU into FeLV-A/61E resulted in multicentric lymp
61 ence microscopy with LysoTracker Red DND-99 (LTR) indicated that E. ictaluri-containing vacuoles (ECV
62                                Additionally, LTRs generated by treatment with 20kHz+1MHz were found t
63 terval, we identify that the insertion of an LTR-retrotransposon in its 11(th) intron results in a co
64  polyadenylation revealed that LTR/Gypsy and LTR/Copia were two major transposable elements within th
65 n, which is conserved among retroviruses and LTR-retrotransposons.
66   Evidence demonstrates that FeLV-945 SU and LTR are required together to fully recapitulate the dist
67 non-essential protein coding genes, rDNA and LTRs.
68 ylaxis should be considered for all RTRs and LTRs.
69 by ten-eleven translocation (TET) enzymes at LTR regions of ERVs, because vitamin C acts as a cofacto
70 sm by which DNA methylation is maintained at LTR retrotransposons and imprinted genes during developm
71                  The amplification of athila LTR-retrotransposons, members of the gypsy superfamily,
72                                         Best LTR responses consisted of 25 (71%) complete remissions
73      IN removes two 3'-nucleotides from both LTR ends and catalyses strand transfer of the recessed 3
74 py numbers of NLRs were greatly increased by LTR-retrotransposon-mediated retroduplication.
75                     In addition to canonical LTR-RTs with 5'-TG...CA-3' termini, LTR_retriever also i
76 spergillus colonization is frequent among CF-LTRs and a positive intraoperative Aspergillus culture p
77 lus colonization on the risk for IA among CF-LTRs.
78                 Overall, 22.5% (20/93) of CF-LTRs developed IA.
79                Seventy percent (65/93) of CF-LTRs had pretransplant Aspergillus colonization.
80 ngle-center retrospective cohort study of CF-LTRs was conducted between 2006 and 2010.
81 ylaxis was administered to 61% (57/93) of CF-LTRs.
82 stic fibrosis-lung transplant recipients (CF-LTRs) may be at greater risk of IA following lung transp
83 psis (Arabidopsis thaliana), the constructed LTR library showed excellent sensitivity and specificity
84  by retroviruses such as HIV-1, and controls LTR/non-LTR retrotransposition in marsupials.
85 of two or more parental genes, demonstrating LTR-retroposition as a novel mechanism of exon shuffling
86  T-bet > Eomesodermin (Eomes) differentiated LTR controllers from viremic relapsers and reciprocally
87  and CD4(+)T-bet(+) induction differentiated LTR controllers from early viremic relapsers, correlatin
88 nternal retrocopies flanked by discontinuous LTR retrotransposons.
89 is even higher, because we show that dormant LTR promoter activity can rescue loss of an essential up
90 3K9me3 levels and derepression of endogenous LTR- and LINE-repetitive DNA elements during differentia
91 ong-term mitotic maintenance of the episomal LTR circles.
92 cent studies cataloging the diversity of ERV LTRs acting as important transcriptional regulatory elem
93                                         ERVL LTRs thus offer means for a comprehensive survey of the
94                             Altogether, ERVL LTRs provide molecular mechanisms for stochastically sca
95 steady, and long-term amplification of a few LTR retrotransposon families.
96 mmediately cotranscribed with their flanking LTR retrotransposons.
97 e molecular features that likely account for LTR exaptation in developmental and tissue-specific gene
98 le progression into mitosis are required for LTR-mediated viral expression, suggesting that the evolu
99                                       Fungal LTR retrotransposons prevent mutagenic insertions throug
100                                 Furthermore, LTR with high levels of RBC MV >/=225/muL were also asso
101  whereas the presence of LINE in P2 or gypsy LTR retrotransposon in P3 reduced expression of the repo
102 n contrast with the LINE in P2 and the gypsy LTR retrotransposon in P3 which act as silencers.
103                      Here we describe HERV-H LTR-associating protein 2 (HHLA2) as a member of the B7
104  NF-Y sites are in select subclasses of HERV LTR repeats.
105 o large loci (>50 kbp) characterized by high LTR density.
106 anism encompassing NFkappaB/SP1-mediated HIV LTR activation.
107 e transfected with different variants of HIV LTR promoters and then exposed to METH.
