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240 publications mentioning hsa-mir-181d (showing top 100)

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-181d. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 283
We hypothesized that, in conjunction with the host pro-inflammatory response during early infection, miR-181 expression might be up-regulated in HeV-infected mammals, but perhaps the virus co-opts this up-regulation to support infection and viral spread in the host. [score:9]
Expression of miR-181 is up-regulated in circulating biofluids derived from in vivo mo dels of henipavirus diseasePrevious studies have reported that members of the miR-181 family are involved in different aspects of immune regulation [43– 45]. [score:9]
Importantly, levels of EphA5 and EphA7, but not EphA4, are reduced by overexpression of both miR-181a and miR-181d, indicating that these class A Ephs are target genes for the miR-181 family, and that the pro-fusion phenotype of miR-181 are, at least in part, due to its downregulation of specific class A Ephs. [score:8]
Expression of miR-181 is up-regulated in circulating biofluids derived from in vivo mo dels of henipavirus disease. [score:8]
As each miRNA can act as a suppressor of many target genes, we hypothesized that miR-181 and miR-17~93 families promoted henipavirus infection by suppressing multiple anti-viral host genes. [score:7]
This led us to hypothesize that miR-181 supported fusion by down -regulating the expression of one or more novel cellular factor(s) that antagonizes expression and/or activity of the henipavirus entry receptors, ephrin-B2 or–B3. [score:6]
miR-181 targets EphA5, EphA7 and EphB4, but not EphA4, for downregulation. [score:6]
Thus, a potential mo del for the pro-viral mechanism of miR-181 posits that the miRNA down-regulates expression of Ephs, increasing the pool of unbound ephrin-B2 or ephrin-B3 for henipavirus G glycoproteins to attach and trigger entry/membrane fusion. [score:6]
Intriguingly, even though the 3’UTR of EphB4 transcripts does not contain any sequence that is complementary to the seed region of miR-181, EphB4 levels were downregulated by miR-181 expression. [score:6]
These data show that endogenous levels of the henipavirus fusion regulators EphA5, A7 and B4 can all be significantly suppressed by miR-181 expression. [score:6]
We opted to assess all Ephs with putative miR-181 target sites as predicted by TargetScan [39, 40], namely EphA4, A5 and A7 (S4 Table). [score:5]
Verified miR-181 and miR-17~93 target genes predominantly inhibit henipavirus infection. [score:5]
Target cells (HeLa) were pre -transfected with either miR-181d agonist or the control agonist (miNEG), stained with a live cell membrane dye, and co-cultured for 24 h with effector cells expressing both glycoproteins or HeV G alone. [score:5]
Select Eph receptors inhibit HeV infection and cell-cell-fusion and are miR-181 target genes. [score:5]
Over -expressing miR-181a and miR-181d caused a significant reduction in EphA5 and A7 mRNA levels, with the latter showing the greatest reduction in gene expression (Fig 7D). [score:5]
Cross-referencing of results from the siRNA screen of host genes associated with HeV infection suggests that miR-181 and miR-17~93 target multiple host genes which are anti-viral for HeV, and that the net outcome of cellular expression of miR-181 or miR-17~93 is likely a host microenvironment that is more conducive for henipavirus infection. [score:5]
Since miR-181 specifically promotes infection of henipaviruses but not other paramyxoviruses, it is quite likely miR-181 increases membrane fusion by directly targeting viral and/or host molecules unique to the henipavirus fusion machinery. [score:4]
In fact, miR-181 downregulated ephrin-B3 and and HeV F glycoprotein by about 30 to 40%. [score:4]
Collectively, these observations demonstrate in two different in vivo mo dels that members of the miR-181 family are up-regulated early in the host during HeV infection, implicating a biological role for miR-181 in host immunity as well as in henipavirus pathogenesis. [score:4]
In contrast, EphA4 levels were not impacted by miR-181d, and were only modestly (11%) affected by miR-181a, demonstrating some level of specificity in the regulation of Eph receptor expression by miR-181. [score:4]
Consistent with this, we observed that miR-181 is up-regulated in sera of ferrets and blood of horses as early as day 1 during a henipavirus infection. [score:4]
We also sought to determine whether miR-181 preferentially regulates the expression of host proteins localized in a particular subcellular compartment. [score:4]
Reminiscent of what was observed in mice treated with LPS [46], this early up-regulation appears to be transient, as by day three, levels of miR-181a and miR-181d began dropping to baseline levels. [score:4]
The screens, in addition to subsequent validation work, demonstrate a key role for miR-181 family members in regulating henipavirus syncytia formation and infection, and suggest several host miRNAs, including miR-17~93, as potential candidates for novel therapeutic targets. [score:4]
The mo del of miR-181 -mediated immune pathogenesis has potential implications for risk factors associated with susceptibility to henipavirus disease, as well as for the strategic design and development of novel immunotherapy for henipavirus infections. [score:4]
Perhaps surprisingly, S3 Fig shows that expression levels of the host and viral molecules which are known to be directly involved in fusion were not appreciably boosted by miR-181d. [score:4]
Accordingly, human EphB4 does contain a putative miR-181 binding site in its ORF, providing an avenue for miR-181 regulation of its expression. [score:4]
In stark contrast to henipaviruses, miR-181 has been shown to be inhibit infection of porcine reproductive and respiratory syndrome virus [63]. [score:3]
Collectively, these data suggest that the net outcome of miR-181 or miR17~93 expression is a cellular microenvironment that is more conducive for henipavirus infection. [score:3]
Here, total small RNA was purified from the stored blood samples of these horses, and the relative expression of miR-181a and miR-181d on 0, 1, 3, 5, 7 and 9 d. p. e. were determined by qRT-PCR (Fig 8C). [score:3]
Expression of entry receptors ephrin-B2/B3 and viral fusion glycoproteins are not appreciably enhanced by miR-181. [score:3]
qRT-PCR analysis of miR-181 expression. [score:3]
Given the substantial impact of miR-181 on cell-cell fusion (Fig 5B and 5C), it was intriguing that the miRNA did not considerably enhance expression levels of host and viral molecules known to be involved in entry and fusion. [score:3]
Pie charts show the relative proportions of pro- and anti-viral target genes for miR-181 (C) and for miR-17~93 (D), with the number of genes printed. [score:3]
To this end, the list of experimentally-validated miR-181 targets (n = 78 genes) was obtained from miRTarBase was subjected to annotation enrichment analysis using the DAVID web service. [score:3]
Experimentally validated target genes for miR-181 and miR-17 families (miRTarBase, and their corresponding impact on HeV infection). [score:3]
Following qRT-PCR, miR-181 expression was analysed using the ΔΔC [T] method and normalised to U6. [score:3]
Impact of members of Eph receptor family on HeV infection [14] and their putative miR-181 binding sites (TargetScan). [score:3]
Members of the miR-181 and miR-17~93 families strongly promoted Hendra virus infection and appear to suppress multiple antiviral host molecules. [score:3]
Viral RNA synthesis is augmented by miR-181 over -expression. [score:3]
S4 TableImpact of members of Eph receptor family on HeV infection [14] and their putative miR-181 binding sites (TargetScan). [score:3]
That said, algorithmic analysis by TargetScan [39, 40] of all human Ephs does not predict miR-181 binding sites in the 3’ UTR of the mRNAs of EphB3 or EphB4 (S4 Table). [score:3]
Collectively, our data supports a mo del where simultaneous inhibition of multiple anti-fusion Ephs from both receptor classes by miR-181 contributes to greatly enhanced membrane fusion and infection. [score:3]
Additionally, miR-181 expression in human kidney tissues were found to be associated with increased transcription of genes of inflammation pathways [47]. [score:3]
In contrast, target cells treated with miR-181d agonists formed larger multinucleated cells. [score:3]
It is tempting to speculate that the host pro-inflammatory response (of which blood miR-181 is correlated with) promotes the early phase of virus spread in the host, thereby contributing to disease progression and pathogenesis [43, 44, 46]. [score:3]
HeLa cells were transfected with miR-181d-specific agonists to effectively over-express miR-181d. [score:3]
Dual miRNA screens reveal miR-181 and miR-17~93 families as promoters of henipavirus infection that target multiple anti-viral genes. [score:3]
corroborate what was observed by visual inspection, indicating that miR-181 overexpression induced a drastic 9- to 10-fold increase in fusion events relative to control (Fig 5C). [score:3]
This supports the mo del that miR-181 enhances syncytia formation by targeting Ephs that naturally associate with the henipavirus entry receptors ephrin-B2 and B3. [score:3]
A subset of class A Eph receptors contain putative miR-181 target sites. [score:3]
This analysis demonstrated an enrichment of miR-181 target genes associated with the nucleoplasm (p = 4.6e-5), while proteins associated with plasma membrane localization were not significantly enriched (p = 0.7). [score:3]
For instance, the ratio of anti-viral to pro-viral hits for validated miR-181 targets was 2.2 to 1 (Fig 2C). [score:3]
Values represent the sum of all the Z-scores, and demonstrate the predominance of anti-viral genes among the miR-181 and miR-17 targets. [score:3]
To test this hypothesis, we firstly mined the miRTarbase database [27] to identify all experimentally-validated target genes for miR-181 and miR17~93 families. [score:3]
Expression levels of miR-181 in biofluids of animals infected with HeV are increased. [score:3]
Infection promotion is primarily mediated via the ability of miR-181 to repress Eph receptors that negatively regulate henipavirus glycoprotein -mediated cell-cell fusion. [score:2]
To address whether miR-181 promotes entry of henipaviruses, a cell-cell fusion assay was performed using 293T effector cells expressing HeV F and G-glycoproteins [14]. [score:2]
Thus, we next investigated if miR-181 overexpression would enhance expression of the virus entry receptors ephrin-B2 and -B3, as well as the viral fusion glycoproteins F and G. miR-181a agonists were included in this analysis, subsequent to the validation of their pro-fusion nature in infection and fusion assays (S2 Fig). [score:2]
These results indicate that, in addition to its role in regulating fusion, miR-181 might act via other anti-viral host mediators to induce a situation that is broadly supportive of henipavirus replication. [score:2]
Previous studies have reported that members of the miR-181 family are involved in different aspects of immune regulation [43– 45]. [score:2]
Considering that EphB4 is most antagonistic towards fusion (Fig 7C), it likely makes the most significant contribution to the pro-fusion phenotype of miR-181. [score:1]
