ライフサイエンスコーパス: antagomir

1 fied and cholesterol-conjugated RNAs termed 'antagomirs'.

2 nic microRNAs by antisense oligonucleotides (antagomirs).

3 ated when miR-328 was inhibited by selective antagomir.

4 3'-UTR activity was blocked by a miR-199a-5p antagomir.

5 ein levels could be reversed with an miR-346 antagomir.

6 following treatment with miR-27b and miR-29b antagomiRs.

7 noparticles, conjugated to LNA-based miR-10b antagomirs.

8 at blocking miR-122 in murine livers with an antagomiR-122 (miRNA inhibitor) results in miR-122* accu

9 Proteomics analysis of livers from antagomiR-122-treated mice revealed novel regulators of

10 sterol measurements showed reduced levels in antagomir-122-treated mice.

11 The anti-angiogenic effect of antagomir-132 was reflected by a reduction in angiogenic

12 of miR-132 by the provision of anti-miR-132 (antagomir-132) nanoparticles to HSV-infected mice led to

13 he restoration of CDC73 levels by the use of antagomir-155 may also have an important role in therape

14 ivo silencing of miR-155 by the provision of antagomir-155 nanoparticles to herpes simplex virus 1-in

15 ells and were specifically lowered by either antagomir-155 or elevated expression of SHIP1.

16 rsely, the delivery of a miR-155 antagonist (antagomir-155) to KB cells overexpressing miR-155 result

17 88 by intra-bone marrow injection of aptamer-antagomiR-188 increased bone formation and decreased bon

18 alloproteinases 2 and 9 in mice treated with antagomiR-195.

19 Meanwhile, treatment with antagomir-21 decreased STAT3 phosphorylation, alleviated

20 Transfected antagomir-21 decreased the IL-6-induced cardiac fibrobla

21 ent in cells treated with the miR-21 eraser, antagomiR-21, and in miR-21 knockout mice.

22 he role of miR-21 in vivo, empty vector- and antagomiR-21-transduced B16 melanoma cells were injected

23 n systemic administration of MSC loaded with antagomiR-222/223.

24 Inhibition of miR-23b using antagomir-23b oligonucleotide (AM23b) reversed the PS-in

25 Furthermore, treatment with antagomiR-29c resulted in a 46 +/- 5% cell death in PC12

26 ize relative to the administration of mutant antagomir-320 and saline controls.

27 Conversely, in vivo treatment with antagomir-320 reduced infarction size relative to the ad

28 Infusion of antagomir-352 increased the number and proliferation of

29 In addition, antagomir-352 up-regulated the expression of insulin-lik

30 n of CDH2 in normal and IPF fibroblasts, and antagomiR-630 abrogated the effect of mEV on CDH2 expres

31 ltaneous in vivo blockade of both miRNAs via antagomiR (a chemically modified miRNA inhibitor) inject

32 treatment of tumor-bearing mice with miR-10b antagomirs-a class of chemically modified anti-miRNA oli

33 rmed bone marrow cells with mir-196-specific antagomir abrogates their replating potential in methylc

34 rthermore, in vivo silencing of miR-22-3p by antagomiR administration lowered random as well as fasti

35 Furthermore, macrophage transfection with antagomirs against miR-155 and miR-146b prevented both t

36 Intravenous administration of antagomirs against miR-16, miR-122, miR-192 and miR-194

37 Furthermore, systemic treatment of mice with antagomiRs against these miRs relieved claudin-14 gene s

38 , injection of an antisense oligonucleotide (antagomiR) against miR-25 markedly halted established he

39 Finally, we show that antagomirs, although incapable of silencing miRNAs in th

40 Antagomir AM27b regulated E2F1 expression, but did not a

41 se therapeutic potential of miRNAs and their antagomirs, an ever growing number of delivery approache

42 and both intrathecal delivery of a miR-21-5p antagomir and conditional deletion of miR-21 in sensory

43 B16 cells with lentivirus encoding a miR-21 antagomir and isolated miR-21 knockdown B16 cells.

44 Studies using cellular delivery of miR-210 antagomir and mimic demonstrated a key role of miR-210 i

45 d -phosphorus medium), and experiments using antagomirs and mimics to modify miR-29b, miR-133b, and m

46 0% in MCF-7 cells transfected with a miR-328 antagomir, and disruption of miR-328 response element wi

47 Treatment with an miR-21-specific antagomir (Ant-21) increased phosphatase and tensin homo

48 We used antagomirs (antago) to reduce the level of miR-31 in pri

49 We used antagomirs (antago) to reduce the levels of miR-205 and

50 ssion of miR-433 but were induced by miR-433 antagomir (anti-miR-433).

