ライフサイエンスコーパス: silencer

1 pears to overcome inhibition mediated by the silencer.

2 in mice harboring point mutations in the Cd4 silencer.

3 s may similarly disrupt function of the ESS1 silencer.

4 e of Sir proteins and, in part, on the HMR-I silencer.

5 development and in DN cells lacking the CD4 silencer.

6 itment of histone acetyl transferases to the silencer.

7 by putatively disrupting an exonic splicing silencer.

8 on-sensitive and limited to the unmethylated silencer.

9 protein (hnRNP) A1-dependent exonic splicing silencer.

10 e element further supports its activity as a silencer.

11 riptional silencing on the Abf1p side of the silencer.

12 ting that it is the inherent property of the silencer.

13 ne c-MYC promoter region functions as a gene silencer.

14 novel functional components of the splicing silencer.

15 ypersensitivity (DHS) site located 3' to the silencer.

16 lement 1), can act as both an enhancer and a silencer.

17 s self-perpetuating independently of the Cd4 silencer.

18 as carriers for chemotherapy agents and gene silencers.

19 spread from these sites independently of the silencers.

20 the internal regions of HMR as well as with silencers.

21 ns were recombinationally separated from the silencers.

22 nteracted with Sir1 and recruits Sir1 to the silencers.

23 nhancers or create predicted exonic splicing silencers.

24 for ARS318 (HMR-I), which is one of the HMR silencers.

25 ents (REs) such as enhancers, repressors and silencers.

26 ons that contribute to the activities of the silencers.

27 gypsy LTR retrotransposon in P3 which act as silencers.

28 ency responders and Class II sRNAs acting as silencers.

29 pressive features that may act as long-range silencers.

30 d photocurrents three times those of earlier silencers.

31 riants (n = 16,384) of the HIV exon splicing silencer 3 (ESS3) 7-nt apical loop.

32 e-dimensional structure of the exon splicing silencer 3 (ESS3) from HIV-1 has been determined using N

33 mbinatorial inputs from one enhancer and two silencers acting at long range.

34 iption factor-binding site and abrogates the silencer activity in luciferase assays, an effect mimick

35 Potentiation of the silencer activity is demonstrated after CTCF protein is

36 l leads to CD4 commitment, whereas continued silencer activity leads to CD8 commitment.

37 croRNA, including miR1, which exerted robust silencer activity over the induction of GATA-6 leading t

38 rotein CTCF to the target promoters, and the silencer activity requires the binding of the REST/NRSF

39 KvDMR1 also contains chromatin insulator or silencer activity.

40 s APOE CGI exhibits transcriptional enhancer/silencer activity.

41 The identification of TRIM28 as a retroviral silencer adds to the growing body of evidence that many

42 ed silencing and interacted with core miRISC silencers Ago2 and Rck/p54 in an RNA-dependent manner an

43 We also discovered that, although the HMR-E silencer alone was sufficient to block transcription of

44 -kb silencer and the DHS, but not the 0.4-kb silencer alone, failed to maintain CD4 expression upon p

45 r, we found that in Saccharomyces cerevisiae silencers also influence the extent of silenced chromati

46 om a 1.8-Mb region of human chromosome 7 for silencer and EB activities.

47 tive elongation factor b (P-TEFb) appose the silencer and enhancer in CD4-negative thymoma cells and

48 We previously identified a recombination silencer and heterochromatin targeting element in the Vk

49 Runx1 binds the silencer and represses CD4 transcription in immature thy

50 kb sequence in intron 1 including the 0.4-kb silencer and the DHS, but not the 0.4-kb silencer alone,

51 e sites, the Sir proteins are recruited to a silencer and then associate with adjacent chromatin.

52 effects were also seen: Effective enhancers, silencers and 3' splice sites tend to be single stranded

53 osophila melanogaster, temperature-sensitive silencers and activators are widely used to control the

54 veloped an experimental strategy to identify silencers and EBs using transient transfection assays.

55 of sequences acted in a dual manner, as both silencers and EBs.

56 Silencers and enhancer-blockers (EBs) are cis-acting, ne

57 s been shown that Sum1-1p is directed to the silencers and internal regions of the HM loci, and inter

58 including enhancers, promoters, insulators, silencers and locus control regions.