108 NFkappaB/SP1-dependent activation of the HIV LTR and with the subsequent alterations of NPC neurogene
109  induced transcriptional activity of the HIV LTR promotor, an effect that required both NFkappaB and
110 y contribute to the sensitization of the HIV LTR to subsequent exposure to VOR, and to increase viral
111  HIV and with basal transcription of the HIV LTR, potently inhibiting replication of R5 HIV but not C
112 R) element and other distal sites on the HIV LTR.
113                                     However, LTR sequences are disproportionately present in human lo
114 lyze the DNA methylation pattern of 4799 IAP LTR retrotransposons in embryonic stem, somatic and Neur
115    About half of the variably methylated IAP LTRs tend to be hypomethylated in ES cells, and nearly a
116 mulation of mutations in initially identical LTRs.
117 ading-empowered Perl program that identifies LTR-RTs and generates high-quality LTR libraries from ge
118 e successfully used programs for identifying LTRs and non-LTR retrotransposons in eukaryotic genome s
119                                 Importantly, LTR-driven transcription was restricted to tumorigenic c
120 r follow-up time, the risk of skin cancer in LTR is comparable to that of kidney transplant recipient
121 features and risk factors of skin cancers in LTR treated mainly with tacrolimus.
122 , RSK2 appears to be selectively involved in LTR stimulation by both KSHV ORF45 and HIV-1 Tat.
123  CMV promoter, suggesting a role of SSRP1 in LTR-driven gene expression but not in viral DNA integrat
124 -10) in BAL fluid are associated with ACR in LTRs, suggesting a potential mechanistic role in the pat
125 ssociation between CXCL10 (IP-10) and ACR in LTRs.
126 chanistic role in the pathogenesis of ACR in LTRs.
127  cells in BAL was significantly increased in LTRs exhibiting viral control compared to those with CMV
128  nucleolin binding aptamer greatly increased LTR promoter activity.
129 fers a unique target to specifically inhibit LTR-retrotransposons, and tRF-targeting is a potentially
130 e maintenance of HIV-1 latency by inhibiting LTR-driven HIV-1 gene transcription in a nuclear factor
131 us estimate, and revealed a high Solo:Intact LTR ratio of 8.2.
132 ogeny population of chromosomally integrated LTR retrotransposons consisting of pairwise recombinatio
133                        Here, we investigated LTRs with intrapulmonary HCMV replication for the chemok
134 e insulator was inserted into the lentiviral LTR.
135                     If we provide lentiviral LTRs with a "twin-site", here an FF3 fusion, the presenc
136                                However, many LTR retrotransposons and imprinted genes are impervious
137 s suggest random activation of a few or many LTR retrotransposons families in particular lineages ove
138                                         MMTV-LTR promoter-driven HA-14-3-3zeta transgenic mice (MMTV-
139 ssing human FLAG-PAD2 downstream of the MMTV-LTR promoter develop spontaneous neoplastic skin lesions
140 acted by a similar cis mechanism to modulate LTR enhancer function in activating transcription of dow
141 ing gene evolution-D6Ertd527e-in which an MT LTR provided a promoter and the 5' exon with a functiona
142 y used programs for identifying LTRs and non-LTR retrotransposons in eukaryotic genome sequences.
143 rspersed element 1 (L1) is an autonomous non-LTR retroelement that is active in mammalian genomes.
144          LINE-1 (or L1) is an autonomous non-LTR retrotransposon in the human genome, comprising 17%
145 or many related bacterial and eukaryotic non-LTR retroelement RTs.
146 gates the hypothesis that RNH domains in non-LTR retrotransposons have a single origin and provides e
147 oviruses such as HIV-1, and controls LTR/non-LTR retrotransposition in marsupials.
148 s type 1 (HIV-1) and the mobility of LTR/non-LTR retrotransposons.
149 n-long terminal repeat (LTR) and MGEScan-non-LTR are successfully used programs for identifying LTRs
150 ough members of the L1 (LINE-1) clade of non-LTR retrotransposons can be deleterious, the L1 clade ha
151 , and harbors features characteristic of non-LTR retrotransposons.
152                                       R2 non-LTR retrotransposons insert at a specific site in the 28
153 , LTR_retriever also identifies noncanonical LTR-RTs (non-TGCA), which have been largely ignored in g
154                 The majority of noncanonical LTRs are Copia elements, with which the LTR is four time
155    We identified seven types of noncanonical LTRs from 42 out of 50 plant genomes.
156 pression in NF-kappaB mediated activation of LTR-driven gene-expression.
