ライフサイエンスコーパス: miR

1 miR-1 recruited P-selectin, thymic stromal lymphopoietin

2 miR-125a-5p and L-plastin may be relevant targets for in

3 miR-127(PD) decreased the viability and motility of TNBC

4 miR-146a was originally identified as an anti-inflammato

5 miR-147 was also downregulated by directly incubating th

6 miR-206 is required for skeletal muscle regeneration in

7 miR-211 has previously been shown to be a direct regulat

8 miR-221, miR-222, miR-21-5p and miR-27a-5p were signific

9 miR-223 expression was decreased in breast cancer of lum

10 miR-223 is enriched in hemECs and in oligopotent nascent

11 miR-223 restricts the EHT of lymphoid-myeloid lineages b

12 miR-24-3p and miR-145-5p were highly expressed in human

13 miR-31 deletion resulted in suppression of miR-31-associ

14 miR-451 is highly conserved in vertebrates and regulates

15 miR-451 is the only known miRNA whose processing bypasse

16 To date, microRNA-1 (miR-1) is the only microRNA known to be regulated in the

17 ing a CaMKIIalpha promoter and microRNA-128 (miR-128) binding sites, and labeled CaMKIIalpha(+) cells

18 20a-FOXE1-PDGFRA) and eight miRNAs (miR-140, miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR-451a and

19 cytes, the expressions of microRNA (miR)-17, miR-18a, miR-19a, miR-19b, and miR-20a, which all belong

20 ression of some microRNAs, including miR-17, miR-150, and miR-155, suggested that microRNAs might pla

21 1-PDGFRA) and eight miRNAs (miR-140, miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR-451a and miR-92a

22 hogenesis including miR-200, miR-7, miR-184, miR-212/miR-132, and miR-130a/b/miR-152.

23 els than control BEC; and that microRNA-18a (miR-18a) normalized AVM-BEC function and phenotype, alth

24 e expressions of microRNA (miR)-17, miR-18a, miR-19a, miR-19b, and miR-20a, which all belong to the m

25 and eight miRNAs (miR-140, miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR-451a and miR-92a) were di

26 ions of microRNA (miR)-17, miR-18a, miR-19a, miR-19b, and miR-20a, which all belong to the miR-17~92

27 t miRNAs (miR-140, miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR-451a and miR-92a) were discovered

28 (miR-140, miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR-451a and miR-92a) were discovered in both h

29 on assays detected positive signals of the 2 miR expression in alveolar epithelial cells.

30 eclinical evidence for the use of miR-30c-2*/miR-497 delivery and AURKA inhibition in the treatment o

31 olved in T2D pathogenesis including miR-200, miR-7, miR-184, miR-212/miR-132, and miR-130a/b/miR-152.

32 miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR-451a and miR-92a) were discovered in both humans and

33 nt change in the expression of a total of 21 miR after CI and 47 miR after EVR.

34 s including miR-200, miR-7, miR-184, miR-212/miR-132, and miR-130a/b/miR-152.

35 miR-221, miR-222, miR-21-5p and miR-27a-5p were significantly inc

36 miR-221, miR-222, miR-21-5p and miR-27a-5p were significantly increased in

37 beta-catenin, Notch1, GATA6, CDX2, miR-34a, miR-181a, and miR-93 were determined in 24 paired GC tis

38 miRNA expression (e.g., upregulated miR-34a, miR-7, and miR-181b).

39 Out of 381 miRs screened in the perivascular tissues in response to

40 E-specific dysregulated miRNAs (miR-200c-3p, miR-25-3p, and miR-302a-3p) and genes (EPHA2, JUN, KLF4,

41 l CREB1-regulating miRNAs, namely miR-22-3p, miR-26a-5p, miR-27a-3p, and miR-221-3p.

42 MI, and sex, baseline levels of miR-3187-3p, miR-4302, and the miRNA combination of miR-3187-3p/miR-1

43 SE-specific dysregulated miRNAs (miR-367-3p, miR-519d-3p, and miR-96-5p) and genes (NR2F1 and NR2F2).

44 02, and the miRNA combination of miR-3187-3p/miR-103a-3p predicted differences in MMTT C-peptide AUC/

45 12-month visit; the combination miR-3187-3p/miR-4723-5p predicted proportions of subjects above/belo

46 s strongly suggest that microRNAs (miR-24-4, miR-21), cytoskeleton remodeling, response to stimuli, a

47 ression of a total of 21 miR after CI and 47 miR after EVR.