59 The proteins nucleate at silencers and spread distally, utilizing the Sir2 NAD(+)

60 lished by the combined actions of cis-acting silencers and trans-acting proteins, including Sir2p, Si

61 ons had a higher ratio of splicing enhancers/silencers and were more conserved across mammals than th

62 ments (CREs, i.e., enhancers, promoters, and silencers) and the trans factors (e.g., transcription fa

63 egulatory sequence, such as an enhancer or a silencer, and a promoter.

64 Runx3 bind to the Ifng promoter and the Il4 silencer, and deletion of the silencer decreases the sen

65 suggest that the 5'ss D2, the proximal GGGG silencer, and the ESE act competitively to determine the

66 Genomic signals such as enhancers, silencers, and repetitive DNA, while required for the es

67 ng strong but spatially delimited binding to silencers, and weaker and more variable Ume6-dependent b

68 vely target CRF neurons with the optogenetic silencer archaerhodopsin tp009 (CRF-ArchT) to examine th

69 fied TRIM28 (Kap-1), a known transcriptional silencer, as an integral component of the complex.

70 scopy to analyze the dynamic effects of four silencers associated with diverse modifications: DNA met

71 itial hnRNP A1 binding to an exonic splicing silencer at the 3' end of human immunodeficiency virus t

72 oteins were recruited to HMR-E and telomeric silencers at equivalent rates.

73 In S. cerevisiae, Sir1 is recruited to the silencers at HML and HMR via its ORC interacting region

74 er mapping in T. delbrueckii revealed single silencers at HML and HMR, bound by Td-Kos3, Td-Sir2, and

75 lent information regulator (Sir) proteins to silencers at the silent mating-type loci and to telomere

76 Using silencer blocking, transgene protection and repressor bl

77 iation, but is not essential for enhancer or silencer blocking.

78 protein is knocked down, suggesting a novel silencer-blocking activity for CTCF.

79 y might contribute to Sir1's selectivity for silencer-bound ORCs in vivo.

80 in detail the interaction between enhancers, silencers, boundary elements and promoters at individual

81 eage choice, whereby inactivation of the DRE silencer by a strong TCR signal leads to CD4 commitment,

82 e exonic enhancers and CUG-BP1 to the exonic silencer by RNA affinity chromatography.

83 In contrast, a long-range silencer cassette downstream from Hand2 likely mediates

84 more closed state with the tTS transcription silencer caused missegregation and loss of the HAC.

85 t binding of Mi-2beta with Ikaros to the Cd4 silencer caused silencer inactivation, thereby allowing

86 regulators, including potential activators, silencers, chromatin remodelers, and ancillary factors.

87 ion and affinity purification to isolate the silencer complex assembled in vitro and identify the con

88 es the formation of a NFkappaB p50-C/EBPbeta silencer complex in the regulatory sequence.

89 the optimal target was mapped to a splicing silencer containing two pseudoacceptor sites sandwiched

90 o promote silencing and found that the HMR-E silencer contributed to an increased steady-state associ

91 gative thymocytes, Ikaros binding to the Cd4 silencer contributed to its repressive activity.

92 g through multiple nonconsensus sites in the silencer core.

93 ember of the Polycomb Group (PcG), is a gene silencer critical for proper development.

94 er and the Il4 silencer, and deletion of the silencer decreases the sensitivity of Il4 to repression

95 encers, it is possible that the promotion of silencer degradation by viral transactivators may be a c

96 Excessive intronic length and silencer density tend to delay splicing.

97 f nucleosomes and directional silencing by a silencer depend on ORC and Abf1p.

98 We propose a silencer-dependent model of lineage choice, whereby inac

99 sly, we reported that the neuron-restrictive silencer element (NRSE) of mu opioid receptor (MOR) func

100 gradient via a conserved Schnurri/Mad/Medea silencer element (SSE) unlike NEEs at brk, sog, rho, and

101 tic stem and progenitor cell (HSPC)-specific silencer element (the Gata1 methylation-determining regi

102 RSF DNA-binding sequence (neuron restrictive silencer element [NRSE]), in vitro and in vivo, reduced

103 and show that it contains a transcriptional silencer element acting on both the AWT1 and WT1-AS prom

104 (ASO) that blocks an SMN2 intronic splicing silencer element and efficiently promotes exon 7 inclusi

105 maining independent causal variant disrupt a silencer element and putatively increase ESR1 and RMND1

106 form a G-quadruplex structure that acts as a silencer element for c-MYC transcriptional control.

