ライフサイエンスコーパス: anti-miR

1 ion modulates the transcriptomic response to anti-miR.

2 erexpression of miR-29a and inhibition using anti-miRs.

3 ithelial cells after knockdown of MIR29 with anti-MIRs.

4 Our results demonstrate that the anti-miR-10 inhibitor not only decreases RhoGTPase/survi

5 Intranasal delivery of ADEVs loaded with anti-miR-106b ameliorates morphine-mediated primary cili

6 Intranasal delivery of ADEVs loaded with anti-miR-106b decreased the expression of miR-106b in as

7 Weekly treatments of mice with MN-anti-miR-10b and low-dose doxorubicin resulted in comple

8 cells were also transfected with a specific anti-miR-10b inhibitor in order to silence miR-10b expre

9 Our results demonstrate that anti-miR-10b inhibitor not only enhances HOXD10 expressi

10 CSCs were also transfected with a specific anti-miR-10b inhibitor to silence miR-10b expression and

11 We found that combination treatments with anti-miR-122 and a DAA had additive or synergistic antiv

12 has been exploited for the development of an anti-miR-122 antagomir as a host-targeting antiviral, th

13 istration of 2 mg kg(-1) chemically modified anti-miR-122 complexed with iNOP-7 resulted in 83.2 +/-

14 systemic delivery of a chemically stabilized anti-miR-122 complexed with interfering nanoparticles (i

15 te targeted N-acetylgalactosamine conjugated anti-miR-122 oligonucleotide, was well tolerated and res

16 Intravenous injection of rAAV9 expressing anti-miR-122 or anti-let-7 TuDs depleted the correspondi

17 atment in HCV-replicating cells with DAA and anti-miR-122 sharply reduced HCV RNA amounts.

18 atasvir, and sofosbuvir) in combination with anti-miR-122 treatment against HCV genotype 1a in cell c

19 rAAV producing anti-miR-122 TuD but not anti-let-7 TuD reduced serum ch

20 and has implications for the development of anti-miR-122-based HCV drugs.

21 s was achieved by combining daclatasvir with anti-miR-122.

22 antly decreased by combining simeprevir with anti-miR-122.

23 n miR-124a levels with Ccl2 expression, with anti-miR-124a increasing Ccl2 mRNA levels in Klf2(+/+) m

24 Anti-miR-125b and anti-miR-155 prevented CD154-mediated

25 levated responsiveness to IFN-gamma, whereas anti-miR-125b treatment decreases CD80 surface expressio

26 Therapeutic depletion of miR-126 with an anti-miR-126 (miRisten) inhibits AML cell survival, redu

27 miRisten, a CpG-conjugated anti-miR-126 oligonucleotide now in clinical trials (NCT

28 Modulation of miR-126 by anti-miR-126 or miR-mimic-126 treatment resulted in sign

29 Anti-miR-126 transfection markedly impaired the capacity

30 Finally, we determine that anti-miR-128 partly neutralizes the IFN-mediated block o

31 Notably, we observe that anti-miR-128 partly neutralizes the IFN-mediated block o

32 We found that anti-miR-129 reversed the expression of CD200R1, as well

33 We found that anti-miR-129 reversed the expression of CD200R1, as well

34 n BALB/c mouse by stereotactically injecting anti-miR-129-5p and assessing the phagocytosis in ex viv

35 Finally, experiments with arsenic, anti-miR-129-5p, ROCK1 & Rac1 siRNA in various combinati

36 in BALB/c mouse by stereotaxically injecting anti-miR-129.

