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1 an ethylene-deficient transgenic line, ACS2-antisense.
2 aracterized long noncoding RNA (lncRNA), SMN-antisense 1 (SMN-AS1), represses SMN2 expression by recr
3 in the consensus two-directional (sense and antisense) "2D" sequences were first characterized by wa
4 ys will aid in the design of next generation antisense agents with improved therapeutic properties.
6 ently for complementation, overexpression or antisense analysis, but sequence changes caused by callu
7 nstrated by the beneficial effect of Cavbeta antisense and gabapentin in allergic airway inflammation
8 reveals a variety of RNAs including numerous antisense and intragenic transcripts, leaderless RNAs, l
9 ing cassettes were constructed around sense, antisense and non-translatable-stop strategies (pGRsense
13 o complementary miRNAs (sense miRNA-122, and antisense antimiR-21) encapsulated in biodegradable poly
14 ions cause retinal degeneration, and show an antisense approach can correct disease-associated phenot
21 isms, with the majority of transcripts being antisense copies of proviruses located within introns.
22 sites can arise at differing frequencies in antisense depending on the overlapping transcript type.
23 fore open new pathways for research into the antisense, diagnostic, and nanotechnology oligonucleotid
26 ctly (p <0.0001) detect the origin (sense vs antisense DNA strands) of DNA methylation at splice site
27 2'-O-methoxyethyl phosphorothioate-modified antisense drug being developed to treat spinal muscular
28 tment with volanesorsen, a second-generation antisense drug targeting apoC-III, were determined in 2
29 or their delivery, and the current status of antisense drug therapy clinical trials for gastrointesti
30 involved in pre-mRNA to mRNA maturation with antisense drugs can lead to efficient gene silencing and
31 ively decreased production of both sense and antisense expanded transcripts, as well as their transla
34 his finding also makes it possible to assess antisense gene regulation efficiency of these brush-DNA
41 s obtained after deletion of Haglr, the Hoxd antisense growth-associated long noncoding RNA (lncRNA)
42 domain of the RNA editing enzyme ADAR to an antisense guide RNA, specific adenosines can be converte
45 ITD(+) AML samples using locked nucleic acid antisense inhibitors, results in an elevated IFN respons
46 neurodegenerative disease associated with an antisense insertion of a SINE-VNTR-Alu (SVA)-type retrot
47 es, the barriers to oral-based therapies and antisense-interfering technologies, the approaches that
48 ding RNA (lncRNA) HOTAIR (for HOX Transcript Antisense Intergenic RNA) mediates a physical interactio
52 the sense protein-coding transcript and the antisense lncRNA increase dramatically in sporozoites.
54 og (PTEN) pseudogene as a model system, that antisense lncRNAs interact first with a 5' UTR-containin
56 te also correlates with the expression of an antisense long non-coding RNA (lncRNA) that has previous
57 tion as distantly-acting control elements of antisense long non-coding RNAs, which in turn regulate t
58 highlight that together with coding genes, (antisense) long non-coding RNAs are deregulated in skin
61 ligonucleotides (SSOs) are short, synthetic, antisense, modified nucleic acids that base-pair with a
63 ss-of-function assays (via microinjection of antisense morpholino or CRISPR-Cas9) confirm that AChE i
64 y, knockdown of zebrafish otg using specific antisense morpholino promoted nuclear accumulation of be
70 SP gene suppression in both wild-types, ACS2-antisense, nor/nor and Nr/Nr, but not the rin/rin mutant
72 pha bioactivity) or knockdown of TNFRI using antisense oligodeoxynucleotide against TNFRI reduced mec
73 eatment of GN mice with connexin 43-specific antisense oligodeoxynucleotide improved functional and s
74 ter intrathecal injection of a gene-specific antisense oligodeoxynucleotide to knock down the express
76 Escherichia coli, we have developed a short antisense oligomer designed to inhibit the expression of
80 ted with disease following treatment with an antisense oligonucleotide (ASO) targeted to the site of
82 For this study, we compared a novel Gen 2 antisense oligonucleotide (ASO) that inhibits angiotensi
83 many as a half million components persist in antisense oligonucleotide (ASO) therapeutics because it
86 pivotal proof of principle that therapeutic antisense oligonucleotide (ASO) treatment can effectivel
89 a mixed modality approach combining an Xist antisense oligonucleotide and a small-molecule inhibitor
91 ect of IONIS-APO(a)-LRx, a ligand-conjugated antisense oligonucleotide designed to be highly and sele
93 d elements involved in mRNA processing using antisense oligonucleotide drugs can be used as a strateg
97 ive subcutaneous injections of placebo or an antisense oligonucleotide targeting ANGPTL3 mRNA in a si
98 pendent clinical trials with drisapersen, an antisense oligonucleotide targeting exon 51: an open lab
101 X011) is a second generation highly specific antisense oligonucleotide that inhibits the production o
104 uppressing MdMYB39L expression in pollen via antisense oligonucleotide transfection significantly red
105 t the combinatorial effect of suboptimal SMN antisense oligonucleotide treatment and PLS3 overexpress
107 atient-derived xenograft (PDX) mouse models, antisense oligonucleotide-mediated (ASO-mediated) skippi
108 geting mast cells in vitro and in vivo using antisense oligonucleotide-mediated exon skipping of the
109 binding sites based on insensitivity to DNA antisense oligonucleotide-mediated RNase H digestion.