Similar to results observed in ferret, transient yet significant increases in circulating miR-181 molecules were observed during the early stages of infection. [score:1]
However, and rather intriguingly, unlike miR-181 (Fig 4), members of the miR-17~93 family appear to also exhibit pro-viral effects on a paramyxovirus from a different subfamily than the henipaviruses. [score:1]
The seed sequence of the miRNAs in this family (AAAGUG) is distinct from that of miR-181. [score:1]
Considering the striking pro-fusogenic activity of miR-181, we wondered whether this effect is unique to the miR-181 family of miRNAs. [score:1]
Thus, miR-181 promotes henipavirus infection at, or prior to, the step of viral RNA synthesis. [score:1]
To assess whether the pro-viral effects of miR-181 are specific to HeV, the in vitro activity of miR-181d agonists were tested on a range of viruses from different subfamilies of the Paramyxoviridae family. [score:1]
Interestingly, this infection enhancement seems to be primarily mediated via the ability of miR-181 to significantly augment henipavirus glycoprotein -mediated cell-cell fusion, implicating miR-181 in the enhancement of henipavirus entry. [score:1]
We found that miR-181 did not affect infection by paramyxoviruses from other genera, indicating specificity in the henipavirus-miR181 virus-host interaction. [score:1]
Congruent with this notion, viral RNA synthesis in a single round of infection is elevated in cells transfected with miR-181 agonists. [score:1]
miR-181 impacts henipavirus infection but not paramyxoviruses from other genera. [score:1]
In addition to miR-181, most members of the miR-17~93 family were pro-viral (Fig 2B). [score:1]
In order to narrow down the possible mechanisms by which miR-181 promotes henipavirus infection, we next sought to delineate the part of the virus life cycle at which miR-181 promotes infection. [score:1]
All four members of the miR-181 family exhibited consistent pro-viral phenotypes in both the agonist and antagonist screens (Figs 1D and 2A). [score:1]
miR-181 significantly enhances HeV F- and G -mediated cell-cell fusion. [score:1]
miR-181d promotes wild-type HeV infection. [score:1]
This pro-fusion effect is specific to the miR-181 family, as transfection with agonists of another strongly pro-viral miRNA (miR-17), did not appreciably alter syncytia formation. [score:1]
Even though it was not predicted to contain any miR-181 binding sites, EphB4 was the most anti-viral hit of the class B receptors in the RNAi screen and was previously shown to compete with HeV G glycoprotein for ephrin-B2 binding [38], so it was incorporated into our study as well. [score:1]
miR-181d promotes henipavirus infection specifically. [score:1]
We found that, as early as one d. p. e., miR-181a and miR-181d became elevated in the serum of these ferrets during the course of infection (Fig 8B). [score:1]
The scale of the pro-viral impacts of miR-181 members is especially remarkable if we compare their effects to that of miR-146a (Fig 2A), which we previously validated as pro-viral for HeV [22]. [score:1]
Since henipavirus mediated cell-cell fusion is both a surrogate mo del for virus entry as well as a natural phenomenon during late stages of infection, it is likely that in addition to enhancing henipavirus entry, miR-181 also promotes more efficient cell-to-cell spread of this virus by merging the cytosols of neighbouring cells more rapidly. [score:1]
Both complementary screens converged on members of four miRNA families (miR-181, miR-17~93, miR-520h, miR-548d) that strongly promoted henipavirus infection. [score:1]
Even though the role of miR-181 in inflammation and NKT-cell maturation has been documented [23, 43– 46], little has been reported about its role in the infection of other viruses. [score:1]
All four members of the miR-181 family significantly promoted HeV infection (Fig 2A). [score:1]
These results indicate that the enhancement effects of miR-181 are specific to the henipavirus genus. [score:1]
miR-181 significantly enhances HeV RNA synthesis and F- and G -mediated cell-cell fusion. [score:1]
In contrast, pre-treatment of cells with miR-181d agonists increased the amount of HeV RNA by approximately 3-fold relative to cells treated with control agonist. [score:1]
Initial in silico analysis revealed that EphA4, EphA5 and EphA7 possess putative miR-181 binding sites in the 3’ UTRs of their transcripts. [score:1]
Cells were transfected with miR-181 agonists, and then infected with a high MOI (5) of HeV. [score:1]
To evaluate whether these anti-fusion Ephs are suppression targets of miR-181, the mRNA levels of the Ephs in agonist -transfected cells were measured by qRT-PCR. [score:1]
Screen results suggested that miR-181d is one of the most pro-viral members of the family (Fig 2A, S1 Table and S2 Table), hence miR-181d was chosen as a representative member of the miR-181 family in the majority of subsequent experiments. [score:1]
Interestingly, miR-181 -transfected cells induced substantially more, and larger, syncytia. [score:1]
We first looked at whether viral RNA synthesis was induced by miR-181 during a single round of HeV infection. [score:1]
This provides a coherent mechanistic mo del for how miR-181 may expedite host entry and virus spread during infection. [score:1]
In sum, these results indicate that HeV-glycoprotein mediated cell-cell fusion is greatly stimulated by miR-181, but not by miR-17, suggesting that miR-181 specifically facilitates henipavirus infection by enhancing host entry and, quite possibly, by supporting cell-to-cell spread during late stages of infection via syncytia formation. [score:1]
We show that miR-181 promoted infection of both wild-type HeV and NiV infections. [score:1]
Since all four members of the miR-181 family were pro-viral hits using this approach, we focused our validation efforts on miR-181. [score:1]
miR-181 promotes Hendra virus infection of human cells. [score:1]
1005974.g002 Fig 2(A and B) from miRNA screens for all miR-181 (A) and miR-17~93 (B) family members, represented by robust Z-scores. [score:1]
This study implicates miR-181 and certain class A Eph receptors as critical modulators of henipavirus membrane fusion, and highlights how the natural innate immune response of the host can be exploited by a RNA virus to promote cell-to-cell spread. [score:1]
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[+] score: 168
To conclude, we show a novel regulatory mechanism of PEAK1 expression in CRC in which miR-181d suppresses its direct target, PEAK1, in turn regulating CRC invasion and metastasis. [score:10]
The results showed that silencing miR-181d upregulated PEAK1 and strengthened cell invasion in vitro, whereas overexpressing miR-181d inhibited PEAK1 expression as well as cell proliferation, invasion and migration in vitro. [score:10]
It has been reported that miR-181d is downregulated in glioma and acts as a tumor suppressor by targeting KRas and Bcl-2 [40]. [score:8]
The results make it evident that miR-181d affects PEAK1 expression by directly binding to the 3′UTR region of PEAK1 and validating that PEAK1 is a direct target of miR-181d. [score:7]
c Western blot to measure PEAK1 protein levels in CRC cells transfected with miR-181d mimics or inhibitor for 72 h. d Western blot showed that overexpression of miR-181d or knockdown of PEAK1 downregulated p-Erk1/2 levels. [score:7]
Zhang W miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expressionNeuro Oncol. [score:6]
We performed a bioinformatics search for potential miRNAs targeting PEAK1 mRNA and found that miR-181d had the highest predictive scores, indicating that miR-181d might directly target PEAK1. [score:6]
Our results showed that miR-181d expression was significantly correlated with local relapse and TNM stage, and the downregulation of miR-181d was significantly associated with poorer overall survival in CRC. [score:6]
Downregulation of miR-181d using anti-miR-181d was associated with significantly higher expression of PEAK1 protein (Fig. 6c). [score:6]
miR-181d targets PEAK1 and as a tumor suppressor in CRC. [score:5]
Together, these findings suggest that low expression of miR-181d leads to high expression of PEAK1 in CRC. [score:5]
Hence, miR-181d is an important tumor suppressor miRNA in CRC invasion and metastasis, and PEAK1 is downstream effector of miR-181d in its target network. [score:5]
To determine whether miR-181d affects PEAK1 expression in the intracellular environment in CRC, the expression of PEAK1 was evaluated in HCT 116 and CaCO [2] cells following transfection with either miR-181d mimics or inhibitors (anti-miR-181d). [score:5]
Exogenous over -expression of miR-181d inhibited the proliferation of pancreatic cancer cells [43]. [score:5]
Overexpressing miR-181d resulted in a reduction in PEAK1 expression (Supplementary Figure S 4c). [score:5]
The Kaplan–Meier curve and log-rank test showed that downregulation of miR-181d was significantly associated with poorer overall survival in CRC (Fig. 6j). [score:4]
Wang XF MiR-181d acts as a tumor suppressor in glioma by targeting K-ras and Bcl-2J. [score:4]
To verify whether PEAK1 was a direct target of miR-181d, we cloned the 3′UTR region of PEAK1 mRNA, which included the predicted miR-181d recognition site, and then inserted it into a luciferase reporter plasmid. [score:4]
PEAK1 is a direct target of miR-181d in CRC cells. [score:4]
Our study further demonstrates the importance of PEAK1 in CRC progression and indicates the activation of the EGFR/KRas signaling axis and repression of miR-181d as a potential mechanism for increased PEAK1 expression in CRC. [score:3]
In multivariate analysis using the Cox proportional hazards mo del, miR-181d expression was found to be an independent prognostic factor for CRC (Supplementary Table S 3). [score:3]
Ectopic expression of miR-181d decreases the invasive, migratory and proliferative capacities of CRC cells in vitro. [score:3]
Guo X miR-181d and c-myc -mediated inhibition of CRY2 and FBXL3 reprograms metabolism in colorectal cancerCell Death Dis. [score:3]
As expected, miR-181d over -expression led to a significant decrease in PEAK1 protein levels and in the levels of p-Erk1/2 (Fig. 6d). [score:3]
Transfection with miR-181d mimics resulted in a significant reduction of PEAK1 protein expression (Fig. 6c). [score:3]
High expression of miR-181d was associated with improved overall survival in glioblastoma 41, 42. [score:3]
Taken together, these findings indicate that miR-181d acts as a tumor suppressor in CRC. [score:3]
The results showed that miR-181d was a potential miRNA targeting PEAK1 because miR-181d incompletely complemented the 3′UTR region of PEAK1 (Fig. 6a). [score:3]
As shown in Supplementary Table S 2, miR-181d expression was significantly correlated with tumor location, local relapse and TNM stage. [score:3]
CRC TMA slides used for ISH analysis of miR-181d expression were obtained from the tumor bank of the Department of Pathology of the First Affiliated Hospital, Sun Yat-sen University (Guangzhou, China). [score:3]
Invasion assays showed that ectopic miR-181d expression significantly decreased the invasive ability of HCT 116 cells (Fig. 6e). [score:2]
However, transfection of CRC cells with the miR-181d inhibitor enhanced cell invasion compared with NC cells (Fig. 6e). [score:2]