37 Anti-miR 130a treatment led to reduced airway branching

38 In vivo studies revealed that LNA(TM) anti-miR-130a could up-regulate the AQP4 M1 transcript a

39 Introduction of anti-miR-130a in hepatocytes increased IFITM1 expression

40 tocytes upregulates miR-130a and that use of anti-miR-130a may have potential for restriction of HCV

41 ls with anti-miR-155-5p, anti-miR-21-3p, and anti-miR-130b revealed a considerable increase in SOCS p

42 ivo silencing of miR-132 by the provision of anti-miR-132 (antagomir-132) nanoparticles to HSV-infect

43 Notably, administration of anti-miR-132 inhibited angiogenesis in wild-type mice bu

44 ovascularization, whereas the application of anti-miR-132 inhibits neovascularization by maintaining

45 ly, vessel-targeted nanoparticle delivery of anti-miR-132 restored p120RasGAP expression in the tumor

46 injection of an antagomir targeting miR-132, anti-miR-132, reduced postnatal retinal vascular develop

47 However, overexpression of anti-miR-135a and anti-miR-199a-5p oligonucleotides led

48 onary hypertension in vivo in miR-143-/- and anti-miR-143-3p-treated mice exposed to chronic hypoxia

49 IPF lung fibroblasts transfected with anti-miR-144-3p had increased RXFP1 expression and reduc

50 gh miR-145 silences the expression of c-Myc, anti-miR-145 enhances its expression.

51 Finally, the blockade of miR-145 by anti-miR-145 is able to reverse the p53-mediated c-Myc r

52 A locked nucleic acid-modified anti-miR-146a given before LPS treatment knocked down mi

53 Transfection of anti-miR-146a nucleotides reversed the inhibitory effect

54 Anti-miR-148a also reduced thrombus formation following

55 Within 18 h of transfection with an anti-miR-150 construct, primary B lymphocytes secrete ap

56 These results suggest that shuttling anti-miR-150 molecules from B lymphocytes to T cells req

57 ocytes secrete approximately 3,000 copies of anti-miR-150 molecules per cell.

58 Anti-miR-150 molecules released by B lymphocytes were in

59 Finally, anti-miR-150 synthesized in B cells were secreted both a

60 s, but only extracellular vesicle-associated anti-miR-150 were apparently taken up by CD8 T cells.

61 locking miR-155 expression using a synthetic anti-miR-155 after alloHSCT decreased aGVHD severity and

62 13.1 months, while a two-drug combination of anti-miR-155 and cisplatin resulted in a median PFS of 1

63 ical development and clinical translation of anti-miR-155 and unravels the potential of anti-miR-155

64 ical scenario revealed that monotherapy with anti-miR-155 at a dose of 2.5 mg/kg administered once ev

65 f anti-miR-155 and unravels the potential of anti-miR-155 combination therapies in NSCLC.

66 Moreover, anti-miR-155 delivered systemically showed uptake in the

67 -155 led to preferential accumulation of the anti-miR-155 in hepatocytes.

68 herapeutic effects of nanoparticle-delivered anti-miR-155 in NSCLC, alone or in combination with stan

69 xperiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in v

70 n or by peripheral or centrally administered anti-miR-155 inhibitor in SOD1 mice.

71 ravenous injection of Lac-GLN containing Cy3-anti-miR-155 led to preferential accumulation of the ant

72 Intravenous administration of 1.5 mg/kg anti-miR-155 loaded Lac-GLN resulted in up-regulation of

73 y, we show that an 8-mer locked nucleic acid anti-miR-155 oligonucleotide targeting the seed region o

74 However, treatment of established PNFs using anti-miR-155 peptide nucleic acid-loaded nanoparticles m

75 ene expression between B cells isolated from anti-miR-155 PNA-treated and miR-155-deficient mice.

76 Anti-miR-125b and anti-miR-155 prevented CD154-mediated repression of BCL2

77 The efficacy of anti-miR-155 targeting in multiple lymphoma cell lines w

78 Lac-GLN effectively delivered anti-miR-155 to HCC cells with a 16.1- and 4.1-fold up-r

79 Intraventricular anti-miR-155 treatment derepressed microglial miR-155 ta

80 glial miR-155 targeted genes, and peripheral anti-miR-155 treatment prolonged survival.

81 Finally, we found that anti-Mir-155 treatment reduced clinical severity of EAE

82 Further, we explored the combinations of anti-miR-155 with standard-of-care drugs, and found stro

83 developed for delivery of anti-microRNA-155 (anti-miR-155) to hepatocellular carcinoma (HCC) cells.

