ライフサイエンスコーパス: antisense oligonucleotide

1 fter 4 weeks of treatment with the anti-Apob antisense oligonucleotide.

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

3 es are mainly induced by chemically modified antisense oligonucleotides.

4 CRISPR/Cas9 or by knocking down UBE3A using antisense oligonucleotides.

5 ical trials in patients treated with miR-122 antisense oligonucleotides.

6 ed by targeting SRSF1 sites on exon 11 using antisense oligonucleotides.

7 m and validated their function in vivo using antisense oligonucleotides.

8 purposes using locked nucleic acid-modified antisense oligonucleotides.

9 interfering RNA (siRNA), microRNA (miRNA) or antisense oligonucleotides.

10 nted when CREB was depleted in these rats by antisense oligonucleotides.

11 ormonal manipulation and gene silencing with antisense oligonucleotides.

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

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

14 brain region in the learning, infusion of an antisense oligonucleotide against Arc into the shell imp

15 that Star:Star-mPEG mediated delivery of an antisense oligonucleotide against miR-145 (antimiR-145)

16 methyl-D-aspartate receptor antagonist or an antisense oligonucleotide against the activity-regulated

17 th/without the SIRT1 inhibitor nicotinamide, antisense oligonucleotides against SIRT1 (SIRT1-ASO), IL

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

19 r functional inhibition by sequence-specific antisense oligonucleotides allows the unprecedented telo

20 a mixed modality approach combining an Xist antisense oligonucleotide and a small-molecule inhibitor

21 Three participants who received the antisense oligonucleotide and three who received placebo

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

23 hip between in vivo inhibition of miR-182 by antisense oligonucleotides and improved post-injury kidn

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

25 Huntingtin-lowering strategies include antisense oligonucleotides and RNA interference targetin

26 ly important to design optimal sequences for antisense oligonucleotides and siRNA because both bind t

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

28 ncrease SMN levels including drug compounds, antisense oligonucleotides, and scAAV9 gene therapy have

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

30 oss of contractile function, injection of an antisense oligonucleotide (antagomiR) against miR-25 mar

31 at silencing of brain-specific miR-134 using antisense oligonucleotides (antagomirs) had potent antis

32 onic copolymer, cationic DOTAP liposome, and antisense oligonucleotide (AON).

33 Previously, we showed that naked antisense oligonucleotides (AONs) effectively restored n

34 Antisense oligonucleotides (AONs) hold promise for thera

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

36 Antisense oligonucleotides (AONs) were designed specific

37 Antisense oligonucleotides (AOs) are a promising DMD the

38 Nucleotide-based drug candidates such as antisense oligonucleotides, aptamers, immunoreceptor-act

39 Antisense oligonucleotides are not a new concept, but su

40 Antisense oligonucleotides are small, modified nucleic a

41 lly in areas of myofiber regeneration, where antisense oligonucleotides are stored in macrophages and

42 r" unit in a number of biologically relevant antisense oligonucleotides, are described using 5-methyl

43 Exon skipping uses antisense oligonucleotides as a treatment for genetic di

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

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

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

47 Antisense oligonucleotide (ASO) drugs that trigger RNase

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

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

50 Systemically administered antisense oligonucleotide (ASO) inhibited miR-182 in the

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

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

53 ted with disease following treatment with an antisense oligonucleotide (ASO) targeted to the site of

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

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

56 We identified an exon 11 antisense oligonucleotide (ASO) that increased lamin C p

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

58 For this study, we compared a novel Gen 2 antisense oligonucleotide (ASO) that inhibits angiotensi

59 many as a half million components persist in antisense oligonucleotide (ASO) therapeutics because it

60 Antisense oligonucleotide (ASO) therapeutics show tremen

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

62 d for 4 wk with a 2'-O-methoxyethyl chimeric antisense oligonucleotide (ASO) to decrease hepatic and

63 We utilize an antisense oligonucleotide (ASO) to reduce apoE expressio

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

65 pivotal proof of principle that therapeutic antisense oligonucleotide (ASO) treatment can effectivel

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

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

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

69 We used an antisense oligonucleotide (ASO)-based inducible mouse mo

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

71 We have previously reported on an antisense oligonucleotide (ASO-29) that dramatically imp

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

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

74 The in vivo potency of antisense oligonucleotides (ASO) has been significantly

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

76 Targeted delivery of antisense oligonucleotides (ASO) to hepatocytes via the

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

78 cer therapy, we here report the synthesis of antisense-oligonucleotides (ASO) and thyroid hormone T3