Yang F miR-181d/MALT1 regulatory axis attenuates mesenchymal phenotype through NF-κB pathways in glioblastomaCancer Lett. [score:2]
Colony formation and real-time cell proliferation assays showed that ectopic miR-181d expression decreased colony formation and cell proliferation (Fig. 6g, h). [score:2]
Real-time cell migration assays showed a reduced migration of miR-181d -overexpressing cells (Fig. 6f). [score:2]
In situ hybridization of miR-181d. [score:1]
We also investigated the correlation between the expression levels of miR-181d and the EGFR/Erk signaling pathway. [score:1]
To better understand the role of miR-181d in CRC, the clinical significance and biological function of miR-181d were analyzed. [score:1]
Luciferase reporter constructs containing wild-type or mutated PEAK1 3′ UTRs were co -transfected with miR-181d mimics or NC into HCT 116 cells. [score:1]
Fig. 6 a The conserved miR-181d binding sequence of PEAK1 or its mutated form was inserted into the pMIR reporter. [score:1]
i Representative images for in situ hybridization analysis of miR-181d. [score:1]
HCT 116 cells were stably infected with the pLenti-miR-181d or pLenti-vector (Supplementary Figure S 4b). [score:1]
Guo et al. [44] reported that miR-181d functions as a tumor promoter in CRC. [score:1]
miR-181d is an independent prognostic factor for CRC. [score:1]
The miR-181d binding site in the 3′UTR region of PEAK1 was mutated to obtain the 3′UTR-MutPEAK1-luc plasmid (Fig. 6a). [score:1]
Briefly, ISH was performed using a hsa-miR-181d probe from Exiqon (miRCURY LNA Detection probe, 250 pmol, 5′-DIG and 3′-DIG labeled). [score:1]
Correlations between clinicopathological features and PEAK1/miR-181d expression were calculated according to the Chi-square test. [score:1]
To further investigate the clinical pathology and prognostic significance of miR-181d expression, in situ hybridization (ISH) staining for miR-181d was performed on 353 CRC samples in a tissue microarray. [score:1]
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3
[+] score: 164
c-d CTDSPL expression was significantly inhibited after transfection with si-CTDSPL-1 and si-CTDSPL-2 in MUM2b and OCM1a cells, whereas pRB and E2F1 expression was significantly increased in MUM2b and OCM1a cells after transfection with si-CTDSPL-1 and si-CTDSPL-2. The gray level was analyzed by histogram seperately (*P < 0.05) miR-181 contributes to cell cycle progression via its target CTDSPL, which in turn increases expression of the cell cycle effector pRB/E2F1 in UM cellsOur work found that miR-181b is overexpressed in melanoma tissues and most UM cells and promotes cell cycle progression by repressing CTDSPL expression in UM cells. [score:15]
Although miR- 181c and - 181d mimics and inhibitors could promote and inhibit CTDSPL expression through the same binding site in the CTDSPL gene, miR-181c and miR- 181d were not upregulated in most UM cells except for a slight increase in miR-181c in OCM1 cells and miR-181d in OCM1a cells. [score:10]
In contrast, the fraction of cells in G0/G1 phase was significantly increased by 12-15%, and the period of S-phases was significantly decreased 8-12% after the inhibitors of miR- 181 family members were transfected into OCM1a cells Bioinformatics and molecular biology assays confirmed CTDSPL as a target of miR-181 family membersTo identify the target gene(s) of miR-181, candidate genes were identified using the miRNA target prediction database TargetScan [13] (http://www. [score:10]
The expression levels of miR-181c and miR-181d were not upregulated in most UM cell lines, except for a slight increase in miR-181c in OCM1 cells and a mild upregulation of miR-181d in OCM1a, both less than 10-fold. [score:9]
In contrast, the fraction of cells in G0/G1 phase was significantly increased by 12-15%, and the period of S-phases was significantly decreased 8-12% after the inhibitors of miR- 181 family members were transfected into OCM1a cells To identify the target gene(s) of miR-181, candidate genes were identified using the miRNA target prediction database TargetScan [13] (http://www. [score:9]
d and (f) Overexpression or knockdown of miR-181 expression inhibited or enhanced the Renilla luciferase activity, respectively. [score:8]
e and (g) The Renilla luciferase activity was nearly unchanged after mimics and inhibitors of miR- 181 family members were transfected with the mutated 3’-UTR of CTDSPL miR-181b was extremely overexpressed in melanoma tissues and most UM cellsTo investigate the expression profile of miR-181 family members in UM, microarray technology was used to detect the expression of miR-181 family members in melanoma tissues. [score:7]
Western blot assays further indicated that mimics of miR-181 family members led to the reduced expression of CTDSPL, while inhibitors led to the increased expression of CTDSPL in MUM2b cells (Fig. 2b-c, P < 0.05). [score:6]
miR-181a expression was also upregulated, while miR-181c and miR-181d were essentially unchanged (Fig.   3a). [score:6]
These data provide strong evidence that the miR-181 family members inhibit CTDSPL gene expression by directly binding to sites within its 3’-UTR. [score:6]
miR-181 contributes to cell cycle progression via its target CTDSPL, which in turn increases expression of the cell cycle effector pRB/E2F1 in UM cells. [score:5]
To examine whether miR-181 family members could directly regulate CTDSPL expression, 293 T cells were transfected with a luciferase reporter construct containing the putative wild-type and mutant 3’-UTR of CTDSPL binding sites, together with one of the following miRNAs: miR-181a, -181b, -181c, -181d, miR-NC, as-miR-181a, - 181b, - 181c, or - 181d. [score:5]
e and (g) The Renilla luciferase activity was nearly unchanged after mimics and inhibitors of miR- 181 family members were transfected with the mutated 3’-UTR of CTDSPL To investigate the expression profile of miR-181 family members in UM, microarray technology was used to detect the expression of miR-181 family members in melanoma tissues. [score:5]
miR-181 family members are highly conserved, and their upregulation promotes cell cycle progression. [score:4]
Thus, miR-181 induces cell cycle progression by repressing the downstream target CTDSPL, which in turn results in the phosphorylation of RB and an accumulation of the downstream cell cycle effector E2F1 Recently, miRNAs have emerged as important cellular regulators that mediate cellular proliferation and progression. [score:4]
Fig. 2CTDSPL is a direct target of miR-181 family members. [score:4]
The results demonstrated that mimics of miR-181 family members promoted cell cycle progression, while inhibitors of miR-181 family members led to cell cycle arrest (Fig. 1b-e). [score:3]
There are five predicted target sites in the 3’-UTR of CTDSPL sequence for miR-181 family members. [score:3]
MiR-181 family members were found to be highly homologous across different species and their upregulation significantly induces UM cell cycle progression. [score:3]
miR-181 overexpression in UM cells induces progression through the G1/S transition and promotes S-phase entry. [score:3]
miR-181 family members were predicted to target CTDSPL, which had previously been denoted as RBSP3 (RB1 serine phosphatase from human chromosome 3), a key downstream mediator of cell cycle progression, and has been reported to participate in acute myeloid leukemia pathogenesis [6]. [score:3]
To determine the common target region of the miR-181 family in CTDSPL, a segment of wild-type and mutated 3’-UTR of the human CTDSPL cDNA was constructed. [score:3]
miR-181 family members were found to be highly homologous and have the same target, CTDSPL. [score:3]
However, the expression and function of the miR-181 family members in the pathogenesis of UM had not been established. [score:3]
Fig. 6 miR-181 targets CTDSPL, which modulates the cell cycle effector E2F1. [score:3]
These findings constitute a comprehensive foundation for future research on the important role miR-181 in the developmental pathology of UM. [score:2]
These results highlight that miR-181 family members, especially miR-181b, may be useful in the development of miRNA -based therapies and may serve as novel diagnostic and therapeutic candidate for UM. [score:2]
miR-181 family members are highly conserved, and their upregulation promotes cell cycle progressionTo explore the relationship among miR-181 family members, their sequence homology was investigated. [score:2]
Bioinformatics and molecular biology assays confirmed CTDSPL as a target of miR-181 family members. [score:2]
The expression level of miR-181 family in human uveal melanoma cell lines was measured via real-time PCR (RT-PCR). [score:1]
miR-181 Uveal melanoma CTDSPL E2F1 Cell cycle Recently, miRNAs were found to play critical roles in many different cellular processes, especially in tumor progression. [score:1]
Thus, miR-181 induces cell cycle progression by repressing the downstream target CTDSPL, which in turn results in the phosphorylation of RB and an accumulation of the downstream cell cycle effector E2F1 To explore the relationship among miR-181 family members, their sequence homology was investigated. [score:1]
Next, miR-181 family members were detected in various types of UM cells, including OCM1, SP6.5, VUP, OCM1a, MUM2b and 92-1 cells. [score:1]
MiR-181 family members are key negative regulators of CTDSPL -mediated cell cycle progression. [score:1]
Evolutionary conservation analysis of the miR-181 family members indicated that the sequences of miR-181a, -181b, -181c, and -181d are partly conserved in Homo sapiens, Mus musculus, Rattus norvegicus, Bos taurus and Pan troglodytes (Fig.   1a). [score:1]
The hollow white rectangle indicates the five different gene loci of the miR-181 family members. [score:1]
miR-181a and miR-181b are transcribed from two separated gene loci (miR-181a-1/miR-181b-1 and miR-181a-2/miR-181b-2), while miR-181c and miR-181d are transcribed from another locus [6]. [score:1]
Schematic representation of the pathway modulated by miR-181 in UM cells progressing through the cell cycle. [score:1]
To investigate the potential roles of miR-181 family members, miR-181 family mimics (miR-181a, -181b, -181c, and -181d) or inhibitors (as- miR-181a, -181b, -181c, and -181d) were separately transfected into MUM2b and OCM1a cells. [score:1]
MUM2b (3 × 10 [5]) or OCM1a (5 × 10 [5]) cells were cultured overnight in 6-well plates and transfected with 200 nM miR-NC, miR-181 family mimics, or as- miR-181 family members (GenePharma Co. [score:1]
The predicted sequences to which miR-181 binds in the 3’-UTR of CTDSPL are conserved in humans (Fig.   2a). [score:1]
Fig. 1The conservation and cell cycle analysis of miR-181 family members. [score:1]
The miR-181 family contains four miRNAs (miR-181a/b/c/d). [score:1]
miR-181a, - 181b, -181c and -181d are miR-181 members of the family, which has been rarely studied, especially uveal melanoma. [score:1]
However, the homology among the miR-181 family members and the contribution of miR-181a, -181b, -181c and -181d in UM have not yet been clarified. [score:1]
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4
[+] score: 139
Notably, the expression of most miRNAs was reduced by the upregulation of miR-181d (+miR-181d) or inhibition of β-catenin (−β-catenin), CBP (−CBP), or STAT3 (−STAT3), while expression levels were increased by downregulation of miR-21 (−miR-21) and -23b (−miR-23b). [score:13]