84 A three-drug combination of anti-miR-155, cisplatin, and pembrolizumab resulted in a

85 sfected with an antisense miR-155 inhibitor, anti-miR-155, endogenous hAT(1)R expression and angioten

86 targeting of miR-155 through its antagonist, anti-miR-155, has proven challenging due to its dual mol

87 Transfection of MyLa and HuT78 cells with anti-miR-155-5p, anti-miR-21-3p, and anti-miR-130b revea

88 study highlight the therapeutic potential of anti-miR-155-mediated inhibition of miR-155 in the treat

89 Anti-miR-155-transfected AMs exhibited an increase in SR

90 vivo compared with conventional full-length anti-miR-155.

91 tion of healthy PACs ex vivo-engineered with anti-miR-15a/16 improved postischemic blood flow recover

92 Treatment of mice with systemic delivery of anti-miR-17 and anti-miR-19 reduced tumor growth in flan

93 ition of miR-17 and miR-19a seed families by anti-miR-17 and anti-miR-19, respectively, resulted in d

94 y diverse and rationally designed library of anti-miR-17 oligonucleotides for optimal pharmaceutical

95 b study, development of the first-generation anti-miR-17 ON RGLS4326 for the treatment of autosomal d

96 ith adenine, we discover the next-generation anti-miR-17 RGLS8429 that is devoid of off-target AMPAR

97 Anti-miR-17 treatment attenuates cyst growth in short-te

98 Anti-miR-17 treatment recapitulated the gene expression

99 L tumor cell proliferation and survival, and anti-miR-181a abrogates these effects.

100 Systemic delivery of anti-miR-181b in angiotensin II-infused Apoe(-/-) and Ld

101 n vivo administration of locked nucleic acid anti-miR-181b retarded both the development and the prog

102 On the other hand, introduction of anti-miR-181c restored ATM and phosphorylated Akt.

103 ferase imaging showed that mice treated with anti-miR-182 had a lower burden of liver metastases comp

104 Our results demonstrate that the use of anti-miR-182 is a promising therapeutic strategy for met

105 Specifically, we assessed the effect of anti-miR-182 oligonucleotides synthesized with 2' sugar

106 scriptional profiling of tumors treated with anti-miR-182 or with control oligonucleotides revealed a

107 Anti-miR-182 treatment inhibits the hypertrophic respons

108 esion and migration modulated in response to anti-miR-182 treatment.

109 ce with systemic delivery of anti-miR-17 and anti-miR-19 reduced tumor growth in flank and brain allo

110 and miR-19a seed families by anti-miR-17 and anti-miR-19, respectively, resulted in diminished tumor

111 Furthermore, LNA-anti-miR-192 attenuated proteinuria in these diabetic mi

112 LNA-anti-miR-192 significantly reduced levels of miR-192, bu

113 odified inhibitor of miR-192, designated LNA-anti-miR-192, in mouse models of diabetic nephropathy.

114 Anti-miR-192-5p significantly blocked VAN-induced apopto

115 Anti-miR-197 transfections were performed to test the op

116 nuated HIF-1alpha and ET-1 expression, while anti-miR-199 reversed the effects, suggesting that ethan

117 (COMP), type II collagen, and Sox9, whereas anti-miR-199a(*) increased the expression of these chond

118 However, overexpression of anti-miR-135a and anti-miR-199a-5p oligonucleotides led to a several fold

119 metastases of MDA-MB-231 cells in vivo, and anti-miR-200 treatment in vivo resulted in increased met

120 Anti-miR-200b delivery to murine injury sites likewise e

121 topical tissue nanotransfection of a single anti-miR-200b oligonucleotide was sufficient to restore

122 We transfected human dermal fibroblasts with anti-miR-200b oligonucleotide, then using single cell RN

123 ccelerated wound closure in vitro induced by anti-miR-200c was associated with upregulation of genes

124 he less aggressive Huh7 cell was enhanced by anti-miR-200c+141.

125 The anti-miR-204-induced decrease in Kir7.1 protein levels s

126 ssion in primary cultures of human RPE using anti-miR-204.