107 lation of Cx36 requires a neuron-restrictive silencer element in the Cx36 gene promoter, and the down

108 l analyses show that SNP rs2494737 maps to a silencer element located within AKT1, a member of the PI

109 Loss of expression requires a silencer element previously shown to be controlled by BM

110 Our examples include a particular Dpp Silencer Element upstream of insect brinker genes, in co

111 ed DNA binding motif (the Neuron Restrictive Silencer Element).

112 tone 3'-UTR motif and the neuron-restrictive silencer element, as well as striking examples of novel

113 s by a separate RNA and that the replication silencer element, located within RIV, defines the templa

114 element and a separate, pro-T-cell-specific silencer element.

115 ed the inter-relationship between the UGCAUG silencer elements and the previously identified intronic

116 ure analyses to demonstrate that the two HMR silencer elements are in close proximity and functionall

117 functionally confirmed four enhancer and two silencer elements by performing luciferase reporter assa

118 Strong silencer elements contained a novel CT-rich motif, often

119 xtaposition to one another, and enhancer and silencer elements operate over large distances to regula

120 pression module" and identified enhancer and silencer elements that are likely to be responsible for

121 n, by enabling distal regulatory enhancer or silencer elements to directly interact with proximal pro

122 cruits chromatin-modifying complexes to RE1 'silencer elements', which are associated with hundreds o

123 licing events by the recognition of splicing silencer elements.

124 exonic splicing enhancer and exonic splicing silencer elements.

125 d 37 SRE sets that include both enhancer and silencer elements.

126 es genes subject to control by Mad-dependent silencer elements.

127 stent with the ties functioning as barriers, silencers, enhancers or locus control regions, depending

128 cis-regulatory elements, such as insulators, silencers, enhancers, and promoters, work together to ti

129 on involves long-range communication between silencers, enhancers, and promoters.

130 es due to the function of an exonic splicing silencer (ESS) complex present on the 5' exon RNA.

131 SF2 or to the creation of an exonic splicing silencer (ESS) element that functions by binding of the

132 st all of a diverse panel of exonic splicing silencer (ESS) elements alter splice site choice when pl

133 An exonic splicing silencer (ESS) in the HPV18 nt 612 to 639 region was ide

134 ic analysis revealed that an exonic splicing silencer (ESS) regulated caspase-9 pre-mRNA processing i

135 verts an exonic-splicing enhancer (ESE) to a silencer (ESS), causing frequent exon7 skipping in SMN2

136 splicing enhancers (ESE) and exonic splicing silencers (ESS) in human inherited disease is still poor

137 silencer (ISS), a bipartite exonic splicing silencer (ESS3a/b), and an exonic splicing enhancer (ESE

138 rength of several classes of exonic splicing silencers (ESSs) evolved in a correlated way, whereas sp

139 c splicing enhancers (ESEs), exonic splicing silencers (ESSs), intronic splicing enhancers (ISEs), an

140 uld be designated as enhancers (ESEseqs) and silencers (ESSseqs), with an ESRseq score indicating the

141 Unexpectedly, as a gene silencer, Ezh2 was required to promote the expression of

142 eanalyze Johnson et al.'s neuron-restrictive silencer factor (NRSF) ChIP-Seq data without relying on

143 transcriptional repressor neuron-restrictive silencer factor (NRSF), which negatively regulates Crh g

144 with the function of the neuron-restrictive silencer factor (NRSF/REST), an important transcription

145 ap in vivo binding of the neuron-restrictive silencer factor (NRSF; also known as REST, for repressor

146 We identified the neural-restrictive silencer factor (REST) as a target for modulation of CD5

147 at control degradation of neural-restrictive silencer factor (REST).

148 cing Transcription Factor/Neuron-Restrictive Silencer Factor (REST/NRSF) is a gene-silencing factor t

149 cing transcription factor/neuron-restrictive silencer factor (REST/NRSF) silences neuronal genes in n

150 1-silencing transcription/neuron-restrictive silencer factor (REST/NRSF)--thought to regulate hundred

151 cing transcription factor/neuron-restrictive silencer factor (REST/NRSF).