79 gene-specific method of NMD inhibition using antisense oligonucleotides (ASOs) and combine this appro

80 hods to suppress expression of mRNAs include antisense oligonucleotides (ASOs) and RNA interference (

81 Antisense oligonucleotides (ASOs) and RNA-interference a

82 or toxicity contribute to the limited use of antisense oligonucleotides (ASOs) and siRNA as therapeut

83 Antisense oligonucleotides (ASOs) are an established too

84 RNase H1-dependent antisense oligonucleotides (ASOs) are chemically modifie

85 Antisense oligonucleotides (ASOs) are chemically synthes

86 ly mitigated through chemical modifications, antisense oligonucleotides (ASOs) are gaining recognitio

87 Antisense oligonucleotides (ASOs) are known to trigger m

88 Antisense oligonucleotides (ASOs) are most commonly desi

89 Antisense oligonucleotides (ASOs) are often used to down

90 Antisense oligonucleotides (ASOs) are recognized therape

91 Antisense oligonucleotides (ASOs) are small sequences of

92 Antisense oligonucleotides (ASOs) are synthetic oligonuc

93 Antisense oligonucleotides (ASOs) are versatile tools th

94 hat administering systemically SMN-restoring antisense oligonucleotides (ASOs) at the age of onset ca

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

96 fected 20-mer phosphorothioate-modified (PS) antisense oligonucleotides (ASOs) can recruit paraspeckl

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

98 High affinity antisense oligonucleotides (ASOs) containing bicylic mod

99 The ability to control gene expression with antisense oligonucleotides (ASOs) could provide a new tr

100 Chemically modified antisense oligonucleotides (ASOs) designed to mediate si

101 Antisense oligonucleotides (ASOs) designed to serve as s

102 Here, we show that antisense oligonucleotides (ASOs) effectively suppress P

103 DNA-based antisense oligonucleotides (ASOs) elicit cleavage of the

104 Here, we found that treating mice with apoB antisense oligonucleotides (ASOs) for 6 weeks decreased

105 Antisense oligonucleotides (ASOs) for ApoC-III reduce pl

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

107 on of gene expression by chemically modified antisense oligonucleotides (ASOs) has been well characte

108 Phosphorothioate (PS)-modified antisense oligonucleotides (ASOs) have been extensively

109 Phosphorothioate (PS) antisense oligonucleotides (ASOs) have been successfully

110 Antisense oligonucleotides (ASOs) have been under intens

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

112 etermined whether decreasing TTR levels with antisense oligonucleotides (ASOs) improves glucose metab

113 c loss or systemic knockdown of Malat1 using antisense oligonucleotides (ASOs) in the MMTV (mouse mam

114 Targeted degradation of SMN-AS1 with antisense oligonucleotides (ASOs) increases SMN expressi

115 Antisense oligonucleotides (ASOs) interact with target R

116 Here we show that systemic delivery of Dnm2 antisense oligonucleotides (ASOs) into Mtm1KO mice effic

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

118 Antisense oligonucleotides (ASOs) modified with phosphor

119 Antisense oligonucleotides (ASOs) modulate cellular targ

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

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

122 educed expression of Thrap3 in fat tissue by antisense oligonucleotides (ASOs) regulates a specific s

123 Antisense oligonucleotides (ASOs) targeted to the CAG re

124 We evaluated antisense oligonucleotides (ASOs) targeting Angptl3 mess

125 Antisense oligonucleotides (ASOs) targeting pathologic R

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

127 Single-dose injection of antisense oligonucleotides (ASOs) that target repeat-con

128 y showed that translation can be enhanced by antisense oligonucleotides (ASOs) that target upstream o

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

130 The available strategies include the use of antisense oligonucleotides (ASOs) to alter splicing or k

131 Exon skipping uses antisense oligonucleotides (ASOs) to alter transcript sp

132 ng approach to treat DM1 uses DMPK-targeting antisense oligonucleotides (ASOs) to reduce levels of to

133 this issue of the JCI, successfully utilized antisense oligonucleotides (ASOs) to reduce PMP22 and am

134 Antisense oligonucleotides (ASOs) with phosphorothioate

135 ll-interfering (siRNAs), microRNAs (miRNAs), antisense oligonucleotides (ASOs), aptamers, synthetic m

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

137 In this study, using splice-switching antisense oligonucleotides (ASOs), we increased the synt

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

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

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

141 directed at the ATXN2 gene by screening 152 antisense oligonucleotides (ASOs).