113 gene-specific method of NMD inhibition using antisense oligonucleotides (ASOs) and combine this appro
114 hods to suppress expression of mRNAs include antisense oligonucleotides (ASOs) and RNA interference (
121 The ability to control gene expression with antisense oligonucleotides (ASOs) could provide a new tr
125 c loss or systemic knockdown of Malat1 using antisense oligonucleotides (ASOs) in the MMTV (mouse mam
127 Here we show that systemic delivery of Dnm2 antisense oligonucleotides (ASOs) into Mtm1KO mice effic
131 y showed that translation can be enhanced by antisense oligonucleotides (ASOs) that target upstream o
132 The available strategies include the use of antisense oligonucleotides (ASOs) to alter splicing or k
133 ng approach to treat DM1 uses DMPK-targeting antisense oligonucleotides (ASOs) to reduce levels of to
134 this issue of the JCI, successfully utilized antisense oligonucleotides (ASOs) to reduce PMP22 and am
136 ll-interfering (siRNAs), microRNAs (miRNAs), antisense oligonucleotides (ASOs), aptamers, synthetic m
139 scular dystrophy (DMD), employing morpholino antisense oligonucleotides (PMO-AO) to exclude disruptiv
140 r functional inhibition by sequence-specific antisense oligonucleotides allows the unprecedented telo
141 hip between in vivo inhibition of miR-182 by antisense oligonucleotides and improved post-injury kidn
144 lly in areas of myofiber regeneration, where antisense oligonucleotides are stored in macrophages and
145 cacy, safety, and tolerability of two unique antisense oligonucleotides designed to lower Lp(a) conce
146 o its first human clinical trial, with other antisense oligonucleotides expected to enter trials in t
147 hermore, delayed administration of periostin antisense oligonucleotides in wild-type animals with GN
148 iated delivery of phosphorothioated TRAF3IP2 antisense oligonucleotides into the LV in a clinically r
152 peptide-phosphorodiamidate morpholino (PPMO) antisense oligonucleotides that induced temporary dystro
153 d on a modular hybrid minigene combined with antisense oligonucleotides to enable verification of fun
157 lly manipulated CD46 exon 13 inclusion using antisense oligonucleotides, opening up opportunities for
158 the RNA-binding protein Nanos2 by morpholino antisense oligonucleotides, or knockout of the Nanos2 ge
161 cer therapy, we here report the synthesis of antisense-oligonucleotides (ASO) and thyroid hormone T3
163 ic banana plants repressing either gene (via antisense or RNA interference [RNAi]) were created and e
166 ermine their combined activities, and in the antisense orientation to measure enhancer activities alo
167 l conserved long noncoding RNAs expressed in antisense orientation to myocardial transcription factor
168 NG12-AS1, a nuclear lncRNA transcribed in an antisense orientation to the tumour-suppressor DIRAS3.
169 ulating the self-regulatory circuit of sense-antisense pairs and the exon skipping during alternative
170 NAs can work as regulatory agents beyond the antisense paradigm and that, hence, they could be interf
174 ns, astrocytes, and glia in gray matter, and antisense QAGR proteins accumulate within white matter.
175 A PARTICLE (Gene PARTICL- 'Promoter of MAT2A-Antisense RadiaTion Induced Circulating LncRNA) partakes
181 that the long non-coding RNA HOX transcript antisense RNA (HOTAIR) is overexpressed in pancreatic ca
182 r region drive the overexpression of a novel antisense RNA and contribute to the development of lymph
183 similarly decreased production of sense and antisense RNA foci, as well as DPR proteins, in patient
184 strand and the relative chance of degrading antisense RNA in the other strand-in the same regions of
185 Our results provide direct evidence that L1 antisense RNA plays a functional role in chromosome-wide
186 egrations driving overexpression of the TERT antisense RNA suggest it may have a role in tumorigenesi
187 t al that proposes regulating Wilm's tumor-1 antisense RNA to control pathological bone resorption.
188 n-coding RNA (lncRNA) HOTAIR (HOX transcript antisense RNA) have diverse functional roles in cancer.