127 rotein) consistent with our observation that anti-miR-204/211 decreased transepithelial resistance by

128 MT markers and cell migration is reverted by anti-miR-205.

129 Moreover, anti-miR-206* inhibitor treatment substantially rescued

130 ning the wild-type 3'-UTR or when a specific anti-miR-206* inhibitor was added.

131 nt of RASA1- or SPRED1-suppressed cells with anti-miR-206/21 had little or no impact on the level of

132 ce injected with LM7 stably transfected with anti-miR-20a had fewer metastases than those with contro

133 onal MI rats were then randomized to receive anti-miR-21 (KD21) or scrambled control sequence (Scr21)

134 n-gel electrophoresis of tumors treated with anti-mir-21 and identified the tumor suppressor tropomyo

135 Administration of anti-miR-21 blocked RI-induced cell proliferation and si

136 lly, knockdown of TSG101 increased uptake of anti-miR-21 by cancer cells in vivo following systemic d

137 Anti-miR-21 enhanced PPARalpha/retinoid X receptor (PPAR

138 r ESCRT-I protein, VPS28, improved uptake of anti-miR-21 in parental SKHEP1 cells and restored produc

139 cells were also transfected with a specific anti-miR-21 inhibitor in order to silence miR-21 express

140 cells were also transfected with a specific anti-miR-21 inhibitor in order to silence miR-21 express

141 Our results indicate that anti-miR-21 inhibitor not only enhances PDCD4 expression

142 Our results demonstrate that anti-miR-21 inhibitor not only upregulates PDCD4 express

143 L1-binding peptide covalently linked with an anti-miR-21 inhibitor via click chemistry.

144 A 22-nt anti-miR-21 mesyl phosphoramidate oligodeoxynucleotide s

145 , we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severit

146 e transfected breast cancer MCF-7 cells with anti-miR-21 oligonucleotides and found that anti-miR-21

147 evaluated the therapeutic potential of these anti-miR-21 oligonucleotides in chronic kidney disease.

148 anti-miR-21 oligonucleotides and found that anti-miR-21 suppressed both cell growth in vitro and tum

149 r-21 down-regulated the luciferase activity, anti-mir-21 up-regulated it.

150 roductive free uptake of a miR-21 inhibitor (anti-miR-21).

151 Uptake of anti-miR-21, but not a mismatch (MM) control, induces ex

152 lucidate mechanisms of SKHEP1 sensitivity to anti-miR-21, we conducted an unbiased shRNA screen that

153 f MyLa and HuT78 cells with anti-miR-155-5p, anti-miR-21-3p, and anti-miR-130b revealed a considerabl

154 In addition, anti-miR-21-induced suppression of cell migration was re

155 Furthermore, this anti-miR-21-mediated cell growth inhibition was associat

156 We comprehensively evaluated anti-miR-21-peptide nucleic acid-RENTAC, and fluorophore

157 downregulation of the antiapoptotic Bcl-2 in anti-miR-21-treated tumor cells.

158 poor uptake resulted in improved activity of anti-miR-21.

159 determinant of anti-proliferative effects of anti-miR-21.

160 to SKHEP1 clones with acquired resistance to anti-miR-21.

161 Intracolonic anti-miR-210 also reduced colitis in response to TNBS (2

162 entary locked nucleic acid oligonucleotides (anti-miR-210).

163 Direct delivery of anti-miR-210-3p LNA in the ATenv markedly rescued mice f

164 ne differentiation was largely unaffected by anti-miR-210.

165 ed intracolonically with locked nucleic acid anti-miR-210.

166 ce, or mice pretreated intracolonically with anti-miR-210.

167 vo biodistribution studies demonstrated that anti-miR-214 accumulated at the highest levels in the ki

168 Silencing of miR-214 by anti-miR-214 in whole AV leaflets with the fibrosa expos

169 e with an anti-miR directed against miR-214 (anti-miR-214) before UUO resulted in similar antifibroti

170 Anti-miR 221 treated lungs had more distal branch genera

171 A cholesterol-modified isoform of anti-miR-221 (chol-anti-miR-221) exhibited improved phar

172 fer a preclinical proof of efficacy for chol-anti-miR-221 in a valid orthotopic mouse model of HCC, s

173 bicin resistance with higher efficiency than anti-miR-221 in human breast cancer cells.