48 t some of the regulated isomiRs (e.g. the 5' miR-217 isomiR) are endowed with alternative seed sequen

49 lating miRNAs, namely miR-22-3p, miR-26a-5p, miR-27a-3p, and miR-221-3p.

50 n T2D pathogenesis including miR-200, miR-7, miR-184, miR-212/miR-132, and miR-130a/b/miR-152.

51 y reducing lung fibroblast (LF) microRNA-98 (miR-98) and PPARgamma levels, thus promoting airway remo

52 ricytes were isolated and transfected with a miR-145a mimic, followed by stimulation with lipopolysac

53 nstrated that increasing PELI3 levels with a miR-744-5p antagomir in an inflammatory environment resu

54 ted skeletal muscles, we genetically ablated miR-133b in the mdx mouse model of DMD.

55 In addition, miR-181c significantly regressed tumor growth in the xen

56 helium, but not smooth muscle or adventitia, miR-210 was observed in knockout mice of WT-knockout pai

57 etal muscle insulin metabolism (miR-106b and miR-20b-5p) and miRNAs with functions in both skeletal m

58 iR-200, miR-7, miR-184, miR-212/miR-132, and miR-130a/b/miR-152.

59 me microRNAs, including miR-17, miR-150, and miR-155, suggested that microRNAs might play a significa

60 egulation in endocrine pancreas (miR-15a and miR-17).

61 d further analysis suggested that miR-16 and miR-148a enriched in exosomes from FAK-null CAFs contrib

62 atory and immunologic targets for miR-17 and miR-548b that are known mediators of lung injury.

63 We found that miR-17 and miR-548b were upregulated in alveolar epithelial cells a

64 Notch1, GATA6, CDX2, miR-34a, miR-181a, and miR-93 were determined in 24 paired GC tissues and corre

65 RNA (miR)-17, miR-18a, miR-19a, miR-19b, and miR-20a, which all belong to the miR-17~92 cluster, are

66 on of cuSCC tumors identified miR-30c-2* and miR-497 as underexpressed in TAp63-deficient cuSCC.

67 ts downstream target miRNAs, miR-30c-2*, and miR-497 as major players that can suppress progression a

68 ventricular tissue revealed that miR-21 and miR-221, 2 activators of profibrotic and proliferative p

69 miR-24-3p and miR-145-5p were highly expressed in human kidneys follow

70 We identify miR-143-3p and miR-22-3p as markers of the naive state and miR-363-5p,

71 amely miR-22-3p, miR-26a-5p, miR-27a-3p, and miR-221-3p.

72 egulated miRNAs (miR-200c-3p, miR-25-3p, and miR-302a-3p) and genes (EPHA2, JUN, KLF4, PLXDC2, RND3,

73 gulated miRNAs (miR-367-3p, miR-519d-3p, and miR-96-5p) and genes (NR2F1 and NR2F2).

74 18a, miR-19a, miR-19b, miR-20a, miR-451a and miR-92a) were discovered in both humans and mice.

75 identified 5 miRNA (including let-7f-5p and miR-181a-5p) and 4 tRNA that are responsive to the dynam

76 miR-221, miR-222, miR-21-5p and miR-27a-5p were significantly increased in ex vivo carti

77 ssion (e.g., upregulated miR-34a, miR-7, and miR-181b).

78 miR-22-3p as markers of the naive state and miR-363-5p, several members of the miR-17 family, miR-30

79 er, treatment of established PNFs using anti-miR-155 peptide nucleic acid-loaded nanoparticles margin

80 bial suppression reversibly decreases aortic miR-204 and improves endothelial function, while the end

81 lating miR-122 regulates vascular miR-204 as miR-122 inhibition decreases miR-204 in endothelial cell

82 To assess miR-133b function in DMD-affected skeletal muscles, we g

83 -7, miR-184, miR-212/miR-132, and miR-130a/b/miR-152.