152 anscription factor (REST)/neuron-restrictive silencer factor is important in a broad range of disease

153 anscription factor]/NRSF (neuron-restrictive silencer factor) actively represses a large array of cod

154 TC-binding factor), NRSF (neuron-restrictive silencer factor) and STAT1 (signal transducer and activa

155 factor (REST; also called neuron restrictive silencer factor) binds to a core group of approximately

156 nscription (also known as neuron-restrictive silencer factor) to position 509 of the KCC2 promoter th

157 ctor (REST; also known as neuron-restrictive silencer factor, NRSF) is a universal feature of normal

158 ctor (REST; also known as neuron restrictive silencer factor, NRSF).

159 ctor (REST; also known as neuron restrictive silencer factor, NRSF).

160 We found that the neuron-restrictive silencer factor, which serves as a master repressor of n

161 In Saccharomyces cerevisiae, silencers flank transcriptionally repressed genes to med

162 In Saccharomyces cerevisiae, silencers flanking the HML and HMR loci initiate the est

163 P rs12038474 is located in a transcriptional silencer for CDC42 and the risk allele increases express

164 re-selection stage is independent of a known silencer for Thpok, and requires the last zinc-finger mo

165 In contrast, H-NS, a global transcriptional silencer, formed two compact clusters per chromosome, dr

166 Confirming the silencer function of ISS-N1, an antisense oligonucleotid

167 of the HML-E silencer is more permissive to silencer function than that of HML-I or HMR-E, despite t

168 ndicating that SAS2 plays a positive role in silencer function.

169 DNA sequence elements, such as enhancers and silencers, function to control the spatial and temporal

170 statistically significant enhancers and five silencers functional in either liver or astrocyte cells,

171 levance of exonic splicing enhancer loss and silencer gain in inherited disease.

172 As a Gli-dependent silencer, GRE1 prevents ectopic transcription of Grem1 d

173 n by antagonizing the global transcriptional silencer H-NS.

174 t al. (2014) determine that the chemogenetic silencer hM4Di-DREADD suppresses presynaptic glutamate r

175 transcription of the HMR locus, a secondary silencer, HMR-I, boosted the level of Sir proteins at HM

176 We compared the abilities of two different silencers, HMR-E and a telomeric repeat, to promote sile

177 The Cd4 silencer impeded this disruption but was not essential f

178 ing enhancers and to disrupt exonic splicing silencers, implying positive selection for these splicin

179 ibition involved binding of pStat3 to a gene silencer in a second conserved enhancer region (enhancer

180 function as an enhancer in one tissue but a silencer in another tissue from the same intronic region

181 tively regulated through activity of the Cd4 silencer in CD4(-)CD8(-) double-negative (DN) thymocytes

182 The ESS1 splicing silencer in CD45 exon 4 confers basal exon skipping in r

183 sal, which revealed a continuous role of the silencer in mature CD8 cells while exposing a remarkable

184 nt functions as an enhancer in neurons and a silencer in nonneuronal cells.

185 rmore, TRIC-induced expression of a neuronal silencer in nutrient-activated cells enhanced stress res

186 ssion by interacting with a newly identified silencer in the c-kit gene.

187 otein-coupled receptor hM4D is a presynaptic silencer in the presence of its cognate ligand clozapine

188 biased experimental search for enhancers and silencers in a 153-kb region containing the human apolip

189 noncanonical nucleic acid structures, act as silencers in the promoter regions of human genes; putati

190 ' splice sites is regulated by enhancers and silencers in the spliced exon.

191 Elimination or weakening of predicted silencers in two reporters consistently promoted use of

192 ent of transcriptionally silent chromatin by silencers in yeast.

193 in 1 (SIRT1), a histone deacetylase and gene silencer, in the eutopic endometrium from women with end

194 2beta with Ikaros to the Cd4 silencer caused silencer inactivation, thereby allowing for CD4 expressi

195 Conserved subelements of the silencer include five short repeated sequences that are

196 The silencer information regulator (Sir) family of proteins

197 of all CREs, including promoters, enhancers, silencers, insulators and transcription factor binding s

198 ry elements, including promoters, enhancers, silencers, insulators, and locus control regions.

199 erent regulatory motifs including enhancers, silencers, insulators, barriers, and boundaries act simi

200 ncreased transcriptional repression, and the silencer is also shown to be an in vitro and in vivo tar

201 e, ARS318 becomes active if the nearby HMR-E silencer is deleted.

