ライフサイエンスコーパス: antisense

1 nuclease stability, and specificity of their antisense action, which involves activation of cellular

2 therapeutic index with minimal impairment of antisense activity.

3 o the protein-coding genes, particularly for antisense and intronic lncRNAs.

4 cular diagnostics, and show promise for both antisense and RNAi therapy.

5 NAs can be degraded using ASOs, adding a new antisense approach to modulation of gene expression.

6 StMSI1-OE and StBMI1-1-antisense (AS) lines produced pleiotropic effects, inclu

7 tudy by Deng and colleagues revealed that an antisense (AS) long noncoding RNA named GLS-AS, which is

8 al administration of an oligodeoxynucleotide antisense (AS-ODN) to mRNA for cluster of differentiatio

9 X3X directly binds to (GGGGCC)n RNAs but not antisense (CCCCGG)n RNAs.

10 lencing of cerebellar degeneration-related 1 antisense (CDR1as), a regulator of miR-7, as a hallmark

11 In contrast, antisense cheRNA (as-cheRNA) may play a role in local ge

12 ncreased distal versus proximal ratio of its antisense COOLAIR transcript.

13 function in the formation of the FLC-derived antisense COOLAIR transcripts.

14 ethod, a vivo morpholino (VMO) piggybacks an antisense deoxyoligonucleotide (dO) into the somatic cel

15 ontains a gene expressed in the opposite, or antisense, direction to all other genes.

16 constructs, comprised of spherically-arrayed antisense DNA (liposomal spherical nucleic acids [L-SNAs

17 One antisense drug, nusinersen, has been approved for the tr

18 Most antisense drugs are chemically modified to enhance their

19 Antisense drugs are currently in development for the tre

20 in part on the early success of nusinersen, antisense drugs hold great promise as a therapeutic plat

21 ses, tolerability of intrathecally delivered antisense drugs, and the biodistribution of intrathecal

22 and the biodistribution of intrathecal dosed antisense drugs.

23 The site of methylation is determined by antisense elements in the box C/D RNAs that are compleme

24 ORD97 and CB box C/D scaRNA SCARNA97 contain antisense elements that target the wobble cytidine at po

25 umerous box C/D RNAs in mammalian cells lack antisense elements to rRNAs or snRNAs; thus, their targe

26 ic cause of ALS and FTD, produces sense- and antisense-expansion RNAs and six dipeptide repeat-associ

27 sion enhances the lam1 mutant phenotype, and antisense expression partially rescues the lam1 mutant,

28 The protein product of this antisense gene, called ASP, is poorly characterized, and

29 tional agents, triple therapies that include antisense HK2 oligonucleotides, metformin, and perhexili

30 localizes with the expression of the IL6 RNA antisense in various tissues.

31 s well as injection of miR-19a/b and miR-20a antisense inhibitors into wound edges enhanced inflammat

32 pression data that captures promoter-derived antisense initiation, we find that H2A.Z's bimodal incor

33 CD39-specific antisense is increased in Treg and Th17-cells of Crohn's

34 Antisense knockdown of slincR results in an increase in

35 ession of human vtRNA1-1 inhibits, while its antisense LNA-mediated knockdown enhances p62-dependent

36 We show that these antisense lncRNA can be generated by R-loops that form w

37 cilitate the synthesis of many gene proximal antisense lncRNA.

38 of structural and sequence components of the antisense lncRNA.

39 ith either Kdm6b small interfering RNA or an antisense locked nucleic acid oligonucleotide specific t

40 binding site that controls expression of the antisense long noncoding RNA (lncRNA) CCR5AS.