51 Moreover, miRNA92a antagomir application reduced immune infiltration and ac

52 Our findings show that antagomirs are powerful tools to silence specific miRNAs

53 isorders, and efforts to develop therapeutic antagomirs are underway.

54 mically engineered oligonucleotides, termed 'antagomirs', are efficient and specific silencers of end

55 oited for the development of an anti-miR-122 antagomir as a host-targeting antiviral, the molecular m

56 nesis and highlight the potential of svRNA-N antagomirs as antivirals.

57 gulation of functional ATP6 protein, whereas antagomir blockade restored functional ATP6 protein and

58 ndogenous miR-9 expression by an appropriate antagomiR can significantly inhibit cell growth/viabilit

59 Importantly, a miRNA92a antagomir completely blocked induction of human TFH prec

60 small complementary miRNA sequences known as antagomirs could be used to inhibit miRNA activity, whil

61 right ventricular systolic pressure, and all antagomirs decreased pulmonary arterial muscularization.

62 ed for functional characterization: systemic antagomir depletion and spatiotemporal inhibition using

63 es of primary DCs treated with antisense RNA antagomirs directed against miR-451 secreted elevated le

64 udy was to assess whether a specific miR-122 antagomir down-regulates HCV protein replication and up-

65 tion of different chemically protected miRNA/antagomir duplexes in mouse livers and localization of a

66 Inhibition of both miRNAs by antagomirs during differentiation of the myeloid cell li

67 Both sets of antagomir effects were mimicked by infecting cells with

68 miR-545 function was inhibited by a specific antagomir, endogenous p220 expression increased in G0/G1

69 nhibiting miR-503 by using an antisense RNA (antagomir) enhanced CUGBP1 biosynthesis and elevated its

70 Injection of the specific antagomir for miR-309 resulted in smaller developing ooc

71 ic miR-134 using antisense oligonucleotides (antagomirs) had potent antiseizure effects in animal mod

72 We demonstrate that antagomirs harbor optimized phosphorothioate modificatio

73 and its inhibition by a cholesterol-modified antagomir has been reported to prevent cardiac hypertrop

74 duplexes in mouse livers and localization of antagomirs in a cytosolic compartment that is distinct f

75 In contrast, expression of miR-34a antagomirs in CD44(-) prostate cancer cells promoted tum

76 ommon pathway, and also establish the use of antagomiRs in fish for temporal knockdown of miRNA funct

77 ion, inhibition of miR-K12-11 function using antagomirs in KSHV-infected human primary effusion lymph

78 characterize the properties and function of antagomirs in mice.

79 n endogenous miR-23b was knocked down by its antagomirs in renal cancer cells.

80 r data further validate the effectiveness of antagomirs in vivo and should facilitate future studies

81 i-microRNAs results in functional siRNAs and antagomirs in vivo.

82 iR-126 mimic, whereas inhibition of miR-126 (antagomir) in healthy CD31(+) cells fully mimicked the P

83 oducing modified antisense oligonucleotides (antagomiRs) in ovo during chick development.

84 ppressed osteoblast differentiation, whereas antagomirs increased bone marker expression.

85 vels, while treatment with the corresponding antagomiRs increased cyclin T1 protein levels.

86 were suppressed at 32 degrees C and miR-155 antagomirs increased Ship1 and Socs1 and reversed the al

87 OX-mediated tumor suppression pathway, these antagomirs induced ROS, inhibited HIF signaling and incr

88 ation was significantly increased by miR-494 antagomir infusion, indicating their regulation by miR-4

89 of ZBTB4 or restoration of ZBTB4 by using an antagomir inhibit growth and invasion of breast cancer c

90 Antagomir inhibition of miR-223 reactivated CLDN8 and im

91 The local application of an miR-342-5p antagomir inhibits the development of atherosclerosis in

92 iation, was increased during sepsis and that antagomiR injection reduced its expression.

93 the immunosuppressive mediators, similar to antagomiR injection.

94 also investigated via infusion of a miR-494 antagomir into the central nucleus of amygdala.