157 ronchoalveolar lavage (BAL) fluids (BALF) of LTR at CLAD diagnosis, are elevated and potential progno
158                        The identification of LTR-RTs is critical for achieving high-quality gene anno
159  developed for the de novo identification of LTR-RTs; however, these programs are associated with low
160 ell is a critical component for induction of LTR promoter activity.
161 nism of action was ascribed to inhibition of LTR promoter activity in cells.
162 h the positions and the degradation level of LTR retrotransposons copies.
163 ncy virus type 1 (HIV-1) and the mobility of LTR/non-LTR retrotransposons.
164 nching model for studying the propagation of LTR retrotransposons in these genomes.
165 ectivity depended on specific recognition of LTR loop residues; the mechanism of action was ascribed
166 ck from Tat shifts and expands the regime of LTR bimodality.
167 B pathway, as a potent negative regulator of LTR-dependent HIV-1 transcription.
168 cterized mainly by a reversible silencing of LTR promoter-driven transcription of an integrated provi
169 report an extraordinary impact of a group of LTRs from the mammalian endogenous retrovirus-related ER
170 n and detecting hypomethylation hot spots of LTRs and LINEs.
171                    Three hundred seventy-one LTR were included.
172 nal repeats (LTRs) of individual orthologous LTR-retrotransposons, the rates of synonymous and non-sy
173                                     Overall, LTR sequences and genic sequences showed more rapid nucl
174 se a new computational method called ProtDec-LTR for protein remote homology detection, which is able
175 y used benchmark dataset showed that ProtDec-LTR can achieve an ROC1 score of 0.8442 and an ROC50 sco
176 dentifies LTR-RTs and generates high-quality LTR libraries from genomic sequences.
177         We prospectively studied 27 D(+)R(-) LTRs during primary CMV infection to determine whether a
178             We prospectively studied 23 D+R- LTRs during primary CMV infection to determine whether a
179 R enhancer complex and facilitate long-range LTR enhancer function in activating transcription of dow
180 vised manner via using the Learning to Rank (LTR) algorithm derived from natural language processing.
181 e limitation for lung transplant recipients (LTR) after the first year, and therapies targeting immun
182 T cell memory in lung transplant recipients (LTRs) is critical for host defense and allograft durabil
183  lavage (BAL) of lung transplant recipients (LTRs) to determine the association between CXCL10 (IP-10
184               In lung transplant recipients (LTRs), human cytomegalovirus (HCMV) DNA detection in the
185 porary cohort of lung transplant recipients (LTRs).
186  particularly in lung transplant recipients (LTRs).
187  particularly in lung transplant recipients (LTRs).
188 r data exist on liver-transplant recipients (LTRs).
189 nce the size of localized transport regions (LTRs) in both in vitro and in vivo models while decreasi
190        Cellular and viral factors regulating LTR activity contribute to HIV-1 latency, and certain re
191       Cellular and viral proteins regulating LTR activity contribute to the modulation of HIV-1 laten
192 ted to stimulate HIV-1 long terminal repeat (LTR) activity.
193              : MGEScan-long terminal repeat (LTR) and MGEScan-non-LTR are successfully used programs
194 II (RNAP II) on the 5' long terminal repeat (LTR) but not on the 3' LTR.
195  total HIV-1 DNA and 2-long terminal repeat (LTR) circles by quantitative polymerase chain reaction (
196 ollection of known ERV/long terminal repeat (LTR) elements to annotate the retroviral complement of t
197 ex with the viral cDNA long terminal repeat (LTR) ends termed an intasome.
198  activity of the viral long terminal repeat (LTR) from Vpr-deficient proviruses was significantly red
199 act genomes and normal long terminal repeat (LTR) function.
200 ript that contains the long terminal repeat (LTR) of lambda-olt 2-1 and shows a similar expression pa
201  HspBP1 inhibits HIV-1 long terminal repeat (LTR) promoter activity.
202 ed Tip110 at the HIV-1 long terminal repeat (LTR) promoter and found that Tip110 expression was assoc
203 cription driven by the long terminal repeat (LTR) promoter of HIV-1.
204 tructures in the HIV-1 long terminal repeat (LTR) promoter suppresses viral transcription.