84 to define the role of the SP/NK1R/TGF-beta1/miR-31 axis in regulating biliary proliferation and live

85 , we firstly demonstrated that bioengineered miR-1291 agent was selectively processed to high levels

86 ted by T2DM, while the signature composed by miR-146a, -320a, -422a, and -451a efficiently identified

87 Vimentin levels were reduced by miR-144 and increased by antagomiR-144 in cultured cardi

88 ased on oncomirs from SEVs (caf-miR-205, caf-miR-222, caf-mir-20a and caf-miR-93) is proposed.

89 af-miR-205, caf-miR-222, caf-mir-20a and caf-miR-93) is proposed.

90 r signature based on oncomirs from SEVs (caf-miR-205, caf-miR-222, caf-mir-20a and caf-miR-93) is pro

91 ree age groups, we identified one candidate (miR-216a) implicated in beta cell proliferation for subs

92 s through delivery of microvesicles carrying miR-155 to disease-prone regions.

93 including beta-catenin, Notch1, GATA6, CDX2, miR-34a, miR-181a, and miR-93 were determined in 24 pair

94 uppresses MYO18B mRNA irrespective of CEBPB, miR-520G overexpression or IFN-gamma treatment.

95 Two parasite-derived miRNAs, cel-miR-71-5p and bma-lin-4, and O-150 repeat DNA were asses

96 We also show that the circulating miR-122 regulates vascular miR-204 as miR-122 inhibition

97 C-miR146a reduced expression of classic miR-146a targets (IRAK1 and TRAF6), thereby blocking act

98 The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes

99 evels at the 12-month visit; the combination miR-3187-3p/miR-4723-5p predicted proportions of subject

100 Increased Gas5 RNA level and decreased miR-222 expression were shown in MLN-M isolated from 7 G

101 ular miR-204 as miR-122 inhibition decreases miR-204 in endothelial cells and aorta.

102 te or chronic cocaine exposure downregulated miR-124 levels concomitant with upregulation of PARP-1 p

103 eously upregulating miR-7 and downregulating miR-21 and establishes a roadmap towards clinical transl

104 Endothelial miR-1 regulates eosinophil trafficking in the setting of

105 aining also confirmed the linkage of ERalpha/miR-141-3p/GSN signaling to the HCC progression.

106 rget of miR-124 in neuronal cells, establish miR-124 as a cocaine-regulated miRNA in the mouse NAc, a

107 control (except miR-429) and cancer (except miR-200a and miR141) samples than their respective Ameri

108 er miR-200 levels in Chinese control (except miR-429) and cancer (except miR-200a and miR141) samples

109 somes showed alterations of several exosomal miRs in FAK-null CAFs, and further analysis suggested th

110 cocultured with MDA-MB-231 cells expressing miR-149, epidermal growth factor (EGF) and amphiregulin

111 Over-expressing miR-195 reduces expression levels of its top predicted t

112 63-5p, several members of the miR-17 family, miR-302 family as primed markers.

113 In situ hybridization for miR-517a/c, a C19MC cistron microRNA, in first trimester

114 ant inflammatory and immunologic targets for miR-17 and miR-548b that are known mediators of lung inj

115 Beyond anti-inflammatory functions, miR-146a is a known tumor suppressor commonly deleted or

116 Furthermore, miR-21/221 knockdown significantly attenuated RV but not

117 In addition, high miR-1260b expression in serum was correlated with radiol

118 We also found that high miR-181a is associated with decreased IFNgamma response

119 Further analyses showed significantly higher miR-200 levels in Chinese control (except miR-429) and c

120 Hsa-miR-124-3p had the most predicted mRNA target interactio

121 hsa-miR-223-3p was a key regulator of the TLR and Th17 pathw

122 s at the 3' terminus for hsa-miR-34a and hsa-miR-449a.

123 target sequences at the 3' terminus for hsa-miR-34a and hsa-miR-449a.

124 g II (angiotensin II)-mediated hypertension, miR-214 showed the highest induction (8-fold, P=0.0001).