95 methyl-mimic miR-122, or nonspecific control antagomir, into wild-type (WT) Huh-7 cells or Huh-7 stab

96 silencing of endogenous miR-155 or -802, by antagomir intra-ventricular injection, resulted in the n

97 The inhibition of miR-19a-3p with an antagomir led to a significant increase in 5-LO mRNA exp

98 Genetic deletion of let-7, antagomir-mediated blockage of let-7 and miR-184* action

99 Antagomir-mediated inhibition of svRNA-N significantly r

100 Conversely, antagomiR-mediated miR-23b and -27b silencing produces t

101 recent reports have suggested that an miR-21 antagomir might be therapeutically useful in preventing

102 Antagomir of miR-122 also decreased Bach1 and increased

103 Antagomir of miR-122 reduced the abundance of HCV RNA by

104 We transfected antagomir of miR-122, 2'-O-methyl-mimic miR-122, or nons

105 eleted, elevate mRNA translation, as does an antagomir of miR-122.

106 Furthermore, antagomir of miR-27b suppressed cell invasion in 4175 ce

107 function and survival relative to a control antagomiR oligonucleotide.

108 man embryoid bodies to hsa-miR-1294 mimic or antagomir oligonucleotides yielded directionally opposit

109 man embryoid bodies to the microRNA mimic or antagomir oligonucleotides, and we observed the effects

110 a miR mimic (tumour suppressor miRNA) and an antagomiR (oncomiR inhibitor)-provides outstanding capab

111 Blockage of miR-205 activity with an antagomir or via ectopic expression of miR-184 could be

112 g with miR-205 function by using a synthetic antagomir, or by the ectopic expression of miR-184, lead

113 Inhibition of miR-223 in vivo using specific antagomirs potentiated postnatal retinal angiogenesis in

114 of amygdala, through infusion of a specific antagomir, provoked anxiolysis, mimicking the action of

115 Inhibition of miR-146a with a selective antagomir restored the immunoregulatory activity of nBMS

116 tralizing virus-induced miR-146a by specific antagomiR restores expressions of IRAK1 and TRAF6, augme

117 ypti females after injection of its specific antagomir resulted in severe defects in blood digestion,

118 Blockade of miR-99b expression by antagomirs resulted in significantly reduced bacterial g

119 imilarly, the inhibition of miR-196a with an antagomir results in an increased level of ANXA1.

120 cal administration of cholesterol-conjugated antagomiRs revealed better inhibition of miR-195 compare

121 Use of specific miRNA antagonists, antagomirs, revealed that miR-301a contributed to the de

122 Therefore, miR-92a antagomir seems as a new atheroprotective therapeutic st

123 Temporal-specific knockdown of miR-138 by antagomiRs showed miR-138 function was required during a

124 vitro and in vivo, silencing of miR-10b with antagomirs significantly decreases miR-10b levels and in

125 RNAs can be blocked by a new class of drugs, antagomirs, some of which have been shown to improve car

126 Injection of antagomirs specific to miR-26a into neonatal mice derepr

127 Down-regulation of HCV replication using an antagomir targeted to miR-122 is effective, specific, an

128 apacity, whereas intraocular injection of an antagomir targeting miR-132, anti-miR-132, reduced postn

129 An antagomir to miR-BART20-5p might be an effective therape

130 portantly, in vivo application of a miRNA92a antagomir to nonobese diabetic (NOD) mice with ongoing i

131 trated that in vivo administration of miR-22 antagomir to SHR causes substantial ( approximately 18 m

132 Administration of miR-10b antagomirs to mice bearing highly metastatic cells does

133 /16-1 in cells increased cell death, whereas antagomirs to miR-15a/16-1 abolished the proapoptotic ef

134 Treatment with antagomiRs to miR-29b induced excess fibrosis after aort

135 Antagomirs to miR-326 that knocked down this cell endoge

136 rfusion recovery from hindlimb ischemia, and antagomirs to miR-93 attenuated perfusion recovery.

137 Hence, antagomirs to miR-BART20-5p or miR-494-3p, miR-142-3p mi

138 bioinformatic analysis of messenger RNA from antagomir-treated animals revealed that the 3' untransla

139 Inhibiting proinflammatory miR-155 by antagomir treatment could help reduce this complication

140 In atherosclerotic lesions, the miR-342-5p antagomir upregulated Akt1 expression and suppressed the

141 miR-690 knockdown using peptide nucleic acid-antagomiR was able to unblock and significantly increase

142 Blocking miR-339-3p by an antagomiR was sufficient to increase melanoma cell invas

143 ificance of silencing miRNAs with the use of antagomirs was studied for miR-122, an abundant liver-sp

144 1b(+) cells isolated from mice injected with antagomiRs were able to differentiate ex vivo into macro

145 Additionally, when antagomirs were used to knock down miR-93 and miR-130b i

146 first tested the effects of miR inhibitors (antagomirs), which were specifically designed to block m

147 The miR-10b antagomir, which is well tolerated by normal animals, ap