41 Transcription of an antisense long noncoding RNA (lncRNA) from this antisens

42 Widespread antisense long noncoding RNA (lncRNA) overlap with many

43 study of three patients with this syndrome, antisense-mediated inhibition of hepatic APOC3 mRNA with

44 Antisense-mediated knockdown of endogenous ssbp1 messeng

45 Here we demonstrate that antisense-mediated modulation of pre-mRNA splicing can i

46 Effective delivery of therapeutic antisense micro-ribonucleic acid (antimiR) molecules to

47 tand the structural differences in sense and antisense microRNA-21 by hybridizing them with complemen

48 Inhibition/blockade of antisense might represent a therapeutic strategy to rest

49 ticles co-loaded with antisense-miRNA-21 and antisense-miRNA-10b to pig liver and kidney.

50 delivering PLGA nanoparticles co-loaded with antisense-miRNA-21 and antisense-miRNA-10b to pig liver

51 lences proximal PASs and its inhibition with antisense morpholino oligonucleotides (U1 AMO) triggers

52 Knockdown of msmb3 with antisense morpholino oligonucleotides or disruption of m

53 Antisense morpholino oligonucleotides were targeted to C

54 with a small number shown to be involved in antisense mRNA mediated gene regulation.

55 Gill et al. show that transcription of antisense ncRNAs induces 'elongation marks' on histones

56 thway from length changes and the effects of antisense oligomers blocking formation of specific conta

57 resent a study of systemic treatment with an antisense oligonucleotide (ASO) (ISIS 486178) targeted t

58 olated from nusinersen-treated SMA patients, antisense oligonucleotide (ASO) concentration and full-l

59 Here we describe an antisense oligonucleotide (ASO) directed against human H

60 Antisense oligonucleotide (ASO) drugs that trigger RNase

61 ation and high sensitivity identification of antisense oligonucleotide (ASO) impurities using a Q-Exa

62 Enhancing the functional uptake of antisense oligonucleotide (ASO) in the muscle will be be

63 uterine microinjection of a splice-switching antisense oligonucleotide (ASO) into the amniotic cavity

64 ion following treatment of SCA2 mice with an antisense oligonucleotide (ASO) lowering ATXN2 expressio

65 approach, we found that administration of an antisense oligonucleotide (ASO) targeting mTORC2's defin

66 Recently, nusinersen, an antisense oligonucleotide (ASO) that corrects SMN2 splic

67 deletion can be effectively treated using an antisense oligonucleotide (ASO) that induces exon skippi

68 pping of the mutated exon c.5668 G > T using antisense oligonucleotide (ASO) therapy leads to restora

69 In this study, we utilized an antisense oligonucleotide (ASO) to reduce IDOL expressio

70 Conjugation of antisense oligonucleotide (ASO) with a variety of distin

71 he abundance of the Scn8a transcript with an antisense oligonucleotide (ASO) would delay seizure onse

72 Nusinersen, a splice-switching antisense oligonucleotide (ASO), was the first approved

73 We recently showed that antisense oligonucleotide (ASO)-mediated PrP suppression

74 or mice were treated with vehicle or control antisense oligonucleotide (ASO-CON) or ASO specific for

75 t progress in understanding phosphorothioate antisense oligonucleotide (PS-ASO) interactions with pro

76 A base-pairing, which can be disrupted by U1 antisense oligonucleotide (U1 AMO), triggering PCPA.

77 yde cross-linking of leaf tissue followed by antisense oligonucleotide affinity capture of psbA mRNA;

78 Patients received the hepatocyte-directed antisense oligonucleotide AKCEA-APO(a)-L(Rx), referred t

79 g exon skipping in these transcripts through antisense oligonucleotide delivery in wild-type islets r

80 IONIS-PKK-L(Rx) is a ligand-conjugated antisense oligonucleotide designed for receptor-mediated

81 IONIS-HTT(Rx) (hereafter, HTT(Rx)) is an antisense oligonucleotide designed to inhibit HTT messen

82 manufacture of milasen, a splice-modulating antisense oligonucleotide drug tailored to a particular

83 Finally, we summarize antisense oligonucleotide drugs that have already been a

84 ing PCR specificity, and we cage a biostable antisense oligonucleotide for time-release activation an

85 an optimized, synthetic locked nucleic acid antisense oligonucleotide inhibitor (antimiR-132).