205 proteins is flanked by long terminal repeat (LTR) regions from the retrovirus.
206 th specific classes of long terminal repeat (LTR) retrotransposons and organize into large loci (>50
207 rms appeared to target long terminal repeat (LTR) retrotransposons and other unrelated genes.
208                        Long terminal repeat (LTR) retrotransposons are an abundant class of genomic p
209           BEL/Pao-like long-terminal repeat (LTR) retrotransposons were annotated from the highly ada
210 es (ERVs), also called long terminal repeat (LTR) retrotransposons, begins with transcription by RNA
211 y resembles endogenous long terminal repeat (LTR) sequences, pointing to a select role of BRD4S-BRG1
212 ted in the foamy virus long terminal repeat (LTR) that has high-affinity binding to the CCCTC-binding
213 paB sites in the HIV-1 long terminal repeat (LTR) U3 and could be transferred to MLV.
214 on in H3K27 at the HIV long terminal repeat (LTR), subsequent exposure to the HDACi suberoylanilide h
215 of HIV's promoter, the long terminal repeat (LTR), to generate bimodal ON-OFF expression and that tra
216 n A1 (HMGA1) and viral long terminal repeat (LTR), which led to higher levels of HIV-1 genomic integr
217           We show that long terminal repeat (LTR)-derived transcripts contribute extensively to the c
218 found two instances of long terminal repeat (LTR)-driven provirus transcription but no evidence to su
219 ction by enhancing HIV long terminal repeat (LTR)-driven transcription via the NF-kappaB pathway.
220 ex essential for HIV-1 long terminal repeat (LTR)-mediated and general cellular transcription.
221          In the mouse, long terminal repeat (LTR)-retrotransposons, or endogenous retroviruses (ERV),
222 e element of the HIV-1 long terminal repeat (LTR).
223 1 promoter, termed the long terminal repeat (LTR).
224 istone acetylation and long-terminal-repeat (LTR) transcription.
225 aracterized effects of long-terminal-repeat (LTR)-driven gene expression.
226 ts (LINE), but not in long terminal repeats (LTR).
227  5' and 3' peripheral long terminal repeats (LTRs) containing bidirectional promoters.
228 ansposons often carry long terminal repeats (LTRs) for retrovirus-like reverse transcription and inte
229 ransposons containing long terminal repeats (LTRs) form a substantial fraction of eukaryotic genomes.
230 stitution between two long terminal repeats (LTRs) of individual orthologous LTR-retrotransposons, th
231 ancer elements in the long terminal repeats (LTRs) of murine leukemia virus (MLV)-based vectors and t
232 e prediction of 20.5% long terminal repeats (LTRs) that doubled the previous estimate, and revealed a
233 s and retrotransposon long terminal repeats (LTRs)) were observed throughout the cell cycle.
234 nts (ERVs) containing long terminal repeats (LTRs), are silenced through trimethylation of histone H3
235 A sequences, known as long terminal repeats (LTRs), at its 5' and 3' ends.
236 ents (TEs), including Long-Terminal-Repeats (LTRs) and SINE-VNTR-Alus (SVAs), that significantly affe
237 se lasting >36 months (long-term responders [LTRs]).
238 ng the long terminal repeat-retrotransposon (LTR-RT) type of TE, we estimated their death rates by co
239       Long terminal repeat retrotransposons (LTR-RTs) are prevalent in plant genomes.
240 pG-rich promoter not related to a retroviral LTR, with sites of expression including the placenta as
241  through the use of an endogenous retroviral LTR promoter of the LTR2 family.
242 in differentiating the capacity of high-risk LTRs to establish durable immune control during early ch
243 nd differentiating the capacity of high-risk LTRs to establish immune control during early chronic in
244                                  We selected LTR grafted in our hospital between January 1996 and Dec
245 6 carefully annotated, full-length Sirevirus LTR retrotransposons in maize, we show that their silenc
246 stances along chromosomes and ratios of solo LTRs to intact elements.
247 recombination resulting in a solitary (solo) LTR, although members of one group of human ERVs (HERVs)
248 e approximately full-length (2-LTR) and solo-LTR alleles in addition to the unoccupied site.
249 ic framework to study ERV insertion and solo-LTR formation.
