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1 fied and cholesterol-conjugated RNAs termed 'antagomirs'.
2 P, in this case to target microRNA function (antagomir).
3 nic microRNAs by antisense oligonucleotides (antagomirs).
4 miR-16-5p, miR-125b-5p, and let-7a-5p (i.e., antagomirs).
5 ein levels could be reversed with an miR-346 antagomir.
6 ated when miR-328 was inhibited by selective antagomir.
7 hese effects could be reversed by a miR-181b antagomir.
8 3'-UTR activity was blocked by a miR-199a-5p antagomir.
9 following treatment with miR-27b and miR-29b antagomiRs.
10 noparticles, conjugated to LNA-based miR-10b antagomirs.
11 ling occluded the antiseizure effects of the antagomirs.
12 at blocking miR-122 in murine livers with an antagomiR-122 (miRNA inhibitor) results in miR-122* accu
17 of miR-132 by the provision of anti-miR-132 (antagomir-132) nanoparticles to HSV-infected mice led to
18 els were reduced by miR-144 and increased by antagomiR-144 in cultured cardiac endothelial cells.
19 rkers, and transfection of RA monocytes with antagomir-155 allowed restoration of M2-like polarizatio
20 he restoration of CDC73 levels by the use of antagomir-155 may also have an important role in therape
21 ivo silencing of miR-155 by the provision of antagomir-155 nanoparticles to herpes simplex virus 1-in
23 rsely, the delivery of a miR-155 antagonist (antagomir-155) to KB cells overexpressing miR-155 result
24 88 by intra-bone marrow injection of aptamer-antagomiR-188 increased bone formation and decreased bon
26 sed in Caco-2 cells incubated with IL1B; the antagomiR-200c prevented the IL1B-induced decrease in oc
28 levels of occludin mRNA; gavage of mice with antagomiR-200C reduced levels of MIR200C-3p and prevente
29 /or gavage with an antagonist to MIR200C-3p (antagomiR-200C) or the nonspecific antagomiR (control).
33 he role of miR-21 in vivo, empty vector- and antagomiR-21-transduced B16 melanoma cells were injected
42 n of CDH2 in normal and IPF fibroblasts, and antagomiR-630 abrogated the effect of mEV on CDH2 expres
43 ltaneous in vivo blockade of both miRNAs via antagomiR (a chemically modified miRNA inhibitor) inject
44 treatment of tumor-bearing mice with miR-10b antagomirs-a class of chemically modified anti-miRNA oli
45 rmed bone marrow cells with mir-196-specific antagomir abrogates their replating potential in methylc
46 rthermore, in vivo silencing of miR-22-3p by antagomiR administration lowered random as well as fasti
47 report that targeting miR-135a in vivo using antagomirs after onset of spontaneous recurrent seizures
48 Furthermore, macrophage transfection with antagomirs against miR-155 and miR-146b prevented both t
50 Furthermore, systemic treatment of mice with antagomiRs against these miRs relieved claudin-14 gene s
51 , injection of an antisense oligonucleotide (antagomiR) against miR-25 markedly halted established he
52 er surface area, were used to adsorb miR200c antagomir/agomir molecules as well as assemble lipid mem
55 se therapeutic potential of miRNAs and their antagomirs, an ever growing number of delivery approache
56 nt validation analyses, including the use of antagomir and 3'-UTR reporter vectors with swapped allel
58 and both intrathecal delivery of a miR-21-5p antagomir and conditional deletion of miR-21 in sensory
60 Studies using cellular delivery of miR-210 antagomir and mimic demonstrated a key role of miR-210 i
61 d -phosphorus medium), and experiments using antagomirs and mimics to modify miR-29b, miR-133b, and m
63 0% in MCF-7 cells transfected with a miR-328 antagomir, and disruption of miR-328 response element wi
64 ng miRNA target predictions and RT-qPCR from antagomir Ant-2940-3p-treated fat body tissues identifie
68 lipid nanoparticles (MLNPs) enclosing miR-17 antagomir (Anti-17 MLNPs), which are targeted to mannose
74 mically engineered oligonucleotides, termed 'antagomirs', are efficient and specific silencers of end
75 oited for the development of an anti-miR-122 antagomir as a host-targeting antiviral, the molecular m
77 gulation of functional ATP6 protein, whereas antagomir blockade restored functional ATP6 protein and
78 ndogenous miR-9 expression by an appropriate antagomiR can significantly inhibit cell growth/viabilit
79 mal uptake during NMP conditions facilitated antagomir co-localization with proteins involved in the
82 small complementary miRNA sequences known as antagomirs could be used to inhibit miRNA activity, whil
84 right ventricular systolic pressure, and all antagomirs decreased pulmonary arterial muscularization.