189 studies of the lncRNA HOTAIR (HOX transcript antisense RNA) provide compelling evidence for therapeut
190 romoter for the transcription of a noncoding antisense RNA, asDOG1, that is 5' capped, polyadenylated
191 genetic tools, along with optimized RBSs and antisense RNA, we engineered B. marmarensis to produce e
193 s this, we demonstrate how naturally derived antisense RNA-mediated transcriptional regulators can be
197 replication cohorts, respectively] and PROX1-antisense RNA1 (PROX1-AS1: rs1891059, P = 2.28 x 10(-7)
198 em from Streptococcus pyogenes and synthetic antisense RNAs (asRNAs) in Escherichia coli strains to r
201 ivo, but it is unknown whether the resultant antisense RNAs are a mechanistic by-product of RNA polym
202 siae, results in transcription initiation of antisense RNAs embedded within body of protein-coding ge
203 ng to protein-coding genes, long ncRNAs, and antisense RNAs were due to DNA contamination on the surf
206 we used a pairwise partial loss of function antisense screen for embryonic brain morphology, using t
208 that promotes base pairing between the FinP antisense sRNA and the traJ mRNA to control F plasmid tr
209 r fusion leads to the generation of abundant antisense sRNAs that map to the target gene, with silenc
213 chromosome-wide effects of ASAR6 map to the antisense strand of an L1 retrotransposon within ASAR6 R
215 non-coding RNA (lncRNA) that arises from the antisense strand of SMN, SMN-AS1, which is enriched in n
218 This putative protein is encoded on the antisense strand of the provirus genome and entirely ove
219 s approach is complicated by the presence of antisense strand transcription of expanded GGCCCC repeat
221 ral C4'alpha-epimer monomers in the sense or antisense strands triggered RNAi-mediated gene silencing
226 ne expression or to modify RNA splicing, but antisense technology has not previously been used to dir
227 of USH1C and reveal the potential for using antisense technology to treat vestibular dysfunction.
228 e DM2 CCTGCAGG expansion expresses sense and antisense tetrapeptide poly-(LPAC) and poly-(QAGR) RAN p
230 revented by intrathecal oligodeoxynucleotide antisense to CD44 mRNA, which also prevents hyperalgesia
242 we characterize a broadly expressed natural antisense transcript at the MALAT1 locus, designated as
243 sense transcripts and initiation of a novel antisense transcript downstream of the sgRNA/dCas9-bindi
244 n convergent genes lead to starkly different antisense transcript landscapes between budding and fiss
246 RNA sequencing, we identified 1769 sense and antisense transcript pairs (NAT pairs) in two maize inbr
247 4.32 x 10-10 for the meta-analysis) in novel antisense transcript RP11-206M11.7;rs146091982 (beta = 0
248 , the long-noncoding RNA PEAT (Pax1 enhancer antisense transcript) was induced in sclerotome-directed
249 intergenic RNA, small nucleolar RNA, natural antisense transcript, small nuclear RNA, and small RNA u
253 a13 domain relies on an enhancer that drives antisense transcription at the Hoxa11 locus after activa
255 AFs have also been recently found to enhance antisense transcription from the 3' end of the GAL10 cod
256 t sense transcription did not interfere with antisense transcription from the 3' LTR and vice versa,
257 Spt5 depletion also results in widespread antisense transcription initiating within this barrier r
258 argeted recruitment of NuA4 KAT to the GAL10 antisense transcription initiation site promotes GAL10 a
260 f the ribosomal protein genes, TAF-dependent antisense transcription of GAL10 also requires NuA4 KAT.
262 nally, we show that the enhancer that drives antisense transcription of the mouse Hoxa11 gene is abse
264 as9 targeting to the non-template strand for antisense transcription results in antisense transcripti
265 trand for antisense transcription results in antisense transcription termination, premature terminati
268 chromatin regulatory factors in controlling antisense transcription, thus illuminating chromatin reg
269 ion of sense transcription without affecting antisense transcription, which may be important for long
270 one H2B ubiquitin conjugase facilitate GAL10 antisense transcription, while the Swi/Snf and SAGA chro
271 f a primary molecule by uridylation-induced, antisense transcription-controlled 3'-5' exonucleolytic
276 r results indicate that, among the sense and antisense transcriptomes of these organs, the sense tran
279 Furthermore, we discovered that natural antisense transcripts (NATs) frequently have actively tr
280 ng noncoding RNAs (lncRNAs) that are natural antisense transcripts (NATs) to transcripts encoding cen
281 d transcript isoforms, including eight novel antisense transcripts and their isoforms, as well as a n
282 HSV-1-induced and constitutively transcribed antisense transcripts are highly similar, indicating tha
285 t HSV-1 induces the expression of about 1000 antisense transcripts from the human host cell genome.
286 n at TEs, resulting in an abundance of sense/antisense transcripts leading to high levels of ARGONAUT
290 nsertion mutants reveal that they can act as antisense transcripts to repress expression levels of se
291 ive transcription, a genome-wide increase in antisense transcripts, and a rapid loss of viability of
300 of SMA therapies, and systemically delivered antisense treatment, completely rescued liver pathology.
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