For example, as a tumor suppressor miR-181d was significantly upregulated after knocking down miR-23b, which may synergize with miR-23b suppression to inhibit the growth of glioma cells. [score:11]
Moreover, four genes in this pathway were differentially expressed in the same direction under +miR-181d and −miR23b, including upregulated DNAJB11, CKAP4, and HSP90B1, and downregulated NSFL1C. [score:10]
For example, miR-17 and -106b were both downregulated and acted cooperatively to regulate focal adhesion (hsa04510) and NOD-like receptor signaling pathways (hsa04621) by mediating MAPK9 expression under the manipulation of miR-181d overexpression(Fig. S13). [score:9]
Therefore, downregulation of miR-17 and -106b may synergistically inhibit glioma malignancy after over expressing miR-181d. [score:8]
For example, overexpression of miR-181d has been shown to inhibit the growth of glioma cells [8], [9], while miR-21 or -23b knockdown suppressed glioma invasion and improved prognosis [10], [11]. [score:8]
Another gene, HSP90B1, in protein processing in endoplasmic reticulum, was differentially expressed in the same direction, being downregulated, under miR-181d, −miR-23b, −β-catenin, and –STAT3. [score:7]
In particular, miR-181d was highly upregulated by all the three miRNA targeted interventions, participating in the regulation of 11 biological pathways. [score:7]
For example, the expressions of miR-181c and -181d were decreased after inhibiting β-catenin activity, confirming the positive correlation of miR-181 family members’ expression and β-catenin [43]. [score:7]
Firstly, we investigated the levels of three targeted miRNAs in each manipulation, and found that all the three miRNAs was differentially expressed in accordance with the manipulation, for example, miR-181d was significantly upregulated under +miR-181d (Fig. S1). [score:6]
Since miR-181d was upregulated by all the three manipulations, its target pathways and fold changes are provided. [score:6]
Moreover, our work mainly focused on the experiments with validated effect on glioma inhibition, further experiments with contrary molecular intervention such as transfecting antagmirs to miR-181d into cells can help us to understand better on miRNAs’ regulatory role in gliomagenesis related to each targeted molecule. [score:6]
Excluding −miR-21, which only significantly stimulated the regulation of miR-21 to MAPK signaling pathway, functional synergy was observed between MPRNs activated by miRNA targeted manipulation (+miR-181d and −miR-23b), including three miRNAs, pathways, and regulatory associations in common (Figure 4A). [score:5]
MPRNs were constructed based on differentially expressed miRNAs and mRNAs after targeted manipulating the levels of miR-181d, - 23b, and -21, as well as STAT3, CBP, and β-catenin (Figure 3A). [score:5]
Figure S1 The expression changes of three targeted miRNAs, miR-181d, - 21, and - 23b, under each manipulation. [score:5]
Notably, GO biological processes most significantly affected by differentially expressed mRNAs of these manipulations were specific hallmarks of cancer, including DNA repair (i. e., genomic instability and mutation) for +miR-181d, ubiquitin -dependent protein catabolic process (i. e., dysregulation of cellular energetics) for −miR-23b, DNA replication (i. e., unlimited potential for self-renewal) for −miR-21, angiogenesis for −β-catenin, autophagic cell death (i. e., resisting cell death) for −CBP, and the steroid hormone receptor signaling pathway (i. e., self-sufficiency in growth signals) for −STAT3 [39]. [score:5]
In contrast, expression levels of miR-181 family members, including miR-181d, were significantly reduced after blocking the activity of β-catenin, suggesting that miR-181d might antagonize the effects of β-catenin inhibition, thereby inducing drug resistance. [score:5]
In this study, miRNAs and mRNAs were simultaneously profiled using high-throughput sequencing in human glioma cell lines after interfering with the expression of miR-181d, -21, and -23b, as well as β-catenin, CBP, and STAT3. [score:3]
MiR-181d mimics, and miR-23b and -21 inhibitors as well as control miRNAs, were purchased from Qiagen (Hilden, Germany). [score:3]
Therefore, we inferred that the expression amount of miR-181d and other miRNAs could recapitulate normal physiologic levels. [score:3]
For example, the MPRN for +miR-181d contained a total of nine miRNAs and eight distinct pathways, including miRNAs that regulate cell cycle (hsa04110) and focal adhesion (hsa04510). [score:2]
Since protein processing in the endoplasmic reticulum pathway was shared by +miR-181d, −miR-23b, −β-catenin, and −STAT3, miRNAs regulating this pathway are shown. [score:2]
For instance, protein processing in endoplasmic reticulum (hsa04141) was regulated by miR-181d in both +miR-181d and −miR-23b. [score:2]
The two pathways were cell cycle and protein processing in endoplasmic reticulum, with the former being shared by +miR-181d, −miR-23b, −β-catenin, and –CBP, and the latter being shared by +miR-181d, −miR-23b, −β-catenin, and –STAT3. [score:1]
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5
[+] score: 120
The results showed that miR-181 overexpression significantly decreased the luciferase activity, and mutations in the miR-181 binding site from the DAX-1 3′-UTR abolished this effect, suggesting that miR-181 directly inhibited DAX-1 expression by targeting the 3′-UTR (Fig. 4B). [score:11]
miR-181 targets the DAX-1 3′-untranslated region (3′-UTR) and downregulates its expression. [score:10]
They demonstrate that miR-181 overexpression causes the upregulation of AR target genes, suggesting that the proliferative role of miR-181, at least in part, may be dependent on androgen signaling. [score:8]
In the present study, elevated expression levels of AR target genes and proteins, including prostate-specific antigen, cyclin -dependent kinase (CDK) 1 and CDK2, was observed in LNCaP cells overexpressing miR-181 (Fig. 5). [score:7]
Therefore, these results suggest that miR-181 may negatively regulate DAX-1 expression at the translational level in LNCaP cells. [score:6]
In order to understand the underlying mechanism, potential targets of miR-181 were determined using TargetScan software. [score:5]
Previous studies have demonstrated that the upregulation of hepatic miR-181 promotes the growth, clonogenic survival, migration and invasion of hepatocellular carcinoma cells (7, 8). [score:4]
It was found that miR-181 is significantly upregulated in cancer tissues compared with that in normal adjacent tissues, as shown in Fig. 1. Since miR-181 was found to be upregulated in prostate cancer tissues, the effect of miR-181 on prostate cancer cell growth was investigated. [score:4]
Furthermore, in the present study DAX-1 was identified as a direct target of miR-181 in prostate cancer cells. [score:4]
miR-181 is upregulated in prostate cancer tissues. [score:4]
In addition, miR-181 overexpression was observed to promote the growth of LNCaP tumors in nude mice. [score:3]
The results suggest that miR-181 may be a potential therapeutic target for the treatment of prostate cancer in the future. [score:3]
The expression of miR-181 was analyzed in prostate cancer tissues and adjacent normal tissues using qPCR. [score:3]
DAX-1 was identified as a potential target of miR-181. [score:3]
In addition, the average tumor weight was significantly increased by miR-181 overexpression (Fig. 3C), suggesting that miR-181 may promote tumor growth in vivo. [score:3]
Furthermore, miR-181 overexpression decreased the percentage of cells in the G1 phase and increased the percentage of cells in the S phase (Fig. 2D). [score:3]
miR-181 overexpression promotes prostate cancer cell proliferation in vitro. [score:3]
Furthermore, the expression level of miR-181 is significantly associated with overall survival in hematological malignancies and may be an important clinical prognostic factor for patients with hepatocellular carcinoma (9). [score:3]
Therefore, in the present study, the expression of miR-181 was determined in prostate cancer tissues. [score:3]
A total of 2×10 [5] LNCaP cells stably expressing miR-181 or NC were injected subcutaneously into the dorsal flank of the mice. [score:3]
In the present study, it was demonstrated for the first time, to the best of our knowledge, that miR-181 overexpression may promote cell proliferation and cell-cycle progression in LNCaP cells. [score:3]
In combination, these results further confirm that DAX-1 is an important target gene of miR-181 in prostate cancer cells. [score:3]
Mutations were introduced in potential miR-181 binding sites using a site-directed mutagenesis kit (Qiagen). [score:3]
miR-181 overexpression promotes tumor growth in vivo. [score:3]
Therefore, miR-181 may be an onco-miRNA in the development of prostate cancer. [score:2]
To analyze miR-181 expression, specific stem-loop reverse transcription primers (Invitrogen Life Technologies) were used. [score:2]
The tumor size and volume were markedly increased in mice injected with LNCaP cells overexpressing miR-181 compared with those in control mice (Fig. 3A and B). [score:2]
To investigate whether DAX-1 may be directly targeted by miR-181, a luciferase reporter vector was constructed, containing the putative miR-181 binding sites within the DAX-1 3′-UTR. [score:2]
To further investigate the function of miR-181 on tumor growth in vivo, LNCaP cells with stable overexpression of miR-181 were generated and injected subcutaneously into the dorsal flank of nude mice. [score:1]
Notably, the 3′-UTR of DAX-1 mRNA was observed to contain a complementary site for the seed region of miR-181 (Fig. 4A). [score:1]
Furthermore, miR-181 mimics decreased the endogenous protein levels of DAX-1, as indicated by western blot analysis (Fig. 4C), while the DAX-1 mRNA levels remained unchanged (Fig. 4D). [score:1]
LNCaP cells were transfected with miR-181 mimics or NC (Fig. 2A). [score:1]
In conclusion, the present study provides a novel role for miR-181 in prostate cancer cell proliferation. [score:1]
Furthermore, the targets of miR-181 were investigated in order to determine the underlying mechanism of miR-181 in prostate cancer. [score:1]
Human miR-181 mimics and negative controls (NC) were purchased from Qiagen (Shanghai, China). [score:1]
[1 to 20 of 35 sentences]
6
[+] score: 85
We also found that CARM1 was post-transcriptionally regulated and was directly targeted by miR-181, which represses the 3′ untranslated region (3′UTR) of CARM1 in hESCs. [score:7]
In differentiated hESCs, H3K27 methylation is inhibited because of the reduction of core pluripotency factors, and miR-181 family members are consequently significantly induced and down-regulate CARM1 activity. [score:6]
In this context, we scanned for microRNAs that target CARM1 and finally identified the miR-181 family as the critical regulator of CARM1 expression. [score:6]
In differentiated hESCs, H3K27 methylation is inhibited due to the reduction of core pluripotency factors, and miR-181 family members are subsequently induced and down-regulate CARM1 activity. [score:6]
Taken together, these results show that miR-181 directly regulates CARM1 by targeting its 3′UTR and that miR-181c may play a prominent role among the 4 members during hESC differentiation. [score:5]