86 Antisense oligonucleotide knockdown (ASO-KD) of nicotina

87 ly, treating both mouse models with an APOC3 antisense oligonucleotide lowered both plasma APOC3 and

88 Treatment with the antisense oligonucleotide nusinersen has been shown to i

89 oped QR-313, a clinically applicable, potent antisense oligonucleotide specifically targeting exon 73

90 ly, the first human trial of an HTT-lowering antisense oligonucleotide successfully, and safely, redu

91 A first-in-class HK2 antisense oligonucleotide suppresses HK2 expression in c

92 pendent clinical trials with drisapersen, an antisense oligonucleotide targeting exon 51: an open lab

93 Tofersen is an antisense oligonucleotide that mediates the degradation

94 The approval of an antisense oligonucleotide therapy for SMA was an importa

95 3140969 ) with intravitreal injections of an antisense oligonucleotide to restore correct splicing.

96 rnal administration of a locked nucleic acid antisense oligonucleotide to young-adult aspartoacylase-

97 d by pharmacological inhibition and targeted antisense oligonucleotide treatment, which normalized mi

98 Two different antisense oligonucleotide-based (ASO-based) therapies ar

99 Indeed, antisense oligonucleotide-based exon skipping has shown

100 Distinct and complementary antisense oligonucleotide-based strategies aiming at int

101 In just the past 5 years, over 100 antisense oligonucleotide-based therapies have been test

102 at1 RNA is responsible for these effects, as antisense oligonucleotide-mediated inhibition of Malat1

103 atherosclerotic mice during apolipoprotein B antisense oligonucleotide-mediated lipid lowering.

104 an be tightly regulated by a steric-blocking antisense oligonucleotide.

105 atment with peptide-conjugated exon skipping antisense oligonucleotides (20-week regimen), resulted i

106 ons in the DMD gene can be modified by using antisense oligonucleotides (AONs) to promote skipping of

107 at the subcutaneous administration of Notch2 antisense oligonucleotides (ASO) down-regulates Notch2 a

108 Matrix metalloproteinase 9 (MMP-9) antisense oligonucleotides (ASO) or an MMP inhibitor wer

109 rotensin to improve the productive uptake of antisense oligonucleotides (ASO), we synthesized neurote

110 Antisense oligonucleotides (ASOs) are chemically synthes

111 at gene targeting 2'-O-methyl (2'OMe) gapmer antisense oligonucleotides (ASOs) can have opposing acti

112 Here, we demonstrate that antisense oligonucleotides (ASOs) can reduce mRNA levels

113 e role of PS chirality on the performance of antisense oligonucleotides (ASOs) has been a subject of

114 Antisense oligonucleotides (ASOs) have been under intens

115 Splice-switching antisense oligonucleotides (ASOs) have emerged as an eff

116 Antisense oligonucleotides (ASOs) interact with target R

117 Among various treatments available for DMD, antisense oligonucleotides (ASOs) mediated exon skipping

118 Antisense oligonucleotides (ASOs) modulate cellular targ

119 hanisms, we investigated the impact of Apoc3 antisense oligonucleotides (ASOs) on lipoprotein metabol

120 is well-established that cellular uptake of antisense oligonucleotides (ASOs) proceeds through the e

121 Antisense oligonucleotides (ASOs) targeting pathologic R

122 to reduce gene expression is via the use of antisense oligonucleotides (ASOs) that harness the RNase

123 Antisense oligonucleotides (ASOs) that trigger RNase-H-m

124 ey anti-CoV NA-based technologies, including antisense oligonucleotides (ASOs), siRNAs, RNA-targeting

125 Using non-cleaving antisense oligonucleotides (ASOs), we selectively blocke

126 Splice-switching antisense oligonucleotides (ASOs), which bind specific R

127 rties of nucleic acid-based drugs, including antisense oligonucleotides (ASOs).