174 that a 2'-O-methyl phosphorothioate-modified anti-miR-221 oligonucleotide was most effective at reduc

175 miR-221, we showed that in vivo delivery of anti-miR-221 oligonucleotides leads to a significant red

176 Within the same period, chol-anti-miR-221 reduced tumor cell proliferation and increa

177 Chol-anti-miR-221 significantly reduced miR-221 levels in liv

178 terol-modified isoform of anti-miR-221 (chol-anti-miR-221) exhibited improved pharmacokinetics and li

179 Further, anti-miR-222 or -181b in combination with tamoxifen supp

180 LV-anti-miR-23b also significantly increased the hydroxylat

181 Furthermore, LV-anti-miR-23b significantly decreased endogenous levels o

182 Transfection of anti-miR-24 molecules in EBNA2-expressing lymphoma cells

183 ated by EBNA2, we analyzed its expression in anti-miR-24 transfected lymphoma cells.

184 of an miR-26a inhibitor, locked nucleic acid-anti-miR-26a, increased SMAD1 expression and rapidly ind

185 = 0.046), and inhibition of miR-26a-2 using anti-miR-26a-2 substantially upregulated HOXA5 expressio

186 Because anti-miR-27b compounds that suppress miR-27b inhibit tum

187 Moreover, intraperitoneally delivered anti-miR-27b restored Nischarin expression and decreased

188 t suppress miR-27b inhibit tumor growth, the anti-miR-27b seems to be a good candidate for the develo

189 Bmpr2 mice treated with anti-miR-29 (20-mg/kg injections for 6 weeks) had improv

190 chondrial abnormalities, which improved with anti-miR-29 transfection in vitro; endothelial-like cell

191 em cell lines were similar and improved with anti-miR-29 treatment.

192 Treatment with locked nucleic acid anti-miR-29a significantly improved survival in a mouse

193 V)-transduced BEAS-2B cells, introduction of anti-miR-29b constructs increased the sensitivity to apo

194 n vivo administration of locked nucleic acid anti-miR-29b greatly increased collagen expression, lead

195 miR-29b decreased and anti-miR-29b increased activity of COL1A1, COL5A3, and C

196 ic delivery of locked nucleic acid-modified, anti-miR-29b-reduced endogenous miR-29b levels in the sm

197 Our results demonstrate that the anti-miR-302 inhibitor not only enhances the expression

198 These CSCs were transfected with a specific anti-miR-302 inhibitor to silence miR-302 expression and

199 urthermore, inhibition of hepatic miR-30c by anti-miR-30c increased hyperlipidemia and atherosclerosi

200 The anti-miR-33 conjugated pHLIP constructs are preferential

201 onflicting reports exist about the impact of anti-miR-33 therapy on the levels of very low-density li

202 nd suggest that caution should be taken with anti-miR-33-based therapies because they might raise pro

203 om atherosclerotic lesions targeted by pHLIP-anti-miR-33.

204 and point to a potential therapeutic use for anti-miR-34 as a radiosensitizing agent in p53-mutant br

205 PACS-1 re-expression through LNA-hsa-anti-miR-34a or -449a or through PACS-1 cDNA transfectio

206 Conversely, locked nucleic acid-based anti-miR-34a treatment diminished post-MI miR-34a upregu

207 Further, anti-miR-34a treatment in primary hepatocytes of obese m

208 Importantly, anti-miR-34a-mediated beneficial effects, including decr

209 ct of Tat was neutralized in the presence of anti-miR-34a.

210 hypertrophic marker type X collagen, whereas anti-miR-365 inhibits the expression of these genes.