250 th proviral form, and the more numerous solo-LTR form, thought to result from homologous recombinatio
251                We find that the rate of solo-LTR formation decreases rapidly as a function of ERV age
252  age and that an age dependent model of solo-LTR formation describes the history of ERVs more accurat
253 ship between full-length proviruses and solo-LTRs to help identify large scale co-options in distant
254 estimated their death rates by counting solo-LTRs and truncated elements.
255 H loci are markedly less likely to form solo-LTRs than ERVs from other families.
256                                         Some LTR-derived transcripts are associated with enhancer reg
257      The functional potential of the studied LTRs is even higher, because we show that dormant LTR pr
258 1 (CCNT1), a subunit of P-TEFb, with the Tat-LTR axis.
259 FACT proteins also interfere with HTLV-1 Tax-LTR-mediated transcription and viral latency, indicating
260         In Schizosaccharomyces pombe the Tf2 LTR retrotransposons are transcriptionally silenced and
261                  Interestingly, we find that LTR-driven HIV-1 gene expression is also enhanced by LY6
262 of binding peaks for a TF, and we found that LTR elements dominated these relationships in human.
263                       Finally, we found that LTR-mediated retrocopies are immediately cotranscribed w
264 ess, accumulating evidence has revealed that LTR sequences derived from distantly related ERVs have b
265 is of intronic polyadenylation revealed that LTR/Gypsy and LTR/Copia were two major transposable elem
266                  Overall, our data show that LTR-mediated retroposition is highly conserved across a
267                  Our findings suggested that LTR lncRNAs transcribed from many of the 4000 copies of
268 ricted to tumorigenic cells, suggesting that LTR promoter activity is dependent upon the transcriptio
269    This demonstrates for the first time that LTRs generated with 20kHz+1MHz are also more permeable t
270                                          The LTR with high levels of epithelial MV >580/muL showed a
271                                          The LTR-mediated gene remodeling also extends to hamster, hu
272  the fusion points between the mRNAs and the LTR retrotransposons, we identified shared short similar
273 o leads to increased mRNA synthesis from the LTR by the host RNA polymerase.
274  erythroblasts, lncRNAs transcribed from the LTR retrotransposons of ERV-9 human endogenous retroviru
275 ufficient to increase transcription from the LTR.
276                          Whether and how the LTR lncRNAs serve biological functions are largely unkno
277 gnize G-quadruplex structures present in the LTR promoter.
278 raction translated into stabilization of the LTR G-quadruplexes and increased promoter silencing acti
279                               Folding of the LTR promoter into dynamic G-quadruplex conformations has
280 tly enhanced transcription elongation of the LTR promoter.
281                                   One of the LTR retrotransposon amplification bursts in Zea may have
282 ively active RSK2 is unable to stimulate the LTR, suggesting that ORF45 may preferentially direct thi
283 hoeae-derived supernatants revealed that the LTR-inducing fraction contained a compound having a mass
284 ive transcription elongation factor b to the LTR promoter.
285 ical LTRs are Copia elements, with which the LTR is four times shorter than that of other Copia eleme
286 kness and were primarily associated with the LTR/Gypsy retrotransposons in the heterochromatin flanki
287                                          The LTRs function in a stage-specific manner during the oocy
288                                          The LTRs modulate transcription in both forward (sense) and
289 ssion levels decline during development, the LTRs are marked by histone H3 lysine 4 trimethylation.
290     Within the cis-regulatory portion of the LTRs, a complex palindrome-rich region acts as a hotspot
291   During the posttransplant follow-up, these LTRs displayed HCMV DNA detection in the BALF by PCR, wh
292 ver, both SUPT16H and SSRP1 are recruited to LTR promoter.
293  approaches in a supervised manner via using LTR.
294 ed viruses that express genes from the viral LTR but not from an internal immediate-early CMV promote
295 ion by inducing transcription from the viral LTR.
296 on in SMYD5 cancer cells was associated with LTR and endogenous retrovirus elements and decreased H4K
297  CD4(+)IL-2(+) frequencies, as compared with LTR controllers.
298 analyses show that this retrotransposon with LTRs (Long Terminal Repeats) is widely distributed among
299  we show that insertion of the fission yeast LTR retrotransposon Tf1 is guided by the DNA binding pro
300 ucity of young elements; the rarity of young LTR-RTs is a consequence of fewer births rather than acc

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