128 proteins with phosphorothioate (PS) modified antisense oligonucleotides (ASOs).

129 acokinetic and pharmacodynamic properties of antisense oligonucleotides (ASOs).

130 city of chemically modified phosphorothioate antisense oligonucleotides (PS-ASOs) are not fully under

131 Release of phosphorothioate antisense oligonucleotides (PS-ASOs) from late endosomes

132 Phosphorothioate-modified antisense oligonucleotides (PS-ASOs) interact with a hos

133 ckbone to enable construction of sulfonamide antisense oligonucleotides (SaASOs).

134 (ie, using hepcidin activators like Tmprss6-antisense oligonucleotides [ASOs]) or increase erythropo

135 eated intraperitoneally with LDLR- and SRB1- antisense oligonucleotides and fed a high cholesterol di

136 own and overexpression were undertaken using antisense oligonucleotides and overexpression plasmids.

137 major classes of agents have been developed-antisense oligonucleotides and small interfering RNA.

138 this barrier and enable topical delivery of antisense oligonucleotides capable of specifically targe

139 Gene-specific blocking of EJC deposition by antisense oligonucleotides circumvents aberrant NMD prom

140 trum pan-ErbB inhibitors or erbb4a-targeting antisense oligonucleotides demonstrated reduced locomoti

141 TriMV IRES activity, as did the delivery of antisense oligonucleotides designed to block YX-AUG acce

142 ully conserved in humans and designed custom antisense oligonucleotides for these candidate targets.

143 However, the suitability of antisense oligonucleotides for treatment of DDEB remains

144 By knocking down expression of K-Ras using antisense oligonucleotides in a mouse model of chronic f

145 conclusion, targeting K-Ras expression with antisense oligonucleotides in a mouse model of CKD preve

146 arkably, lowering nigral SRY expression with antisense oligonucleotides in male rats diminished motor

147 istration of a single dose of Plp1-targeting antisense oligonucleotides in postnatal jimpy mice fully

148 er, intracerebroventricular injection of two antisense oligonucleotides in wild-type mice leads to a

149 Depletion of EZH2 by antisense oligonucleotides inhibited p53 GOF mutant-medi

150 de effect of translation-blocking morpholino antisense oligonucleotides is the induction of a set of

151 Treatment with RIPK1 antisense oligonucleotides led to a reduction in aortic

152 Conversely, selective TGLI1 knockdown using antisense oligonucleotides led to decreased breast cance

153 splicing of BRD9 in SF3B1-mutant cells using antisense oligonucleotides or CRISPR-directed mutagenesi

154 down of dominant disease-causing genes using antisense oligonucleotides or inhibitory RNAs, delivery

155 Antisense oligonucleotides represent a novel therapeutic

156 Finally, in vivo administration of antisense oligonucleotides targeting HERNA1 protected mi

157 the invasive growth of glioma, we find that antisense oligonucleotides targeting lncGRS-1 selectivel

158 Localized delivery of antisense oligonucleotides targeting miR-23a and miR-155

159 Antisense oligonucleotides targeting multiple types of n

160 Antisense oligonucleotides targeting the same lncRNAs ex

161 ribe the engineering of chemically optimized antisense oligonucleotides that recruit endogenous human

162 al potential of this strategy, we identified antisense oligonucleotides that stably decrease the leve

163 Many of these efforts employ antisense oligonucleotides to alter pre-mRNA splicing or

164 We administered weekly injections of RIPK1 antisense oligonucleotides to Apoe(-/-) mice fed a chole

165 Finally, we develop splice-switching antisense oligonucleotides to reverse the increased skip

166 ed by converting astrocytes to neurons using antisense oligonucleotides to transiently suppress PTB.