125 -mouse comparison of cuSCC tumors identified miR-30c-2* and miR-497 as underexpressed in TAp63-defici

126 We identify miR-143-3p and miR-22-3p as markers of the naive state a

127 ified regulator of atherosclerotic burden in miR-144 knockout mice receiving a high fat diet.

128 Furthermore, changes in miR-223 levels in the OFC were positively and negatively

129 igation revealed that Dicer was decreased in miR-200a overexpressed BC cells; this resulted in inhibi

130 ival and parasite growth and distribution in miR-155(-/-) and wild-type (WT) C57BL/6 mice.

131 ic shock exhibited a significant increase in miR-19b and a concomitant decrease in syndecan-1 mRNA.

132 s in expression of some microRNAs, including miR-17, miR-150, and miR-155, suggested that microRNAs m

133 ilies involved in T2D pathogenesis including miR-200, miR-7, miR-184, miR-212/miR-132, and miR-130a/b

134 under a hypoxic condition, AR could increase miR-185-5p expression to suppress VEGF-C expression, yet

135 Similarly, neutrophil microvesicles increase miR-155 and enhance NF-kappaB at disease-prone sites of

136 Similarly, rosiglitazone increased miR-98 and reversed nicotine-induced increases in NGF, F

137 s with HCC treated with sorafenib, increased miR-30e-3p circulating levels predicted the development

138 In gene expression studies, SHP inhibited miR-210 expression by repressing a transcriptional activ

139 y overexpression of ATM from a clone lacking miR-181c binding sites.

140 ile the endothelial function of mice lacking miR-204 remained indifferent to the microbial alteration

141 IARS mice were mostly CCL1(+)IL-10(+)LIGHT(+)miR-27a(+) M (M2bM , inhibitor cells for the M1M polariz

142 Notably, higher LOX, ITGA5, or FN1, or lower miR-142-3p levels are associated with shorter survival i

143 These findings confirm macrophage miR-106b-5p secretion from impaired vitamin D receptor s

144 Meanwhile, miR-26a prevents hyperinsulinemia through targeting seve

145 In a feed-forward mechanism, miR-3085-3p then potentiates NFkappaB signaling.

146 tions in skeletal muscle insulin metabolism (miR-106b and miR-20b-5p) and miRNAs with functions in bo

147 at least in part, via activation of microRNA miR-7.

148 keratinocytes, the expressions of microRNA (miR)-17, miR-18a, miR-19a, miR-19b, and miR-20a, which a

149 e aimed to investigate the roles of microRNA(miR)-124, a novel ER stress suppressor, in As-induced ER

150 we identified an autosomal-derived microRNA, miR-1-3p, that has predicted target sites in the transfo

151 with a decrease in its regulatory microRNA, miR-148b-3p.

152 se findings strongly suggest that microRNAs (miR-24-4, miR-21), cytoskeleton remodeling, response to

153 microRNAs (miRs) are small non-coding molecules that regulate post-

154 MicroRNAs (miRs) are small non-coding RNAs that can have large impa

155 tion, analysis of EV cargo implicated miRNA (miR-124) as a potential candidate in the mitigation of R

156 ted several SE-specific dysregulated miRNAs (miR-200c-3p, miR-25-3p, and miR-302a-3p) and genes (EPHA

157 TIMP3) and NSE-specific dysregulated miRNAs (miR-367-3p, miR-519d-3p, and miR-96-5p) and genes (NR2F1

158 miR17/miR20a-FOXE1-PDGFRA) and eight miRNAs (miR-140, miR-17, miR-18a, miR-19a, miR-19b, miR-20a, miR

159 fine TAp63 and its downstream target miRNAs, miR-30c-2*, and miR-497 as major players that can suppre

160 cooperatively to the PDCD4 mRNA and mitigate miR-21-mediated translation repression.

161 p towards clinical translation of modulating miRs for various cancer types.

162 Moreover, miR-223 was found to be enriched in astrocytes and secre

163 -371-373 are the human homologs of the mouse miR-290 family, which are the most highly expressed miRN

164 d four novel CREB1-regulating miRNAs, namely miR-22-3p, miR-26a-5p, miR-27a-3p, and miR-221-3p.