211 We found overexpressed siFas and anti-miR-375 in plasmid encoding shFas and anti-miR-375

212 d anti-miR-375 in plasmid encoding shFas and anti-miR-375 transfected hBMSC-derived exosomes, which s

213 78a using nanoparticles encapsulated with an anti-miR-378a oligonucleotide restored PPARa activity, i

214 78a using nanoparticles encapsulated with an anti-miR-378a oligonucleotide restored PPARa activity, i

215 Knockdown of miR-423-5p with anti-miR-423-5p reversed training-induced bradycardia vi

216 R-433 but were induced by miR-433 antagomir (anti-miR-433).

217 HCC97H cell migration, which was reversed by anti-miR-433.

218 l proliferation, which was not influenced by anti-miR-433.

219 n and invasion and antagonized the effect of anti-miR-433.

220 lines decreases cellular transformation, and anti-miR-494 treatment of primary MYC-driven liver tumor

221 and transfection of PBC cholangiocytes with anti-miR-506 was able to improve their AE2 activity.

222 Anti-miR-540 mitigated ALR depletion-induced steatosis a

223 Treatment with the combination of anti-miR-630 and anti-vascular endothelial growth factor

224 The anti-miR-663 reduced OXPHOS complex activity and increas

225 Oligonucleotides anti-miR-7 inhibited the exendin-4-induced proliferation

226 Furthermore, silencing miR-712 by anti-miR-712 rescues TIMP3 expression and prevents ather

227 herapeutic approach to this disease using an anti-miR-886-3p.

228 Remarkably, administration of anti-miR-9 or JAK inhibitors suppressed MV-induced cell

229 Administration of an anti-miR-92a after disease initiation prevented albuminu

230 The therapeutic effectiveness of anti-miR-92a therapy in treating atherosclerosis and ste

231 Conversely, anti-miR-93 inhibitors increased VEGF release.

232 d in lung homogenates in vivo Treatment with anti-miR-98 alone was sufficient to recapitulate increas

233 re manipulated in LFs with miR-98 inhibitor (anti-miR-98), miR-98 overexpression (miR-98 mimic), or t

234 Treatment of anti-miR-99b-transfected DCs with anti-TNF-alpha antibod

235 ved 'epidrugs' (chromatin modifiers, mimics, anti-miRs) able to prevent transcriptional alterations u

236 for efficient miRNA targeting and show that anti-miR activity is enhanced substantially by the prese

237 We show that anti-miR activity of a Cys-containing PNA is achieved by

238 delivery of an oligonucleotide comprising an anti-miR against miR-126 resulted in significant knockdo

239 Nebulized anti-miRs against miR-25 and miR-138 restore MCU express

240 Treatment with anti-miRs against the miR-17 family reduced cyst prolife

241 In contrast, treatment with anti-miRs against the miR-18, 19, or 25 families did not

242 of PNAs and other oligonucleotides as potent anti-miR agents.

243 data indicate that in vivo administration of anti-miRs allows for efficient miRNA targeting and conco

244 explored the subcellular localization of PNA anti-miRs and our data suggest that anti-miR targeting o

245 the regulation of productive free uptake of anti-miRs and reveal potential avenues for improving oli

246 oblastoma cells) passively took up 8-mer LNA-anti-miRs and specifically inhibited targeted microRNA s

247 g RNAs (siRNAs), microRNAs (miRNAs or miRs), anti-miRs, and mRNA-based platforms holds great promise

248 Anti-miRs are oligonucleotide inhibitors complementary t

249 microRNA-155 by a systemically delivered LNA-anti-miR attenuated cardiac infiltration by monocyte-mac

250 by down-regulating TIMP3, and corresponding anti-miRs can be used to render these tumors responsive

251 d whether locked nucleic acid (LNA)-modified anti-miR chemistries can target cardiac expressed miRNAs

252 by using antisense oligonucleotides, called anti-miRs, complimentary to the miRNA sequences.