202 e positioning in the immediate vicinity of a silencer is independent of its orientation and genomic c

203 Thus, an exonic splicing silencer is involved in the inhibition of splicing of a

204 The context of the HML-E silencer is more permissive to silencer function than th

205 encing in CD8 cells, thus suggesting the Cd4 silencer is not the (only) determinant of heterochromati

206 oncogenic role of EZH2 as a transcriptional silencer is well established; however, additional functi

207 They ensure that the action of enhancers and silencers is restricted to the domain in which these reg

208 partite motif of the human intronic splicing silencer ISS-N1, which controls survival of motor neuron

209 We identify an intronic splicing silencer (ISS) adjacent to the M1 branch point that is s

210 Antisense treatment to SMN2 intron7-splicing silencer (ISS) improves SMN expression and motor functio

211 that ASOs directed against an intron splice silencer (ISS) in the survival motor neuron 2 (SMN2) gen

212 gh a complex network of an intronic splicing silencer (ISS), a bipartite exonic splicing silencer (ES

213 cing enhancers (ISEs), and intronic splicing silencers (ISSs), which are typically located near the s

214 exon 7 and identified two intronic splicing silencers (ISSs): one in intron 6 and a recently describ

215 1 also stimulate the degradation of cellular silencers, it is possible that the promotion of silencer

216 Moreover, ORC could be recruited to the silencers lacking an ACS through its Sir1 interaction.

217 lso binds to an additional intronic splicing silencer, located at the 3' end of intron 10, to promote

218 Silencer mapping in T. delbrueckii revealed single silen

219 50 nucleotides downstream of 3'ss A1; a GGGG silencer motif proximal to 5'ss D2; and an SRp75-depende

220 ucleotide that targets the intronic splicing silencer N1 (ISS-N1), located downstream of the 5' splic

221 bitory region that we term intronic splicing silencer N2 (ISS-N2).

222 neither the initiation of DNA replication at silencers nor the passage of a replication fork through

223 epO, which is the first identified enzymatic silencer of an RRNPP-type quorum-sensing pathway.

224 H-NS appears to act primarily as a silencer of AT-rich genetic material acquired by horizon

225 sion of negative JAK/STAT regulators such as silencer of cell signaling 1 (SOCS1) or protein-tyrosine

226 They further establish Silencer of Death Domains as a novel target for miR-26a,

227 the 3' untranslated region (3'UTR) of SODD (silencer of death domains).

228 BCL11A is a potent silencer of fetal hemoglobin in both mouse and humans.

229 cteria, which functions as a transcriptional silencer of foreign DNA by binding to AT-rich elements,

230 gest that it acts as both an activator and a silencer of gene expression in vivo.

231 ing that H-NS functions as a transcriptional silencer of horizontally acquired genes.

232 An adult stage-specific silencer of the (A)gamma-globin gene was identified betw

233 The RE-1 silencer of transcription (REST) is a transcriptional re

234 er that resembles the binding motif for RE-1 silencer of transcription (REST; also known as NRSF) tra

235 histone deacetylase 2 (PfHda2), is a global silencer of virulence gene expression and controls the f

236 hnRNP H and hnRNP F proteins as being novel silencers of fibroblast growth factor receptor 2 exon II

237 S. cerevisiae Sir1, enriched at the silencers of HMLalpha and HMR A: , was absent from telom

238 22-nucleotide noncoding RNAs that constitute silencers of target gene expression.

239 We identify silencers of the Polycomb group (PcG) as principal contr

240 dentified 456 putative splicing enhancers or silencers, of which 221 were predicted to be tissue-spec

241 development via transient action of the Cd4 silencer; once established, the heterochromatin becomes

242 en reported to function as a transcriptional silencer or activator and to execute these activities th

243 ders or in exonic or intronic RNA regulatory silencer or enhancer elements, as well as in genes that

244 plicing factors with regulatory sites termed silencers or enhancers, RNA-RNA base-pairing interaction

245 nance of epigenetic information in which DNA silencers or nascent RNA scaffolds act as sensors that w

246 Schnurri are required to mediate the ectopic silencer output in the absence of Smad2.

247 In the absence of Runx1 on the silencer, P-TEFb interacts with the transcription comple

248 an inducible proximal promoter, an upstream silencer (PAUSE-1), and a distal transactivator region b

249 We demonstrate that the activity of a silencer pertaining to its potency and directionality is

250 e and potential intersection with epigenetic silencer polycomb repressive complex 2 (PRC2), suggested

251 We conclude that the HML-I and HMR-E silencers promote asymmetric positioning of nucleosomes,

252 Silencers recruit the Sir proteins, which then spread al

253 ed to the telomeric repeat, even though both silencers recruited similar levels of Sir proteins.