165 Neither miR-21 or miR-221 was statistically significantly differ

166 Notably, miR-125b down-regulation in infected cells was not due t

167 formation resulted in a timely abrogation of miR-223 expression, likely due to activation of E2F1, a

168 Exogenous administration of miR-127, which is functionally activated in target cells

169 e control (P <= 0.05) and single blockade of miR-24-3p (P <= 0.01) or miR-145-5p (P <= 0.05).

170 7-3p, miR-4302, and the miRNA combination of miR-3187-3p/miR-103a-3p predicted differences in MMTT C-

171 ssion of Ago2 rescues some of the defects of miR-451 processing.

172 diate inflammatory responses.(,) Deletion of miR-146a in mice phenocopies many aspects of age-depende

173 In vivo, global deletion of miR-155 significantly decreased tumor number and volume,

174 Furthermore, delivery of miR-486-5p antagomirs to preestablished orthotopic GBM n

175 nanoparticles are used for the detection of miR-17.

176 the EsxBA proteins in the downregulation of miR-147.

177 articular, pulmonary vascular engraftment of miR-210-positive interstitial lung macrophages was obser

178 of miR-1185-1, which increased expression of miR-1185-1 and further repressed CD24 translation and co

179 ha(+) cells with naturally low expression of miR-128 (Lm128C cells) in male and female mice.

180 Ectopic expression of miR-15a decreases both mRNA and protein levels of SMPD1.

181 showed a combined loss of the expression of miR-15a/-15b and overexpression of their direct/indirect

182 Tissue expression of miR-181a-5p reflected plasma levels.

183 Exogenous expression of miR-181c inhibited ATM expression and activation of its

184 r findings suggest that higher expression of miR-21 is correlated with poorer glioma prognosis.

185 2.73), indicating that higher expression of miR-21 was significantly associated with worse OS in gli

186 We noted loss of expression of miR-299-3p in prostate tumors compared to noncancerous p

187 TGFbeta1 also induces the expression of miR-3085-3p, but in this instance, it exerts a feedback

188 tion abolished normal rhythmic expression of miR-375 and the functional regulation occurred in the l-

189 one resulted in reduced muscle expression of miR-379 and increased expression of EIF4G2 and DAPIT.

190 PCR) arrays indicated that the expression of miR-522-3p was downregulated in paclitaxel-resistant cel

191 ent with previous transcriptomic findings of miR-128 in regulating gene networks that govern membrane

192 ressed the remodeling-associated increase of miR-21.

193 Selective in vivo inhibition of miR-128-3p in FMRP-deficient astroglia sufficiently resc

194 Inhibition of miR-15a/16-1 function in cerebrovascular endothelium may

195 sed BC cells; this resulted in inhibition of miR-16 maturation and consequently led to increased JNK2

196 Furthermore, introduction of miR-181c significantly inhibited phospho-cyclin-dependen

197 ptide, age, BMI, and sex, baseline levels of miR-3187-3p, miR-4302, and the miRNA combination of miR-

198 population structure, we found that loss of miR-146a depleted a subpopulation of primitive, quiescen

199 MS/MS analysis, we discover that majority of miR-21-5p isolated from human non-small cell lung cancer

200 Misexpression of miR-183 cluster in the human retinal epithelial cells le

201 ore, viral vector-mediated overexpression of miR-124 in the irradiated brain ameliorated RICD and red

202 function, while astroglial overexpression of miR-128-3p strongly and selectively diminishes developme

203 cycle progression, whereas overexpression of miR-181c promoted apoptosis of HCV-infected hepatocytes

204 ioma dataset revealed that overexpression of miR-21 was a potential independent prognostic biomarker

205 sine 9 acetylation on the promoter region of miR-1185-1, which increased expression of miR-1185-1 and

206 to activation of E2F1, a known repressor of miR-223 transcription.

207 oxO-Hippo subnetwork, as well as the role of miR-129-5p in the miR-129-5p-Col1a1 subnetwork.