253 d previously that peptide nucleic acid (PNA) anti-miRs containing a few attached Lys residues were po

254 he miPSA has additional utility in assessing anti-miR cross-reactivity with miRNAs sharing similar se

255 in the study, use of DOPC nanoliposomes for anti-miR delivery serves as a better alternative approac

256 ects of LXA4 in renal epithelia; conversely, anti-miR directed against let-7c attenuated the effects

257 Treatment of wild-type mice with an anti-miR directed against miR-214 (anti-miR-214) before

258 Correspondingly, systemic delivery of miR-15 anti-miRs dose-dependently represses miR-15 in cardiac t

259 ion changes in these genes following in vivo anti-miR dosing, suggesting that derepression of these t

260 diameter of 73 nm, zeta potential of +3.5mV, anti-miR encapsulation efficiency of 88%, and excellent

261 e inhibited miRNAs are sterically blocked by anti-miRs from forming this interaction.

262 In contrast, miR-143 anti-miR had no effect.

263 An miR-138 anti-miR had the opposite effects.

264 et-7 family with a locked nucleic acid (LNA)-anti-miR has the opposite effect.

265 overexpression, and knockdown via mimics and anti-miRs, immunoblotting, dual luciferase reporter assa

266 Indeed, down-regulation of miR-29 with anti-miRs in vitro and in vivo induces the expression of

267 ly dissociate from AGO2-miRNA complexes when anti-miR is spiked into liver lysates.

268 Selective reduction in miR-886-3p by an anti-miR led to elevation of FXN message and protein lev

269 miR-145 deficiency and anti-miR-mediated reduction resulted in significant prot

270 noparticles entered PNFs, suggesting that an anti-miR might have therapeutic potential.

271 of the miR-17~92 cluster family by 8-mer LNA-anti-miRs might be considered for the treatment of SHH m

272 e of miR-338-3p in beta cells using specific anti-miR molecules mimicked gene expression changes occu

273 rdiac fibroblasts were transfected with pre-/anti-miR of miR-29b and miR-30c, and their conditioned m

274 Anti-miRNA (anti-miR) oligonucleotide drugs are being developed to i

275 nal inhibition of the respective miRNAs with anti-miR oligonucleotides resulted in induction of ICAM-

276 Conversely, the transfection of synthetic anti-miR oligonucleotides that inhibit miR-338 increases

277 targeting locked nucleic acid (LNA)-modified anti-miR oligonucleotides, termed tiny LNAs, that inhibi

278 e E14 whole lungs cultured for 48 hours with anti-miRs or mimics to miR-130a and miR-221.

279 nous miR-140 by locked nucleic acid-modified anti-miR partially sensitized resistant colon cancer ste

280 The inhibition of miR-378 by its anti-miR protected cardiomyocytes against H(2)O(2) and h

281 ition studies were performed with pre-miR or anti-miR, respectively.

282 Antisense-mediated knockdown (anti-miR) revealed that miR-206/21 coordinately promote

283 Here we performed an in vivo anti-miR screen to identify the miRNA drug targets withi

284 We entrapped these anti-miR sgammaPNAs in nanoparticles (NPs) formed from a

285 n of PNA anti-miRs and our data suggest that anti-miR targeting of miR-122 may take place in or assoc

286 GLN as a liver-specific delivery vehicle for anti-miR therapy.

287 poorly reflect the binding stoichiometry of anti-miR to miRNA.

288 onstrate that iNOPs can successfully deliver anti-miR to specifically target and silence miRNA in cli

289 We designed anti-miRs to individually inhibit miR-17, miR-18, miR-19

290 rovide a foundation for developing synthetic anti-miRs to therapeutically target the tumor microenvir

291 e effectively downregulated in the tumors of anti-miR-treated mice compared with tumors of control-tr

292 Accordingly, anti-miR treatment causes a specific shift of cognate mi

293 rs that can be upregulated in tumor cells by anti-miR treatment.

294 We developed a novel method for delivering anti-miRs using liposomes for the functional knockdown o

295 ed in miR-145 knockout and mice treated with anti-miRs via measurement of systolic right ventricular

296 In vivo, nebulized anti-miRs were administered to rats with monocrotaline-i

297 or direct measurement of miRNA engagement by anti-miR, which is more robust than conventional pharmac