167 Selective delivery of TRIM37-specific antisense oligonucleotides using antifolate receptor 1-c

168 The protective effect of the SRY antisense oligonucleotides was associated with male-spec

169 Antisense oligonucleotides were used to inhibit miRNAs.

170 huntingtin-lowering approaches such as RNAi, antisense oligonucleotides, and small-molecule splicing

171 ase-causing r(CUG)(exp) has been targeted by antisense oligonucleotides, CRISPR-based approaches, and

172 Further work could bring antisense oligonucleotides, deep brain stimulation, and

173 , whether by direct targeting of SREBP1 with antisense oligonucleotides, or through combinatorial eff

174 s for hearing loss such as gene replacement, antisense oligonucleotides, RNA interference and CRISPR-

175 es (e.g. antibodies) or new modalities (e.g. antisense oligonucleotides, siRNA or PROTAC), feasibilit

176 Antisense oligonucleotides, which were designed based on

177 ormonal manipulation and gene silencing with antisense oligonucleotides.

178 Extracellular application of antisense oligos of FNDC3B and CTSS transcripts inhibits

179 for cell-type specificity of maxRNA, we use antisense oligos to hybridize to single-stranded transcr

180 RNA-based tools such as siRNA, antisense oligos, and morpholinos can be used to silence

181 Both antisense only (ASO)-R-loops and sense/antisense (S/AS)-

182 could be reversed with either CTS, the Cx43 antisense or AKT inhibitor.

183 tive correlation for the expression of sense-antisense pairs, whereas paralogs and divergent transcri

184 ecific Therapeutic (FAST) platform to create antisense peptide nucleic acids (PNAs), gene-specific mo

185 n was performed using a previously described antisense peptide-conjugated phosphorodiamidate morpholi

186 uided to another subset of neoblast mRNAs by antisense piRNAs and binds these without degrading them.

187 iRNA response suppresses transposition until antisense piRNAs are produced, establishing sequence-spe

188 as endogenous viral elements (EVEs), produce antisense piRNAs that are preferentially loaded onto Piw

189 of complementarity between target mRNAs and antisense piRNAs.

190 Antisense Piwi-interacting RNAs (piRNAs) guide silencing

191 piRNAs drive ping-pong amplification of the antisense pool, but how the germline responds to genome

192 isense long noncoding RNA (lncRNA) from this antisense promoter extends through the sense promoter, l

193 ha gene choice involves the activation of an antisense promoter located in the first exon of each Pcd

194 with genetic errors, including cryptic sense/antisense promoters and translation, attenuation, incorr

195 strand of HIV-1 encodes a highly hydrophobic antisense protein (ASP) with no known homologs.

196 We provide evidence that the antisense protein, ASP, of HIV-1 is found within the cel

197 In vivo RNA Antisense Purification (RAP-MS) identifies YBX1 as a dir

198 Using RNA antisense purification and mass spectrometry, we identif

199 Using RNA antisense purification coupled with quantitative mass sp

200 RNA affinity antisense purification-mass spectrometry (RAP-MS) reveal

201 However, the frequency of the antisense RAN translation product poly(PR) is comparable

202 vidence for wide-spread post-transcriptional antisense regulation.

203 ts regulate the expression of both sense and antisense repeats.

204 e, we demonstrate an essential role of GATA6 antisense RNA 1 (GATA6-AS1) in cardiomyocyte differentia

205 (DeltaSUB1) mRNA using SUB1 single-stranded antisense RNA coupled with human Argonaute 2.

206 ses, including transcriptional interference, antisense RNA interactions between the mRNAs of the two

207 Instead, antisense RNA interactions seem to be the system's drivi

208 HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1) is a long no

209 e prospects of nanoparticles, immunotherapy, antisense RNA, and drug-resistance-modulation approaches

210 that relies on the presence of an endogenous antisense RNA, transcribed from the 3'-end of the human

211 n antitoxin, which, in type I systems, is an antisense RNA.