208 We identified the physiological role of miR-1300 as a regulator of endomitosis in megakaryocyte

209 xperiments validated the regulatory roles of miR-340-5p and Foxm1 in the Wnt-FoxO-Hippo subnetwork, a

210 Optimal quantitative sensing of miR-141 was achieved via the first example of an electro

211 miR-31 deletion resulted in suppression of miR-31-associated EGLN3/NF-kappaB-controlled inflammator

212 tudies identify Parp-1 as a direct target of miR-124 in neuronal cells, establish miR-124 as a cocain

213 factor 4 was found to be a direct target of miR-128 and able to modulate the methylation status of t

214 fibrotic responses and SHIP-1 is a target of miR-155.

215 yD88 has been shown to be a direct target of miR-3085-3p and may be responsible for the early inhibit

216 or kappaB (NF-kappaB), as a direct target of miR-31 establishes a functional link between oncomiR-31,

217 3 (FGFR3) was also identified as a target of miR-701-3p.

218 dentify additional cardiovascular targets of miR-144, and subsequently examined the role of a newly i

219 PTEN), which is one of the direct targets of miR-216a, was analyzed using western blot.

220 provides preclinical evidence for the use of miR-30c-2*/miR-497 delivery and AURKA inhibition in the

221 tigated whether stress-induced variations of miR-218 expression in the mPFC can be detected in blood.

222 Lastly, profiling of miRs from CAF exosomes showed alterations of several exo

223 protein, as a new target gene for oncogenic miR-106b, which was identified as an induced miRNA in PC

224 single blockade of miR-24-3p (P <= 0.01) or miR-145-5p (P <= 0.05).

225 Neither miR-21 or miR-221 was statistically significantly different in LV-

226 Mutating the miR-9-3p or miR-9-5p MREs prevented this decrease, demonstrating dir

227 Targeting the SP/NK1R and/or miR-31 may be a potential approach in treating human cho

228 Among these, miR-155 was a top overexpressed miR, and its expression was regulated by RAS/MAPK signal

229 cell cycle regulation in endocrine pancreas (miR-15a and miR-17).

230 Our results demonstrated that pericyte miR-145a mediates sepsis-associated microvascular dysfun

231 Plasma miR-181a-5p was significantly downregulated in non-progr

232 In blood, postnatal miR-218 expression parallels changes occurring in the mP

233 the precursor to oncogenic microRNA-21 (pre-miR-21) for enzymatic destruction with selectivity that

234 translated region of PDCD4 mRNA and prevents miR-21-mediated translation repression.

235 TIMP3 and CPEB3 are putative miR targets in chondrocytes.

236 ngly, FOXM1 was found to negatively regulate miR-23c expression in prostate cancer.

237 nterestingly, HIV-1 infection down-regulated miR-125b expression concurrent with up-regulation of CPS

238 Bioinformatics analysis revealed miR-34a could target 30 genes that are implied in all st

239 enome browser analysis of PACS-1 micro RNAs (miR), revealed two 8-base target sequences at the 3' ter

240 -5 abundance, and we found that EC-selective miR-15a/16-1 deletion enhanced claudin-5 mRNA and protei

241 Serum miR-1 levels had inverse correlations with sputum eosino

242 Serum miR-375 was significantly lower in the peritoneal pouch

243 Among these, serum miR-1260b level was significantly upregulated in patient

244 miR-370-3p into heart failure mice silences miR-370-3p and restores HCN4 mRNA and protein and I(f) i

245 sequences for skeletal muscle cell-specific miR-206.

246 fferential microRNA expression, specifically miR-326, may in part explain regional differences in inf

247 In these studies, miRs predicted to bind to the 3'-UTR of mouse MR were pr

248 sibility of using the EVLP platform to study miR signature in human lungs in response to CI/EVR.

249 A novel tumor suppressor miR-1185-1 is involved in molecular regulation of CD24-

250 According to TCGA data, the tumor suppressor miR-200b is overedited in thyroid tumors, and its levels

251 ased in control mice injected with synthetic miR-144.

252 lectively processed to high levels of target miR-1291-5p in human pancreatic cancer (PC) cells.

253 and luciferase reporter assay confirmed that miR-466o-3p directly targeted WT1 mRNA.

254 ally, pulldown experiments demonstrated that miR-125b physically interacts with CPSF6 3'UTR.

255 Our results demonstrated that miR-1291 was effective to sensitize PC cells to arginine

256 In this study, we present evidence that miR-19b targets syndecan-1 mRNA to downregulate its expr

257 ese results provide conclusive evidence that miR-31 expression is necessary for ESCC development.