254 ochondrial division inhibitor 1 or Drp1 gene silencer reduced mitochondrial fragmentation and increas

255 as2Delta reduces the silencing activities of silencers regardless of their locations and contexts, in

256 eam of the Vkappa genes was increased in the silencer regions upstream of Jkappa1, within the Igkappa

257 A series of splice enhancers and silencers regulate incorporation of SMN2 exon 7; these s

258 exemplifies this process, with enhancer- and silencer-regulated establishment of epigenetic memory fo

259 Two of them, named silencer regulatory sequence 1 (SRS1) and SRS2, are loca

260 TRF2 interacts with the master neuronal gene-silencer repressor element 1-silencing transcription fac

261 also found that the neuronal transcriptional silencer REST is necessary for FBMN migration, and we pr

262 DNA methylation of the silencer results in increased transcriptional repression

263 ays showed that hrp48 protein binding to the silencer RNA can recruit hrp36 and hrp38.

264 eins bind with low affinity to the P-element silencer RNA.

265 These data imply that xDnmt1 has a major silencer role in early Xenopus development before the MB

266 at silencing proteins are first recruited to silencer sequences and then spread from these sites inde

267 recruit limiting Sir3 protein to cis-acting silencer sequences.

268 in silencing: recruitment of Sir proteins to silencers, Sir protein spreading, and transcriptional re

269 treatment of eyes with KA along with a Sarm1 silencer siRNA attenuated KA-mediated degeneration of RG

270 y treating the eyes with KA along with Sarm1 silencer siRNA.

271 ruited by transcription factors bound to the silencers, spread throughout the silenced region.

272 It all comes down to an eighty base pair silencer switch.

273 enhancers and higher frequencies of splicing silencers than average exons.

274 nt splice sites have more enhancers and less silencers than average introns.

275 f decoy splice sites and a higher density of silencers than exons in which splice-site mutation activ

276 of splicing enhancers and lower densities of silencers than their GT 5'ss equivalents.

277 In CD4 cells, Runx1 dissociates from the silencer that has become less accessible, and CD4 transc

278 ors, but p300 recruitment is impaired by the silencer that is associated with the repressor Runx1.

279 ) are involved in the function of a splicing silencer that is created de novo by a total of 83 differ

280 e activation, but Runx1 remains bound to the silencer that retains an open chromatin configuration.

281 ion rely on the function of miRNA, molecular silencers that enact post-transcriptional gene silencing

282 tical strategy is the disruption of splicing silencers that impair exon 7 recognition.

283 e exonic and intronic splicing enhancers and silencers that regulate exon 13 inclusion via trans-acti

284 on of Sir-based silencing, focusing on Sir1, silencers, the molecular topography of silenced chromati

285 sed in macrophages lacking the translational silencer TIA-1.

286 mic function: it activates the translational silencers TIA-1 and TIAR and thus inhibits the translati

287 nner, and could surprisingly replace the Cd4 silencer to induce irreversible Cd4 silencing in CD8 cel

288 histone deacetylase functions as a chromatin silencer to regulate recombination, genomic stability, a

289 The ability of silencers to promote assembly of silenced chromatin over

290 enerate Nb Alb-70-96 named "TNF Receptor-One Silencer" (TROS).

291 nsitive Cd4 allele harboring a removable Cd4 silencer, we found that a tet-controlled repressor recap

292 on-coding RNA XIST functions as a cis-acting silencer when expressed from nine different locations th

293 Sir2p and Sir3p, but not Sir4p, to the HMR-E silencer, where silencing initiates, as well as the effi

294 Each of the four silencers, which flank the silenced loci, includes an or

295 und that H-NS functions as a transcriptional silencer while Ler functions as an antisilencer of LPF e

296 modified duplexes can be highly potent gene silencers, with EC50s in the picomolar concentration ran

297 centrated at and immediately adjacent to the silencers, with lower levels of enrichment over the prom

298 BZLF1 promoter, Zp, are potent transcription silencers within the context of an intact EBV genome.

299 erent combinations of splicing enhancers and silencers without assuming a predefined size or limiting

300 show that the tiRNA-associated translational silencer YB-1 contributes to angiogenin-, tiRNA-, and ox

301 ructures and interact with the translational silencer YB-1.