212 ue transcription units and detects prevalent antisense RNA.

213 art and neural crest derivatives expressed 2 antisense RNA1, a noncoding gene related to cardiovascul

214 ng, poorly translated mRNAs, small RNAs, and antisense RNAs are the main substrates, while rRNA, tRNA

215 entified E(2)-induced and RNase H1-sensitive antisense RNAs located at the 5' and 3' ends of the E(2)

216 ut functional elements e.g. small RNAs, long antisense RNAs or untranslated regions (UTRs) of mRNA tr

217 xpressed between the two ecotypes, including antisense RNAs targeting key regulators of root-growth r

218 d ~200 long, unspliced and exosome-sensitive antisense RNAs that arise from transcription start sites

219 cus aureus, including transcription factors, antisense RNAs, and host elements.

220 epresented among loci with exosome-sensitive antisense RNAs, suggesting a potential for widespread co

221 and searched for the presence of RAPs within antisense RNAs.

222 by a non-translated retrotransposon-like one antisense (Rtl1as) transcript that are decreased in the

223 Both antisense only (ASO)-R-loops and sense/antisense (S/AS)-R-loops sharply peaked around transcrip

224 Antisense silencing results in CD39 upregulation in vitr

225 rGrArGrGrArUrArGrArArUrG-3'), the luciferase antisense siRNA.

226 omachine over other gene therapy approaches (antisense, siRNA, and CRISPR/cas) is its ability to clea

227 21-nt phased siRNAs (phasiRNAs) and natural antisense siRNAs (nat-siRNAs), which direct cleavage of

228 ize and represented a subset of the cellular antisense small RNA population that has previously been

229 RAPs coordinate Rho activity at the antisense strand and terminate antisense transcripts.

230 e of a single 5'p-rN1-(2'-5')-N2 unit in the antisense strand does not alter the 'clover leaf' bend a

231 vestigate 3' exonuclease activity toward the antisense strand metabolism.

232 Extensive modification of the antisense strand minimally affected 5'-phosphorylation o

233 iated up-regulation of MALAT1 as well as its antisense strand TALAM1 occurs in breast cancer cells, b

234 sidues were detrimental at the 5' end of the antisense strand, the siRNAs with ANA at position 6 or 7

235 e strand, but only at a few positions in the antisense strand.

236 a-sensitive quantification of both sense and antisense strands of siRNA independent of structural mod

237 Sense and antisense strands of the parent duplex were synthesized

238 porated at the tested positions of sense and antisense strands.

239 We used a morpholino antisense strategy to knock down the beta1 or beta3 inte

240 sticity on cued heroin seeking, a morpholino antisense strategy was used to knock down expression of

241 Cdk9-dependence of antisense suppression at specific genes correlates with

242 Antisense targeting and genetic ablation of miR-128-1 in

243 Antisense technology can reduce gene expression via the

244 ucleotide class provides a powerful tool for antisense technology.

245 es, which may represent a promising group of antisense therapeutic agents.

246 r virus function, as well as new targets for antisense therapeutics.

247 al for many fields spanning from genomics to antisense therapy and diagnostics.

248 The seed sequences for these miRNAs are antisense to each other and are transcribed from diverge

249 g a new class of viral lytic RNA transcripts antisense to latent EBNAs, we provide a novel mechanism

250 r VZVsncRNA clustering in and near ORF61 and antisense to the latency-associated transcript of VZV ca

251 cting small RNAs (piRNAs), some of which are antisense to the nxf2 transcript, and that the TART-like

252 Intrathecal oligodeoxynucleotide antisense to TLR4 mRNA (TLR4 AS-ODN) prevented OIH and p

253 chX repeats produce abundant piRNAs that are antisense to vasa; however, vasa mRNA escapes silencing

254 LNAA to the four VZVsncRNA antisense to VLT significantly reduced viral spread and

255 NA (VZVsncRNA10, -11, -12, and -13) that are antisense to VLT, a transcript made in lytic infections

256 These results suggest that sncRNA antisense to VZV may regulate VZV growth, possibly by af

257 tandem-Tr1 anchored to the beads through the antisense Tr2 linker and vice versa.