Although the miR-181 family also regulates many target genes [21], [46], [47], [48], [49], it is important to highlight that in mouse ESCs, the miR-181 family regulates another histone modulator, Cbx7, which plays a critical role in maintaining ESC pluripotency [50]. [score:5]
0053146.g002 Figure 2The miR-181 family directly regulates CARM1 expression in hESC. [score:5]
To investigate whether CARM1 can be directly targeted by miR-181, we engineered luciferase reporters that have either the wild-type 3′UTR of CARM1, or a mutant 3′UTR with three point mutations in the target sites as a negative control (Fig. 2C). [score:5]
The miR-181 family directly regulates CARM1 expression in hESC. [score:5]
Enforced Expression of miR-181c Induced hESC Differentiation by Targeting CARM1 We selectively transfected miR-181c mimics in undifferentiated hESCs to study the effect of miR-181 on hESCs differentiation. [score:5]
All the results indicated that CARM1 down-regulation may greatly contribute to the miR-181-meidated hESC differentiation. [score:4]
Future studies will explore how the expression of the miR-181 family is regulated in ESC differentiation and whether other transcriptional factors are associated with CARM1. [score:4]
By contrast, the expression of mutant reporters was not repressed by miR-181 (Fig. 2D). [score:3]
Thus, we suggest that CARM1 is one of the key target genes of the miR-181 family during the progression of ESCs differentiation. [score:3]
Our work suggests that downstream targets of the miR-181 family include epigenetic factors that reconfigure the H3 arginine methylation signature during the process of hESC differentiation. [score:3]
Considering that the sites of the CARM1 3′UTR that are targeted by miR-181 family members are conserved in mammals, we suppose that the interaction between miR-181 and CARM1 is conserved in mESCs. [score:3]
The mature transcripts of the 4 members of the miR-181 family were all found to be significantly increased in differentiated hESCs, and miR-181c had the highest expression level (Fig. 2A). [score:3]
miR-181 Family Members are Critical Regulators of CARM1 during hESC Differentiation. [score:2]
Our results also suggest that the miR-181/CARM1/core-pluripotency-factors regulatory loop may be a novel mo del pathway involved in the modulation of hESC pluripotency (Figure 4E). [score:2]
We selectively transfected miR-181c mimics in undifferentiated hESCs to study the effect of miR-181 on hESCs differentiation. [score:1]
To study the role of endogenous miR-181 in repressing the CARM1 3′UTR reporter in differentiated hESCs, we co -transfected the wild-type 3′UTR luciferase reporter and the negative control luciferase into differentiated hESCs. [score:1]
This finding suggests that the miR-181 family may also promote differentiation by affecting histone modulation in mESCs. [score:1]
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7
[+] score: 82
In light of this, we presume that miR-181 upregulation is an important host protective mechanism against endotoxin shock, because it can shift the immune status from hyperinflammation to endotoxin tolerance via a rapid shutdown of inflammatory cytokine expression without altering anti-inflammatory cytokine expression. [score:8]
The miR-181 mimics also suppressed ouabain -induced TNF-α mRNA expression in A549 cells (Fig 3D) and TNF-α protein expression in human blood monocytes (Supplementary Fig S8A), miR-181d had the strongest effect. [score:7]
Furthermore, when siRNA was used to knock down Egr-1 expression, the ouabain -induced increase in pri-miR-181c/d, mature miR-181c, and mature miR-181d expression was attenuated (Fig 5C). [score:6]
Q-PCR analysis showed that miR-181b, miR-181c, and miR-181d were upregulated in sepsis patients, while miR-181a and miR-16 were unchanged (Fig 4E). [score:4]
Luciferase constructs with mutations in T55 were designated m1, m2, m3, m4, m5, m6, m7, FM (full mutation), and 181BSM (miR181 binding site mutation), respectively. [score:4]
Although ouabain induced miR-181d expression, it still reversed immunoparalysis and delayed TNF-α mRNA decay. [score:3]
Figure 8 HuR competes with miR-181d on the shared target of TNF-α mRNA Effects of miR-181d (left panel) and pRK5-HuR (right panel) on the luciferase activity of cells transfected with TNF-α 3′-UTR and its mutants. [score:3]
When we examined possible competition between the two elements, we found that HuR overexpression counteracted the effect of miR-181d on the T55 WT reporter (Fig 8B). [score:3]
The expression levels of pri-miR-181c/d, miR-181c, and miR-181d after Egr-1 siRNA transfection. [score:3]
To verify database predictions, we showed that “mimics” of miR-181a, miR-181b, miR-181c, and miR-181d inhibited the luciferase activity of a TNF-α 3′-UTR reporter (T789), but had no effect when the miR-181 binding site was mutated (T789 m) (Fig 3C, left panel). [score:3]
HuR competed with miR-181d for binding to a shared TNF-α mRNA target sequence, leading to TNF-α mRNA stabilization. [score:3]
As shown in Fig 8A, miR-181d overexpression reduced T55 (WT) reporter luciferase activity to 53% of the activity observed in control cells; however, the effect of miR-181d on T55FM was less potent (Fig 8A, left panel). [score:3]
Notably, miR-181d failed to alter the general ribosome profile and TNF-α mRNA distribution in polysomes (Supplementary Fig S9A–D), indicating that members of the miR-181 family specifically regulate TNF-α mRNA stability. [score:2]
These conflicting results suggest that additional ouabain -dependent mechanisms counter-regulate miR181d -mediated TNF-α mRNA decay. [score:2]
A mutated version (T789 m) of this construct carrying a 7-bp substitution in the miR-181 binding site was obtained through site-directed mutagenesis. [score:2]
Therefore, we compared the expression of the miR-181 family members in human monocytes isolated from 25 patients with severe sepsis due to infections. [score:2]
In ouabain -treated cells, TNF-α mRNA stability was preferentially regulated by HuR and not by miR-181 family members. [score:2]
Thus, the AREs and the miR-181 binding site within the TNF-α 3′-UTR are cis-regulatory elements that are functionally dependent on each other. [score:2]
Effects of miR-181d and antagomir-181d on the half-life of TNF-α mRNA. [score:1]
The microRNA181 family negatively regulates TNF-α mRNA stability and induces immunoparalysis. [score:1]
However, the miR-181c/d cluster is located in an intergenic region on chromosome 19, and miR-181d is slightly downstream of miR-181c (Supplementary Fig S12A). [score:1]
In fact, only one miR-181 binding site is present in the minimal TNF-α 3′-UTR (T55); in contrast, seven “AUUUA” motifs are located in the immediate vicinity of the miR-181 binding site. [score:1]
However, the effect of HuR on the T55 reporter with a mutated miR-181d binding site (T55BSM) was less potent (Fig 8A, right panel). [score:1]
Ouabain produced two opposite effects on the mRNA stability of TNF-α mRNA mediated by HuR and miR181d. [score:1]
As a result, ouabain -induced HuR nuclear export competed with miR181d for binding to TNF-α mRNA, thereby leading to TNF-α mRNA stabilization and improvement of immunoparalysis. [score:1]
HuR antagonizes miR-181d -mediated TNF-α mRNA destabilization. [score:1]
Notably, miR-181 binding sites are frequently distributed in the 3′-UTRs of many inflammatory cytokines, including IL-1α and TNF-α; surprisingly, no miR-181 binding sites have been found in the 3′-UTRs of anti-inflammatory cytokines such as IL-10 and TGF-β. [score:1]
A549 cells were transfected with 50 nM miR-181d mimics or 200 nM antagomir-181. [score:1]
Twenty-four hours later, these cells were stimulated with 100 nM ouabain for 2 h. Q-PCR analysis was performed to measure the expression levels of pri-miR-181c/d, miR-181c, and miR-181d. [score:1]
Luciferase activity in A549 cells transfected with constructs encoding vector T789-Luc or T789 m-Luc of TNF-α 3′-UTR plus mimics of miR-181a, miR-181b, miR-181c, miR-181d (left panel), or antagomir-181 (right panel). [score:1]
The microRNA181 family consists of four members: miR-181a, miR-181b, miR-181c, and miR-181d. [score:1]
HuR and miR-181d are mutually antagonistic for TNF-α mRNA stabilization. [score:1]
Here, we showed that members of the miR-181 family act downstream of TLR4 signaling to induce TNF-α mRNA degradation. [score:1]
A549 cells were transfected with the indicated constructs, miR-181d or pRK5-HuR. [score:1]
miR-181d greatly shortened the half-life of TNF-α mRNA, while antagomir-181d extended the half-life (Fig 3E). [score:1]
Therefore, it is likely that the binding of HuR to the 3′-UTR of TNF-α triggers a conformational change in the local RNA that masks the miR-181 binding site. [score:1]
Because the miR-181 binding site in the 3′-UTR of TNF-α is located within two adjacent “AUUUA” motifs (Supplementary Fig S14A), we speculated that, after ouabain treatment, HuR might counteract the destabilizing effect of miR-181d on TNF-α mRNA. [score:1]
miR-181c and miR-181d are co-transcribed (Supplementary Fig S12B and C). [score:1]
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8
[+] score: 61
The significance of the differences in the expression was confirmed for four of the miRNAs, including three down-regulated miRNAs namely miR-181d-5p, miR-140-3p and miR-206 and one up-regulated miRNA namely miR-625-5p (P < 0.05) (Fig.   1). [score:9]
The significance of the differences in the expression was confirmed for six of the miRNAs, including two down-regulated miRNAs namely miR-181d-5p and miR-206 and four up-regulated miRNA namely miR-1233-3p, miR-183-5p, miR-421 and miR-625-5p) (P < 0.05) (Fig.   3). [score:9]
The significance of the differences in the expression was confirmed for four of the miRNAs, including three down-regulated miRNAs namely miR-181d-5p, miR-140-3p and miR-206 and one up-regulated miRNA namely miR-625-5p) (P < 0.05) (Fig.   2). [score:9]
In detail, we selected two miRNAs with high fold changes among the up-regulated (miR-625-5p and miR-183-5p) and four miRNAs with high fold changes among the down-regulated ones (miR-181d-5p, miR-206, miR-142-5p and miR-339-5p). [score:7]
To gain insights into the potential impact of the three validated miRNAs (miR-181d-5p, miR-206 and miR-625-5p) in regulating target genes, we applied miRTargetLink [23]. [score:6]
The RT-qPCR showed the same direction of expression changes as the microarray analysis for five miRNAs namely miR-181d-5p, miR-142-5p, miR-206, miR-339-5p and miR-625-5p. [score:4]
The RT-qPCR showed the same direction of expression changes as the microarray analysis for six miRNAs namely miR-181d-5p, miR-1233-3p, miR-183-5p, miR-206, miR-421 and miR-625-5p. [score:4]
The RT-qPCR showed the same direction of expression changes as the microarray analysis for six miRNAs namely miR-181d-5p, miR-142-5p, miR-1233-3p, miR-206, miR-339-5p and miR-625-5p. [score:4]
Bioinformatics analysis helped to gain insights into the potential impact of the three validated miRNAs (miR-181d-5p, miR-206 and miR-625-5p) on target genes (Additional file 3: Figure S2). [score:3]
Together, the three miRNAs namely miR-181d-5p, miR-206 and miR-625-5p were significantly deregulated in all subgroups of TOF patients. [score:2]