142 Angelman syndrome by reducing Ube3a-ATS with antisense oligonucleotides (ASOs).

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

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

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

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

147 otide strategies to silence gene expression, antisense oligonucleotide-based cancer therapy has not b

148 Indeed, antisense oligonucleotide-based exon skipping has shown

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

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

151 Using a morpholino-antisense-oligonucleotide-based zebrafish model for CHAR

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

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

154 ve shown that a locked nucleic acid-modified antisense oligonucleotide complementary to the CAG repea

155 , we utilized very short chemically modified antisense oligonucleotides composed exclusively of locke

156 tion of the binding domain or treatment with antisense oligonucleotides compromises Musashi function.

157 bilization of pausing, were competitive with antisense oligonucleotide concentration, suggesting that

158 itionally, systemic treatment with a peptide-antisense oligonucleotide conjugate designed to induce D

159 with pre-existing dystrophic pathology using antisense oligonucleotides conjugated to a cell-penetrat

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

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

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

163 We present an untemplated, single-component antisense oligonucleotide delivery system capable of reg

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

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

166 ect of IONIS-APO(a)-LRx, a ligand-conjugated antisense oligonucleotide designed to be highly and sele

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

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

169 cacy, safety, and tolerability of two unique antisense oligonucleotides designed to lower Lp(a) conce

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

171 Nusinersen is an antisense oligonucleotide drug that modifies pre-messeng

172 d elements involved in mRNA processing using antisense oligonucleotide drugs can be used as a strateg

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

174 stream of SMN2 exon 7 using Morpholino-based antisense oligonucleotides (E1(MO)-ASOs).

175 o its first human clinical trial, with other antisense oligonucleotides expected to enter trials in t

176 We still do not have a marketed antisense oligonucleotide for a cancer indication.

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

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

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

180 Weekly administration of FII antisense oligonucleotide "gapmer" to Berkeley SCD mice

181 drisapersen, a 2'-O-methyl-phosphorothioate antisense oligonucleotide, given for 48 weeks.

182 e show that acute depletion of Platr14 using antisense oligonucleotides impacts the differentiation-

183 uently, down-regulation of PDI expression by antisense oligonucleotides impaired the spreading of cel

184 e GSK126, or decreasing its expression using antisense oligonucleotides, impeded osteoclast different

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

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

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

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

189 ntracerebroventricular administration of the antisense oligonucleotides in the presymptomatic phase e

190 hermore, delayed administration of periostin antisense oligonucleotides in wild-type animals with GN

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

192 Antisense-oligonucleotide-induced exon skipping allows s

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

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

195 iated delivery of phosphorothioated TRAF3IP2 antisense oligonucleotides into the LV in a clinically r

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

197 Antisense oligonucleotide knockdown (ASO-KD) of nicotina

198 Antisense oligonucleotide knockdown of hepatic ASS1 expr

199 Antisense oligonucleotide knockdown of hepatic mitochond

200 In contrast, antisense oligonucleotide knockdown of HTT in WT co-cult

201 PSC-derived human cortical neurons following antisense oligonucleotide knockdown.

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

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

204 Antisense oligonucleotides linked by phosphorothioates a

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

206 Antisense oligonucleotides may be coupled to high-affini

207 atient-derived xenograft (PDX) mouse models, antisense oligonucleotide-mediated (ASO-mediated) skippi

208 geting mast cells in vitro and in vivo using antisense oligonucleotide-mediated exon skipping of the

209 (1) restoration of dystrophin expression by antisense oligonucleotide-mediated exon-skipping in mdx

210 renia-related lncRNA was explored in vivo by antisense oligonucleotide-mediated gene knockdown in the

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

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

213 binding sites based on insensitivity to DNA antisense oligonucleotide-mediated RNase H digestion.

214 pies such as mipomersen, a second-generation antisense oligonucleotide, microsomal triglyceride trans

215 ort new insights into these mechanisms using antisense oligonucleotide mimics of a pause RNA hairpin

216 Antisense oligonucleotides, miRNA sponges, and CRISPR/Ca

217 phase 1 study have shown that an oral SMAD7 antisense oligonucleotide, mongersen, targets ileal and

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

219 isense oligonucleotide or a mismatch control antisense oligonucleotide once a week for 1 or 4 weeks b

220 lly manipulated CD46 exon 13 inclusion using antisense oligonucleotides, opening up opportunities for

221 t mice were treated with either an anti-Apob antisense oligonucleotide or a mismatch control antisens