85 ed for functional characterization: systemic antagomir depletion and spatiotemporal inhibition using
86 es of primary DCs treated with antisense RNA antagomirs directed against miR-451 secreted elevated le
87 udy was to assess whether a specific miR-122 antagomir down-regulates HCV protein replication and up-
88 tion of different chemically protected miRNA/antagomir duplexes in mouse livers and localization of a
92 contrast, inhibition of renal miR-466o-3p by antagomiR, either prior to or after ADR injection, subst
93 miR-545 function was inhibited by a specific antagomir, endogenous p220 expression increased in G0/G1
94 nhibiting miR-503 by using an antisense RNA (antagomir) enhanced CUGBP1 biosynthesis and elevated its
96 ic miR-134 using antisense oligonucleotides (antagomirs) had potent antiseizure effects in animal mod
98 and its inhibition by a cholesterol-modified antagomir has been reported to prevent cardiac hypertrop
100 134 using antisense oligonucleotides, termed antagomirs, has potent and long-lasting seizure-suppress
101 at increasing PELI3 levels with a miR-744-5p antagomir in an inflammatory environment resulted in red
103 duplexes in mouse livers and localization of antagomirs in a cytosolic compartment that is distinct f
105 ontrolled delivery of miR-133a-3p mimics, or antagomirs in diseased endothelial cells, might open new
106 ommon pathway, and also establish the use of antagomiRs in fish for temporal knockdown of miRNA funct
107 ion, inhibition of miR-K12-11 function using antagomirs in KSHV-infected human primary effusion lymph
110 r data further validate the effectiveness of antagomirs in vivo and should facilitate future studies
112 iR-126 mimic, whereas inhibition of miR-126 (antagomir) in healthy CD31(+) cells fully mimicked the P
116 were suppressed at 32 degrees C and miR-155 antagomirs increased Ship1 and Socs1 and reversed the al
117 OX-mediated tumor suppression pathway, these antagomirs induced ROS, inhibited HIF signaling and incr
118 ation was significantly increased by miR-494 antagomir infusion, indicating their regulation by miR-4
119 of ZBTB4 or restoration of ZBTB4 by using an antagomir inhibit growth and invasion of breast cancer c
125 methyl-mimic miR-122, or nonspecific control antagomir, into wild-type (WT) Huh-7 cells or Huh-7 stab
126 silencing of endogenous miR-155 or -802, by antagomir intra-ventricular injection, resulted in the n
127 rior intracerebroventricular injection of an antagomir, kainic acid-induced seizures were delayed and
132 recent reports have suggested that an miR-21 antagomir might be therapeutically useful in preventing
133 ain biologically active Agomir (miRNA mimic)/Antagomir (miRNA inhibitor) adsorbed on magnetic ZnO par
140 man embryoid bodies to hsa-miR-1294 mimic or antagomir oligonucleotides yielded directionally opposit
141 man embryoid bodies to the microRNA mimic or antagomir oligonucleotides, and we observed the effects
142 a miR mimic (tumour suppressor miRNA) and an antagomiR (oncomiR inhibitor)-provides outstanding capab
146 g with miR-205 function by using a synthetic antagomir, or by the ectopic expression of miR-184, lead
147 Inhibition of miR-223 in vivo using specific antagomirs potentiated postnatal retinal angiogenesis in
148 ar tropic nanoparticles that deliver miR-30c antagomiRs promoted PAI-1-dependent tumor growth and inc
149 Cell transfection with miR-223 mimic or antagomiR proved the role of this microRNA in EV-induced
150 of amygdala, through infusion of a specific antagomir, provoked anxiolysis, mimicking the action of
151 Inhibition of miR-146a with a selective antagomir restored the immunoregulatory activity of nBMS
152 tralizing virus-induced miR-146a by specific antagomiR restores expressions of IRAK1 and TRAF6, augme
153 COPD small airway epithelial cells, using an antagomir, restores sirtuin-1 and suppresses markers of
154 ypti females after injection of its specific antagomir resulted in severe defects in blood digestion,
157 cing sirtuin-1/6, and its inhibition with an antagomir results in their restoration, reducing markers
158 cal administration of cholesterol-conjugated antagomiRs revealed better inhibition of miR-195 compare
161 Temporal-specific knockdown of miR-138 by antagomiRs showed miR-138 function was required during a
162 vitro and in vivo, silencing of miR-10b with antagomirs significantly decreases miR-10b levels and in
163 RNAs can be blocked by a new class of drugs, antagomirs, some of which have been shown to improve car
165 Down-regulation of HCV replication using an antagomir targeted to miR-122 is effective, specific, an
166 apacity, whereas intraocular injection of an antagomir targeting miR-132, anti-miR-132, reduced postn
169 portantly, in vivo application of a miRNA92a antagomir to nonobese diabetic (NOD) mice with ongoing i
170 trated that in vivo administration of miR-22 antagomir to SHR causes substantial ( approximately 18 m
171 ciated cultures of MG using either mimics or antagomiRs to increase or reduce expression, respectivel
173 /16-1 in cells increased cell death, whereas antagomirs to miR-15a/16-1 abolished the proapoptotic ef
176 rfusion recovery from hindlimb ischemia, and antagomirs to miR-93 attenuated perfusion recovery.
180 tested the impact of exogenously loading of antagomirs to specific Nrf2-related miRNAs on CHF-EV-ind
181 bioinformatic analysis of messenger RNA from antagomir-treated animals revealed that the 3' untransla
183 Both Mir324 knockout (KO) and miR-324-5p antagomir treatment significantly reduce dendritic spine
184 subregion, and Mir324 KO, but not miR-324-5p antagomir treatment, shift dendritic spine morphology, r
186 In atherosclerotic lesions, the miR-342-5p antagomir upregulated Akt1 expression and suppressed the
187 miR-690 knockdown using peptide nucleic acid-antagomiR was able to unblock and significantly increase
189 ificance of silencing miRNAs with the use of antagomirs was studied for miR-122, an abundant liver-sp
190 1b(+) cells isolated from mice injected with antagomiRs were able to differentiate ex vivo into macro
192 first tested the effects of miR inhibitors (antagomirs), which were specifically designed to block m