The diagnostic accuracy of only three of the validated miRNAs namely miR-181d-5p, miR-206 and miR-625-5p by ROC analysis was high with AUCs of 0.987, 0.993 and 0.769 respectively in all TOF patients and 0.990, 0.994 and 0.749 respectively in the subset of TOF patients without symptomatic right heart failure. [score:1]
Three miRNAs namely miR-181d-5p, miR-206 and miR-625-5p were validated by RT-qPCR in all TOF groups. [score:1]
Strong interaction was observed between miR-181d-5p and BCL2 and is highlighted in ‘Green’ in the resulting network (Additional file 3: Figure S2). [score:1]
These results indicate the high diagnostic accuracy of miR-181d-5p and miR-206 and a moderate accuracy of miR-625-5p in differentiating TOF patients from healthy controls. [score:1]
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9
[+] score: 47
Moreover, H19 expression upregulated β-catenin expression via binding and inhibiting miR-181d, which negatively regulated β-catenin mRNA, thereby contributing to H19 oncogenic functions in glioblastomas. [score:11]
Furthermore, miR-181d overexpression decreased the β-catenin levels, and H19 upregulation facilitated β-catenin accumulation by aborting the inhibition of miR-181d in both U87 and U251 cells (Fig. 7D). [score:8]
Since miR181d inhibits β-catenin expression by directly binding the 3′-UTR of the β-catenin message 28, and β-catenin acts as an intracellular signal transducer in the Wnt signaling pathway involved in EMT-like in GBM 40, we verified H19 sponge activity towards miR-181d affects β-catenin levels in U87 and U251 cells. [score:6]
Using RNAHYBRID Bioinformatic tools, we found that H19 contained a putative binding site for miR-181d, which is known to directly target β-catenin 28 (Fig. 7A). [score:4]
H19 affects β-catenin expression by regulating miR-181d activity. [score:4]
As shown in Fig. 7B, miR-181d mimics did not affect H19 expression by qPCR. [score:3]
The miR-181d, miR-16-1 and scrambled miRNA mimics were chemically synthesized by Ribo (Guangzhou, China), and small interfering RNA (siRNA) oligonucleotides targeting Hif-1α, SP1 and PTEN were chemically synthesized by GenePharma (Shanghai, China). [score:3]
These data confirmed that H19 acts as a molecular sponge for miR-181d that abolishes miR-181d inhibition of β-catenin. [score:3]
H19 antagonizes miR-181d blocking β-catenin repression. [score:1]
After transfection with a reporter gene containing mutated binding sites for miR-181d, the reduced luciferase activity was not observed with miR-181d mimics (Fig. 7C). [score:1]
The miR-181d binding site from the H19 lncRNA (NR_002196), along with a mutated version of the sequence, was also chemically synthesized and cloned into a reporter plasmid (GV306-basic). [score:1]
These data suggest that the putative miR-181d binding site is essential for the interaction of miR-181d and H19 RNA. [score:1]
After transfecting a luciferase reporter plasmid harboring the putative miR-181d binding site from H19, the relative luciferase activity decreased in cells transfected with miR-181d mimics but not miR-16-1 mimics, the miRNA could not combine with H19 as previously reported 29. [score:1]
[1 to 20 of 13 sentences]
10
[+] score: 41
In this study, we report that lncRNA by competitively binding the miR-181 family, upregulating Bcl-2, and then suppressing gastric carcinogenesis (Fig.   5d). [score:6]
Furthermore, ectopic expression of MEG3 in HGC-27 and MGC-803 cells inhibited cell proliferation, migration, invasion, and promoted cell apoptosis, which might be due to MEG3 sequestering oncogenic miR-181 s in GC cells. [score:5]
Furthermore, MEG3 affected GC cell phenotypes in a miR-181 sites -dependent manner, which occurs without changes in the levels of miR-181 isoforms, suggesting that MEG3 regulates miR-181 activity by altering miRNA targeting. [score:4]
These findings suggest that lncRNA MEG3, a ceRNA of miR-181 s, could regulate gastric carcinogenesis and may serve as a potential target for antineoplastic therapies. [score:4]
We also showed that MEG3 inhibited GC cell proliferation, migration and invasion by operating as a competing endogenous RNA (ceRNA) for the miR-181 microRNA (miRNA) family. [score:3]
b The expression of MEG3 and Bcl-2 mRNA in HGC-27 cells transfected with empty vector, wild type MEG3 or mutant MEG3 as indicated; c Immunoblot analysis of Bcl-2 protein in HGC-27 cells transfected with empty vector, wild type MEG3 or mutant MEG3 as described in B; d A Schematic mo del of MEG3/miR-181/Bcl-2 cascade in gastric carcinogenesis. [score:3]
Taken together, our research demonstrated that MEG3 acted as a key regulator in human gastric carcinogenesis and revealed roles of MEG3 in regulating miR-181-Bcl2 axis. [score:3]
Studies have reported that miR-181 targets multiple Bcl-2 family members in astrocytes [24]. [score:3]
Subsequently, we constructed a series of luciferase reporters containing the wild type MEG3 (pMIR-MEG3-WT), or mutant MEG3 with mutations of single (pMIR-MEG3-MUT1, 2, 3, 4) or all four predicted miR-181 binding sites (pMIR-MEG3-MUT1-4). [score:2]
The miR-181 family contains four miRNAs (miR-181a/b/c/d), which are transcribed from three separated gene loci. [score:1]
The lower panel: the prediction for miR-181 s binding sites on MEG3 transcript. [score:1]
MEG3 is physically associated with miR-181 family. [score:1]
Among the results, we found 4 miR-181 family binding sites scattering the MEG3 transcripts, suggesting its ceRNA potential for miR-181 s (Fig.   3a). [score:1]
Fig. 3The interaction of MEG3 with miR-181. [score:1]
We found that transfection of HGC-27 cells with miR-181a mimic reduced the luciferase activities of the MEG3-WT reporter vector but not empty vector or all miR-181 site mutant reporter vector (Fig.   3b), suggesting the binding of miR-181a to these sites. [score:1]
a The upper panel: schematic outlining the predicted binding sites of miR-181 s on MEG3. [score:1]
The red nucleotides are the complementary sequences to miR-181 seed sequences. [score:1]
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[+] score: 39
Based on findings using the TargetScan software, miR-368 targets MINT31, miR-181d, 30a-3p, 30c, 30d, 30e-3p, 370, 493-5p, and 532-5p target CDH13, and miR-181d targets RASSF1. [score:9]
org) we identified nine miRNAs that regulate these three genes: miR-368 targeting MINT31, miR-181d, miR-30a-3p, miR-30c, miR-30d, miR-30e-3p, miR-370, miR-493-5p and miR-532-5p targeting CDH13, and miR-181d targeting RASSF1. [score:8]
In addition, expressions of miR-181d (P = 0.07), miR-30a-3p (P = 0.12), miR-493-5p (P = 0.06) and miR-368 (P = 0.08) were downregulated in Her2/neu -positive ovarian carcinomas (data not shown). [score:6]
In multivariate analyses, higher expression of miR-181d, miR-30c, miR-30d, and miR-30e-3p was associated with significantly better disease-free or overall survival. [score:5]
Expression of miR-30a-3p was significantly higher in well-differentiated carcinomas (grade 1) compared to poorly differentiated carcinomas (grade 3) (P = 0.02) and expression of miR-181d was marginally higher in well-differentiated carcinomas (grade 1) compared to poorly differentiated carcinomas (grade 3) (P = 0.08). [score:3]
Expression of miR-181d, miR-368, and miR-370 was significantly different between cell lines and normal ovaries as well as between cell lines and benign tumors. [score:3]
In addition, miR-181d, miR-30c and miR-30e-3p were also significantly associated with disease-free survival in the multivariate analysis. [score:3]
In a univariate mo del investigating disease-free survival, there was a moderate decreased risk of recurrence for miR-181d (P = 0.25), miR-30c (P = 0.14), miR-30d (P = 0.07), and miR-30e-3p (P = 0.11). [score:1]
An additional three miRNAs (miR-181d, miR-30a-3p, miR-532-5p) were significantly different between borderline and carcinoma tissues. [score:1]
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[+] score: 35
miR-181, miR-183 and miR-200 miRNAs Families Members are Similarly down-regulated during in vitro DecidualizationInterestingly, three miRNAs families (miR-181, miR-183 and miR-200) were down-regulated during the decidualization process. [score:7]
miR-181, miR-183 and miR-200 miRNAs Families Members are Similarly down-regulated during in vitro Decidualization. [score:4]
The molecular pathways potentially regulated by the mir-181, miR-200 and miR-183 families with the potential target genes are listed below the histograms. [score:4]
Interestingly, three miRNAs families (miR-181, miR-183 and miR-200) were down-regulated during the decidualization process. [score:4]
Surprisingly, from the total 33 differentially expressed miRNAs during our in vitro decidualization mo del, only two (miR-181b and miR-181d) have been previously identified in the Qian et al study [22]. [score:3]
For the mir-181 family, which includes six miRNAs precursors (mir-181a-1, mir-181a-2, mir-181b-1, mir-181b-2, mir-181c and mir-181d) located at three different loci (chromosomes 1, 9 and 19), the corresponding mature miRNA expression in decidual cells decreased (Figure 1B). [score:3]
By using the Diana miR-Path database [21], we searched for the molecular pathways potentially regulated by the mir-181 family. [score:2]
The top two molecular pathways potentially regulated by the miR-181 family are TGFß signaling and T cell receptor. [score:2]
Another interesting finding is that all the members of three different miRNAs families (miR-181, miR-200 and miR-183) have been identified to be similarly regulated. [score:2]
B, miR-181 C, miR-200 and D, miR-183 family members’ expression in the E+P decidualized hESCs for 9 days if compared to the non decidualized control hESCs. [score:2]
miR-181, miR-183 and miR-200 miRNAs families members are similarly regulated during in vitro decidualization. [score:2]
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[+] score: 34
miR-181 inhibits differentiation of AML cells into granulocytes and macrophages by down -regulating their direct targets PRKCD, CTDSPL, and CAMKK1 and then affecting the PRKCD-P38-C/EBPα pathway and reducing pRB phosphorylation. [score:7]
Expression of all miR-181 family members was reduced in adult AML patients (M1-M3 subtypes), suggesting all function as tumor suppressors. [score:5]
The in vivo expression of miR-181 partially reversed the lack of myeloid differentiation in AML patients and in the mice with CD34 [+] HSPCs from AML patients [37] It has been demonstrated that, in normal hematopoiesis, some miRNAs were involved in progenitor lineage commitment[38] and controlling HSC [39- 41] by coordinate repression of multiple targets [42]. [score:5]
The down-regulation of miR-181 was associated with leukemia invasiveness, and miR-181 has been well studied to be a prognostic predictor of AML [6, 36, 96, 97]. [score:4]
In AML CD34 [+] HSPC xenograft mice, inhibition of miR-181 increased differentiation of myeloid progenitors, reduced engraftment and infiltration of leukemic HSPCs into bone marrow and spleen, and ameliorated symptoms of leukemia. [score:3]
Su et al [37] demonstrated that miR-181 inhibition is a potential new treatment strategy for AML. [score:3]
These findings suggest that miR-181 is a potential target for AML therapy. [score:3]
Knockdown of miR-181 in cultured bone marrow blasts from AML patients partially reversed blockage of myeloid differentiation. [score:2]