258 We find that miR-451, which derives from a hairpin with a suboptimal

259 sequencing and flow cytometry, we found that miR-155 promotes the activation of effector T cell popul

260 We found that miR-17 and miR-548b were upregulated in alveolar epithel

261 RNA is through miRNA sponging, we found that miR-671-5p more potently silenced an axis of CDR1as and

262 integrated screening approach, we found that miR-671-5p reduces LUSC metastasis by inhibiting a circu

263 Bioinformatics analysis predicts that miR-379 targets EIF4G2, a translational factor, which is

264 Luciferase reporter assay revealed that miR-124 post-transcriptionally regulates Parp-1 3'UTR ac

265 analysis of ventricular tissue revealed that miR-21 and miR-221, 2 activators of profibrotic and prol

266 Here we show that miR-17-92 forms a regulatory loop with the transcription

267 ive RT-PCR and Cyquant assay, we showed that miR-124 protects against As-induced cytotoxicity in neur

268 Subtype-specific analysis showed that miR-200b had an overall elevated level in serous cancer

269 of tumor-stroma interactions by showing that miR-149 downregulation in TNBC enhances reciprocal growt

270 These data suggest that miR-149 downregulation functionally contributes to breas

271 These results suggest that miR-H1/H6 plays an important role in facilitating effici

272 ll CAFs, and further analysis suggested that miR-16 and miR-148a enriched in exosomes from FAK-null C

273 are targets of the miR-183 cluster, and the miR-183 cluster dysregulation causes certain defects in

274 ion of the circadian rhythm and sleep by the miR-375-timeless interaction.

275 Accordingly, mutations in the miR-125b seed sequence abrogated the regulatory effect o

276 rk, as well as the role of miR-129-5p in the miR-129-5p-Col1a1 subnetwork.

277 Mutating the miR-9-3p or miR-9-5p MREs prevented this decrease, demon

278 Compared with wild type, ablation of the miR-144/451 cluster increased plasma vimentin, while vim

279 state and miR-363-5p, several members of the miR-17 family, miR-302 family as primed markers.

280 pathway of photoreceptors are targets of the miR-183 cluster, and the miR-183 cluster dysregulation c

281 multivariate Cox regression analysis of the miR-21 expression in the TCGA glioma dataset revealed th

282 q revealed a significant derepression of the miR-21 targetome in antimiR-21-treated myocardium and a

283 These results dissect the role of the miR-211-DUSP6-ERK5 axis in melanoma tumor growth and sug

284 k at least in part through regulation of the miR-424(322)/503 cluster.

285 For in vivo study, the miR-216a mimics/inhibitors conjugated to the nanoparticl

286 that AR could transcriptionally suppress the miR-185-5p expression in the presence of functional VHL-

287 iR-19b, and miR-20a, which all belong to the miR-17~92 cluster, are upregulated during wound repair.

288 We validated the miR-744 binding site in the 3' untranslated region (UTR)

289 Among these, miR-155 was a top overexpressed miR, and its expression

290 sion to suppress VEGF-C expression, yet this miR-185-5p effect on VEGF-A was reversed via AR's positi

291 In triple-negative breast cancer (TNBC), miR-127 downregulation correlates with decreased disease

292 , intraperitoneal injection of an antimiR to miR-370-3p into heart failure mice silences miR-370-3p a

293 erential miRNA expression (e.g., upregulated miR-34a, miR-7, and miR-181b).

294 andard low dose radiation (2 Gy) upregulates miR-15a and decreases SMPD1 levels.

295 utic efficacy of simultaneously upregulating miR-7 and downregulating miR-21 and establishes a roadma

296 t the circulating miR-122 regulates vascular miR-204 as miR-122 inhibition decreases miR-204 in endot

297 The vascular miR-204 is sensitive to microbiota, and microbial suppre

298 ulation occurred in the l-LNv neurons, where miR-375 modulated the circadian rhythm and sleep via tar

299 erous cancer compared with controls, whereas miR-429 was significantly elevated in clear cell and end

300 Here we assessed whether miR-218 in the mPFC confers resilience or susceptibility