258 ressed in many tumor types together with its antisense transcribed pseudogene RPSAP52.

259 ing to the long noncoding RNA (lncRNA) BACE1-antisense transcript (BACE1-AS), resulting, in turn, in

260 n is mediated by the frequency (frq) natural antisense transcript (NAT) qrf.

261 restricted to neurons by expression of UBE3A antisense transcript (UBE3A-ATS) from the paternally inh

262 uld trigger phasiRNA production from its own antisense transcript and the derived phasiRNAs might rev

263 We identify XSR, an RSX antisense transcript expressed from the active X chromos

264 e, we showed that loss of the paternal Ube3a antisense transcript resulted in both unique and overlap

265 ntified COMET (Correlated-to-MET), a natural antisense transcript that was highly expressed in carcin

266 potently silenced an axis of CDR1as and its antisense transcript, cerebellar degeneration related pr

267 Gm15441 expression suppresses its antisense transcript, encoding thioredoxin interacting p

268 Natural antisense transcript-derived small interfering RNAs (nat

269 ally in reverse direction, thus producing an antisense transcript.

270 of inhibitory RAPs (iRAPs) in modulation of antisense transcription (AT) using in silico and in vivo

271 Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse

272 regulation of viral gene expression by EBNA-antisense transcription during lytic EBV infection.

273 sets; ablation of both pathways de-represses antisense transcription of over half the genome.

274 inhibition or H2Bub1 loss induces intragenic antisense transcription of ~10% of fission yeast genes,

275 upstream and downstream of genes, increased antisense transcription overlapping gene bodies, and red

276 At Arabidopsis thaliana FLC, antisense transcription quantitatively influences transc

277 Hypomethylation of genes also activates antisense transcription, which is modestly enhanced by H

278 Thus, antisense transcription-mediated promoter demethylation

279 tely considered as a +1 H2A.Z nucleosome for antisense transcription.

280 expression causes the selective reduction of antisense transcription.

281 We revisited the antisense transcriptome in cells with impaired AT regula

282 Cis-Natural Antisense Transcripts (cis-NATs), which overlap protein

283 romosomes, are testis-expressed, and produce antisense transcripts and short RNAs.

284 Proximal polyadenylation of the antisense transcripts by FCA, an RNA-binding protein tha

285 ental expression patterns of Ube3a sense and antisense transcripts by postnatal day 2 (P2) in hypotha

286 The increase of antisense transcripts from the cluster at 29 degrees C c

287 Moreover, levels of sense and antisense transcripts increase at boundaries of PTUs in

288 We show that FACT and H2Bub globally repress antisense transcripts near the 5' end of genes and insid

289 Antisense transcripts originate either at gene promoters

290 The expression of these novel antisense transcripts to EBNA were verified by 3' rapid

291 tivities for proximal polyadenylation of the antisense transcripts to FLD/LD/SDG26-associated H3K4 de

292 rmation about potentially novel transcripts (antisense transcripts, alternative splice isoforms, and

293 cripts resembling enhancer RNAs, pri-miRNAs, antisense transcripts, and promoter upstream transcripts

294 expressed during latency, expression of EBNA-antisense transcripts, which is restricted in latent cel

295 tivity at the antisense strand and terminate antisense transcripts.

296 ular coloboma phenotype following morpholino antisense translation-blocking knockdown and downstream

297 tative primary piRNA transcripts overlapping antisense transposons.

298 hile being organized as an overlapping sense/antisense unit.

299 we identify de novo production of sense and antisense ZAM-derived piRNAs that display a germinal mol

300 polymerase chain reaction assay that targets antisense ZIKV RNA (asRNA) to assess ZIKV replication co