Accumulating evidence indicates that the miR-181 family plays important roles in AML pathogenesis [36]. [score:1]
These results demonstrate critical but complex roles of miR-181 in AML, and more importantly, the temporal changes of miRNA expression and function during AML progression highlight a rigorous evaluation of miRNA -based therapy in AML. [score:1]
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[+] score: 32
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-134, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-330, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-505, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-505, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-181d, which regulates the three genes shown in Figure 3, down-regulates MGMT mRNA and protein expression in glioblastoma cells (Zhang et al., 2012b), is involved in MAPK signaling in pancreatic cancer cells (Ikeda et al., 2012), and is upregulated by hepatic transforming growth factor beta (TGFβ) in promoting hepatocarcinogenesis (Wang et al., 2010). [score:9]
miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression. [score:6]
MiR-17-5p and miR-181d, which are downregulated in formaldehyde -treated human lung epithelial cells, were predicted to regulate the greatest number of genes in the brains of MAM -treated Mgmt [−/−] mice (Figure 3). [score:5]
These include miR-17-5p and miR-181d, which regulate genes involved in tumor suppression, DNA repair, amyloid deposition, and glutamatergic and dopaminergic neurotransmission. [score:4]
MiR-181d also regulates the expression of calcium/calmodulin -dependent protein kinase II delta (CAMK2D). [score:3]
MiR-181d regulates the expression of CAMK2D, GRM5, NTS, and RFC1. [score:3]
A comparison of all 89 formaldehyde-modulated miRNAs in human lung epithelial cells (Rager et al., 2011) with the miRNAs predicted here to regulate genes in the brains of MAM -treated Mgmt [−/−] mice show overlap of 6 miRNAs: miR-107, miR-152, miR-17-5p, miR-181d, and miR-454-3p. [score:2]
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[+] score: 32
Given that miR-181d is down-regulated with the overexpression of HER2 in both cell lines and clinical samples, miR-181d may be classified as a tumor suppressor miRNA and may target an oncogene. [score:10]
Even though miR-181c is possibly co-expressed or repressed with miR-181d, there has not been many research done regarding this co -expression or repression. [score:5]
Among these differentially expressed miRNAs, miR-146a-5p, miR-195-5p, and miR-181d are potentially involved in breast cancer development based on previous research and therefore they were selected for further statistical analysis. [score:4]
Expression and prognostic values of miR-181d, miR-195-5p and miR-146a-5p in clinical breast cancer samples. [score:3]
However, it has been observed that the miR-181 family (miR-181a, miR-181b, miR-181c, and miR-181d), more precisely miR-181c, is activated by HER2 expression [13]. [score:3]
Figure 2(a, c, e) Relative expression levels of miR-181d, miR-195-5p and miR-146a-5p in breast cancer subtypes. [score:3]
Three miRNAs miR-146a-5p, miR-95-5p and miR-181d show their expected expression profile in HER2 -positive breast cancers when compared with other subtypes of breast cancers. [score:2]
The amount of information and connection between miR-181d and cancer is scarce and it is even more in HER2 positive breast cancers. [score:1]
Unlike the previous two miRNAs, miR-181d has not been extensively studied. [score:1]
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[+] score: 32
In addition to remarkable changes in miR-449a expression, SIRT1 protein expression was significantly downregulated in the cells transfected with miR-449a mimics (Figure 6B), but no effect of miR-181d mimics transfection on SIRT1 protein expression was observed (Figure 6C). [score:10]
Based on this mechanism, we hypothesize that the downregulated miR-449a and miR-181d might release the tight suppression of SIRT1 expression in T-2 toxin treated cells. [score:8]
In T-2 toxin treatment, two miRNAs, miR-449a and miR-181d, have been found to be significantly downregulated via the screening of predicted miRNAs that potentially target the SIRT1 3′UTR. [score:6]
Two putative miRNAs, miR-449a and miR-181d, were selected for further analysis because they were significantly downregulated by T-2 toxin, showing 0.6- and 0.7-fold changes in HepG2 cells relative to the untreated control and 0.6- and 0.3-fold changes in HEK293T cells (Figure 6A). [score:4]
The SIRT1 expression level in HepG2 and HEK293T cells transfected with miR-181d mimics was analyzed by western blotting. [score:3]
To evaluate the potential roles of miR-449a and miR-181d in SIRT1 expression, we transfected miR-449a and miR-181d mimics into HepG2 and HEK293T cells, respectively. [score:1]
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[+] score: 27
The sequences for control and miR-181a inhibitors were as follows: control inhibitor, 5′-CAGUACUUUUGUAGUACAA-3′ and miR-181 inhibitor, 5′-ACUCACCGACAGCGUUGAAUGUU-3′. [score:7]
MiR-181a down-regulates triglycerides and total cholesterol levels in vivoWe have recently characterized the inhibitory function of miR-181 in the regulation of embryo implantation in mice (unpublished data). [score:5]
The findings that IDH1 is a direct target of miR-181 and the opposite phenotypes displayed by miR-181a TG and IDH1 TG mice led us to test the possibility that miR-181a may regulate lipid metabolism through IDH1. [score:5]
To knockdown miR-181a in mice, six-week old miR-181 WT male mice were given administration of nanoparticles packed with either control or miR-181a inhibitors four times at one-week intervals 33. [score:4]
To determine whether miR-181a is involved in the regulation of lipid metabolism, six-week old miR-181 TG and WT male mice were fed with high fat diet (HFD) for 10 weeks. [score:2]
To explore whether miR-181a is involved in the regulation of lipid metabolism, both miR-181 TG and WT mice were fed with high fat diet (HFD), and after 10 weeks of feeding, miR-181a TG mice exhibited smaller size and lower body weight than miR-181a WT mice (Figures 1A and 1B) while these mice showed no obvious differences in food intake (Supplementary Figure S1B). [score:2]
We have recently characterized the inhibitory function of miR-181 in the regulation of embryo implantation in mice (unpublished data). [score:2]
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[+] score: 24
Some of the EV miRNAs (miR-181d-3p, miR-155-3p, miR-185-5p, miR-3940-3p, miR-4532, miR-7107-5p miR-504-3p, miR-320d, miR-19b-3p and miR-22-3p) up-regulated in female OA synovial fluid were down-regulated in response to estrogen treatment in human and mouse cells 51– 54. [score:7]
We also found that miR-185-5p and miR-7107-5p significantly (p < 0.05) down regulated expression of CREB -binding protein whereas miR-181d-3p did not show significant change in expression of CREB -binding protein (Fig.   5). [score:6]
Further detailed analysis showed that 6 miRNAs (miR-181d-3p, miR-3940-3p, miR-155-3p, miR-4532, miR-185-5p, miR-7107-5p) target 9 genes of the ovarian steroidogenesis pathway and the same number of miRNAs (miR-4532, miR-181d-3p, miR-185-5p miR-6865-3p, miR-4459, miR-7107-5p) target 14 genes of the estrogen signaling pathway. [score:5]
Surprisingly, miR-181d-3p significantly (p < 0.01) up-regulated nuclear receptor co-repressor (n-COR) and no change in TIF2 (Transcriptional Intermediary Factor 2). [score:4]
We did not find any significant changes in content of miR-181d-3p and miR-7107-5p in EVs cargo. [score:1]
Scrambled (Negative control) miRNA and miRNA mimics for miR-181d-3p, miR-185-5p and miR-7107-5p were purchased from QIAGEN. [score:1]
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The miR-181 family is particularly enriched in the brain and is involved in autism spectrum disorders [56], schizophrenia [57], Alzheimer disease [58], where they are mainly found to be upregulated. [score:6]
Note that prenatal stress downregulated miR-181 and miR-186 expression in the frontal cortex. [score:6]
Downregulation of miR-181 contributes to accelerated HIV -associated dementia in opiate abusers [59]. [score:4]
Downregulation of miR-181 was shown to have protective effects against apoptosis and mitochondrial dysfunction [60]. [score:4]
At the cellular level, miR-181 regulates apoptosis factors such as bcl-2 in astrocytes. [score:2]
miR-181 and miR-186 were chosen for verification using qRT-PCR analysis. [score:1]
Stress also led to critical decreases in let-7c, miR-23b, miR-181, and miR186 amounts. [score:1]
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[+] score: 23
Specifically, miR181-a is present in both bovine oocytes and embryos with increased expression in early stages of development then drops to low levels in the blastocyst and is thought to regulate nucleoplasmin2 a protein important in nuclear organization (Lingenfelter et al., 2011). [score:5]
Activin and TGF beta regulate expression of the microRNA-181 family to promote cell migration and invasion in breast cancer cells. [score:4]
Cutting edge: microRNA-181 promotes human NK Cell development by regulating notch signaling. [score:3]
MiR-181 and miR-370 were found to be expressed in the control media regardless of BSA supplementation (Table 3). [score:3]
When BSA was not supplemented in SOF media, miR-181 showed expression though right at threshold cut off in one blastocyst pool and was not detected in the second pool making the data not conclusive. [score:3]
In BSA supplemented media, the expression of both miR-181 and miR-370 was detected though not statistically significantly different between embryos of varying quality or above the baseline control. [score:3]
MiR-181 has been associated with roles in genes relating to cancer (Neel and Lebrun, 2013), immune function through NK cell development (Cichocki et al., 2011) and embryonic development (Lingenfelter et al., 2011). [score:2]
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21
[+] score: 23
This miRNA regulates the expression of the cell cycle regulator p27 [kip1], which is normally induced during monocytic differentiation, thus ectopic expression of miR-181 counteracts monocytopoiesis [54]. [score:7]
Increased expression levels of miR-181 were associated with favourable outcome in AML with both normal and abnormal karyotypes [75, 104, 105], and connected with CEBPA mutations [105]. [score:4]
In this case, the downregulation of the miR-181 family was suggested to contribute to an aggressive leukemia phenotype through mechanisms associated with the toll-like receptors and interleukin-1 β  [73]. [score:4]
Among the deregulated miRNAs in AML, these studies identified miRNAs already known to be hematopoietic specific (e. g., miR-142-5p, miR-223, and miR-181) or reported to be highly expressed in other hematological malignancies and solid tumours (e. g., miR-221, miR-222, miR-17-92 cluster and miR-155) [6, 18, 20, 21, 69]. [score:4]
Conversely, miR-181 levels are decreased by VitD3 treatment [54]. [score:1]
In contrast, in different studies performed on a high-risk subgroup with normal karyotype, decreased levels of miR-181 were identified [73]. [score:1]