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

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

224 Knock-down of InsP3R1 expression by antisense oligonucleotides or knock-down or knock-out of

225 the RNA-binding protein Nanos2 by morpholino antisense oligonucleotides, or knockout of the Nanos2 ge

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

227 scular dystrophy (DMD), employing morpholino antisense oligonucleotides (PMO-AO) to exclude disruptiv

228 Eye drops of aganirsen, an antisense oligonucleotide preventing insulin receptor su

229 Knockdown of miR-29a by antisense oligonucleotides promoted HDAC4 action, nephri

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

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

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

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

234 The anti-Apob antisense oligonucleotide reduced plasma cholesterol by

235 Targeting tRNA(Arg)(UCU) with an antisense oligonucleotide replicated effects of Hili and

236 Antisense oligonucleotides represent a novel therapeutic

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

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

239 pinocerebellar ataxias, including the use of antisense oligonucleotides, short-interfering RNAs, as w

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

241 CSK9 synthesis in the endoplasmic reticulum (antisense oligonucleotides, siRNAs), and interfere with

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

243 Injection of morpholino (MO)-modified antisense oligonucleotides specifically designed to knoc

244 We also reduced MeCP2 using an antisense oligonucleotide strategy, which has greater tr

245 ockdown of total alpha-synuclein with potent antisense oligonucleotides substantially reduces inclusi

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

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

248 ive subcutaneous injections of placebo or an antisense oligonucleotide targeting ANGPTL3 mRNA in a si

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

250 Antisense oligonucleotides targeting C9orf72 have shown

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

252 nslated dipeptides, which were suppressed by antisense oligonucleotides targeting human C9orf72.

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

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

255 Antisense oligonucleotides targeting multiple types of n

256 Antisense oligonucleotides targeting the same lncRNAs ex

257 We further showed that antisense oligonucleotides targeting the SF2 binding sit

258 An intrathecally delivered antisense oligonucleotide that aims to lower huntingtin

259 We generated a C6 antisense oligonucleotide that blocks MAC formation by i

260 Custirsen is a second-generation antisense oligonucleotide that inhibits clusterin produc

261 X011) is a second generation highly specific antisense oligonucleotide that inhibits the production o

262 Tofersen is an antisense oligonucleotide that mediates the degradation

263 FXI-ASO (ISIS 416858) is a second-generation antisense oligonucleotide that specifically reduces fact

264 The only approved SMA treatment is an antisense oligonucleotide that targets the intronic spli

265 In contrast, similarly targeted MOE-gapmer antisense oligonucleotides that degrade RNA but do not e

266 peptide-phosphorodiamidate morpholino (PPMO) antisense oligonucleotides that induced temporary dystro

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

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

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

270 The development of antisense oligonucleotide therapy is an important advanc

271 3140969 ) with intravitreal injections of an antisense oligonucleotide to restore correct splicing.

272 models using a therapeutic splice-switching antisense oligonucleotide to restore SMN and a complemen

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

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

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

276 he contact system, we used DNase, RNase, and antisense oligonucleotides to characterize the FeCl3 mod

277 d on a modular hybrid minigene combined with antisense oligonucleotides to enable verification of fun

278 Here, we exploited synthetic antisense oligonucleotides to inhibit the RNA levels of

279 We used Cavbeta antisense oligonucleotides to knock down Cavbeta and gab

280 We used antisense oligonucleotides to knock down Lxralpha in mic

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

282 time window of response to administration of antisense oligonucleotides to SMA mice with an intermedi

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

284 uppressing MdMYB39L expression in pollen via antisense oligonucleotide transfection significantly red

285 insulin receptor 2'-O-methoxyethyl chimeric antisense oligonucleotide-treated rats.

286 t the combinatorial effect of suboptimal SMN antisense oligonucleotide treatment and PLS3 overexpress

287 Antisense oligonucleotide treatment caused dose-responsi

288 We find that antisense oligonucleotide treatment induces a broad phen

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

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

291 The antisense oligonucleotides used for exon skipping are de

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

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

294 Using antisense oligonucleotides we demonstrated that disrupti

295 loying heat-inducible transgenic strains and antisense oligonucleotides, we demonstrate that decrease

296 Antisense oligonucleotides were designed based on the se

297 Both antisense oligonucleotides were safe.

298 When C9ORF72 was overexpressed or antisense oligonucleotides were targeted to the C9orf72

299 Antisense oligonucleotides were used to inhibit miRNAs.

300 Antisense oligonucleotides, which were designed based on