Microarray analysis identified different miRNAs modulated during monocytic differentiation of AML cell lines, in particular miR-424, miR-32, and miR-181 [49– 51]. [score:1]
Increased miR-181 levels characterized these leukemias [71], a miRNA known to be involved in lymphoid lineage differentiation and to inhibit monocytopoiesis [18, 54]. [score:1]
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[+] score: 22
More relevant microRNAs detected were miR-181d and miR-191, implicated in circadian transcription factor regulation in mouse liver, suggesting the importance of the cyclic expression of these microRNAs for the cyclic regulation of the expression of clock genes like CLOCK and BMAL1 in the liver [116]. [score:7]
Zhang W. Zhang J. Hoadley K. Kushwaha D. Ramakrishnan V. Li S. Kang C. You Y. Jiang C. Song S. W. miR-181d: A predictive glioblastoma biomarker that downregulates mgmt expression Neuro. [score:6]
Accordingly, circulating levels of miR-181 have been suggested to be a potential biomarker of non-alcoholic fatty liver disease [124], and have been found to be decreased in monocytes of obese subjects, although weight loss normalized its expression [125]. [score:5]
Figueredo et al. have recently demonstrated daily variation in miR-16 and miR-181 expression in human leukocytes, both microRNAs peaked between 8:00 a. m. and 16:00 p. m. [121]. [score:3]
miR-181 has been associated with glioblastoma [122] and it has been proposed to be a modulator of the lipid droplet content in human hepatic cells [123], suggesting a link with lipid metabolism. [score:1]
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First, the heterogeneity existed in our meta-analysis and was probably due to the differences in baseline demographic characters of population, the tumor types, the disease stages, the cut-off value of miR-181 expression, the duration of follow-up, etc. [score:5]
MiR-181 family is one of those miRNA families, which generally express in 70 species and various human cancers [6]. [score:3]
In recent years, the miR-181 family was found dysregulated in a variety of human cancers and significantly associated with clinical outcome of cancerous patients. [score:2]
These findings indicated the significance of miR-181 in human hematopoietic development. [score:2]
MiR-181 preferably expresses in hematopoietic cell lineages and is involved in erythropoiesis, granulocytic and megakaryocytic differentiation [33]– [36]. [score:2]
This family includes 4 members (miR-181a, miR-181b, miR-181c and miR-181d) and they are highly conserved in the seed-region sequence and RNA secondary structure. [score:1]
For PubMed, the contextual query language (CQL) was “ (mir-181[Title/Abstract]) OR (microRNA-181[Title/Abstract]) OR (mir-181a[Title/Abstract]) OR mir-181b[Title/Abstract]”; for EMBASE, the CQL was “(mir-181 or microRNA-181 or mir-181a or mir-181b). [score:1]
Forest plots of studies evaluating HR of overall survivals comparing high and low miR-181 expression. [score:1]
The importance of miR-181 in hematopoiesis leaded most studies to focus on the role of miR-181 family in hematological malignancies. [score:1]
First, lack of abundant miR-181a/b expression data in global population makes it difficult to set a standard value for the measurement of miR-181/b. [score:1]
Most of the studies used quantification real-time PCR to measure the expression level of miR-181 (TaqMan: 6 and Stem-loop: 2), and others used microarray method. [score:1]
In recent years, miR-181 family has been found associated with tumorigenesis. [score:1]
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[+] score: 20
FAS has target sites for miR-195, miR-181d and miR-16 that were all downregulated in the liver of the obese minipigs. [score:6]
ADIPOR2 is targeted by the downregulated miRNAs miR-181d, miR-92a, miR-204 and miR-196b-5p. [score:6]
MiR-181d (FC 2.27; p value 0.03) was the most downregulated while miR-195 and miR-16 were down regulated with fold changes < -1.5 and p values < 0.05. [score:5]
MiR-181d is downregulated in serum of NAFLD patients [66]. [score:3]
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[+] score: 20
hESC were transfected with a miR-181a inhibitor or a miRNA inhibitor negative control (miRNA inhibitor control, 100 nM) for 24 h, and then cells were treated with or without 0.5 mM 8-Br-cAMP and 1 μM MPA (8Br + MPA) for an additional 72 h. miR-181 family (A), FOXO1A (B), PRL (C), IGFBP1 (D), DCN (E), and TIMP3 (F) mRNA expression levels were examined by qRT-PCR. [score:9]
miR-181a inhibitor specifically suppressed endogenous miR-181a expression without affecting miR-181b, miR-181c, or miR-181d levels in hESC (Figure  2A). [score:7]
Various potential miR-181 family targets, such as ETS1, CREB1/3, Esr1, and PGR, are involved during differentiation and decidualization events [16- 18]. [score:3]
MicroRNA-181a (miR-181a), which belongs to the miR-181 family, is a key modulator of cellular differentiation. [score:1]
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[+] score: 20
Auxiliary pairing regulates miRNA–target specificity in vivoAs a striking indication that auxiliary pairing regulates miRNA–target specificity, duplex structure analysis revealed distinct binding patterns for members of miRNA seed families (for example, let-7, miR-30, miR-181 and miR-125) (Fig. 4d). [score:7]
identified functional, non-canonical regulation globally for miR-128 and miR-124 (Fig. 2), and for individual miR-9, miR-181, miR-30 and miR-125 targets (Fig. 4f and Fig. 8b–m). [score:4]
As a striking indication that auxiliary pairing regulates miRNA–target specificity, duplex structure analysis revealed distinct binding patterns for members of miRNA seed families (for example, let-7, miR-30, miR-181 and miR-125) (Fig. 4d). [score:4]
Analysis of miR-125 and miR-181 families revealed additional intra -family target preferences (Supplementary Fig. 9a–d). [score:3]
Similarly, miR-181 family members were enriched in both seed -dependent and -independent classes. [score:1]
Interestingly, a number of major miRNAs enriched for seedless interactions (for example, miR-9, miR-181, miR-30 and miR-186) have AU-rich seed sites, indicating that weak seed-pairing stability may favour seedless non-canonical interactions 10. [score:1]
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[+] score: 20
The most highly connected microRNAs in the network included miR-638, miR-18a-3p, miR-483-3p, miR-181d, and miR-30c, which had greater than 50 positively or negatively correlated predicted targets, suggesting that these microRNAs may be important regulators of gene expression associated with emphysema severity. [score:6]
A subset, including miR-638, miR-30c, and miR-181d, had expression levels that were associated with those of their predicted mRNA targets. [score:5]
Five of these microRNAs (miR-638, miR-181d, miR-18a-3p, miR-30c, and miR-483-3p) were correlated with ≥50 of their predicted targets, suggesting that these microRNAs may play a key role in gene regulation in emphysema. [score:4]
Expression values derived from microarray and RT-PCR data were significantly correlated for four of the eight miRNAs (Pearson; P ≤ 0.05; Additional file 1: Figure S2) and just below statistical significance but trending in the correct direction for a fifth microRNA, miR-181d (P = 0.06). [score:4]
These include Let-7c, Let-7d, Let-7e, and Let-7f from the Let-7/miR-98 family, miR-181c and miR-181d from the miR-181/4262 family, and miR-30a-3p, miR-30c, miR-30e-5p, and miR-30e-3p from the miR-30/384-5p family. [score:1]
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28
[+] score: 20
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Finally, other subsets of miRNAs were either up-regulated (miR-23a-3p, miR132-3p, miR-146a-5p, miR-154-3p, miR-181d-5p, miR-212-3p, miR-212-5p, miR-344b-5p, miR-380-3p, miR-410-3p, miR-433-3p and miR-3584; Fig. 2, Supplementary Fig. S4), or down-regulated (miR-29c-5p, miR-30a-5p, miR-30c-2-3p, miR-30e-3p, miR-138-5p, miR-140-3p, miR-551b-3p and miR-652-3p; Fig. 2, Supplementary Fig. S5) during all phases of the disease. [score:9]
Some miRNAs (miR-129-1-3p; miR-129-2-3p, miR-129-5p, miR181c-5p, miR181d-5p, miR-409a-5p, miR-655 and miR-874-3p) were up-regulated (Fig. 2, Supplementary Fig. S3A), whereas others (miR-296-5p, miR-500-3p and miR-652-3p) were down-regulated only in the chronic phase, while not being significantly altered during latency (Fig. 2, Supplementary Fig. S3B). [score:7]
In fact, the expression patterns of miR-20b-5p, miR-142-3p, miR-181d-5p, miR-212-5p, miR-344b-5p and miR-674-3p were identical to those observed using the microarray, and those of miR-21-5p and miR-146a-5p were very similar, although not identical (Fig. 4). [score:3]
Cluster 4 included miR-181c-5p and miR-181d-5p. [score:1]
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[+] score: 19
Besides miRNA 181a, miR-220b, miR-513a-3p, miR-181b, miR-181c, miR-181d, miR-548n and miR-127-5p, are also predicted to target and regulate the expression of OPN. [score:6]
OA patients have higher expression of miR-220b, miR-513a-3p and miR-548n, but lower expression of miR-181a, miR-181b, miR-181c, miR-181d and miR-127-5p, compared to non-OA patients (Fig. 1A). [score:4]
As OPN increased in the pathogenesis of OA 32, we focused on the down-expressed miRNA, including miR-181a, miR-181b, miR-181c, miR-181d and miR-127-5p. [score:3]
This compelling study is indicating miR181 family members have critical importance in the establishment and development of OA. [score:2]
In total, eight potential regulatory miRNAs, including miR-220b, miR-513a-3p, miR-181a, miR-181b, miR-181c, miR-181d, miR-548n and miR-127-5p, were identified by the five algorithms. [score:2]
miR-miR181 family members have been reported to regulate the differentiation stages of chondrocyte and chondrocyte formation 40. [score:2]
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30
[+] score: 18
Other miRNAs from this paper: hsa-mir-134, hsa-mir-149, hsa-mir-130b, hsa-mir-491, hsa-mir-146b
Although, the miR-181d and miR-146b are significantly changed in both the resistant cell line, both the miRNAs are up-regulated in SCC131/R cells while these are down-regulated in SCC084/R (Supplementary Table S5). [score:7]
However, only 26 out of the 40 miRNAs (miR-181d and miR-146b were excluded as they displayed opposite expression status in SCC084/R and SCC131/R) yielded experimentally known target mRNAs. [score:5]
Consequently, the level of miR-181d expression also revealed as a putative biomarker for lymph-node metastasis of oral cancer 49, and correlated with clinicopathological features in ovarian cancer 50 and suggested as a predictive biomarker for glioblastoma 51. miR-181d was found to be up regulated in breast cancer compared to normal adjacent tumour tissues 52. [score:3]
Finally, we have established 6 miRNA signatures (miR-130b, miR-134, miR-149, miR-491, miR-181d, miR-146b) which are significantly (p ≤ 0.05) differentially expressed and common in both the cisplatin resistant cell lines (SCC084/R and SCC131/R) compared to their parental cell lines (SCC084 and SCC131) (Fig. 7C and). [score:2]
There are 6 miRNAs, miR-130b, miR-134, miR-149, miR-491, miR-181d, miR-146b, which are common in both the resistant cells. [score:1]
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31
[+] score: 18
During myogenesis it is up-regulated by SRFs and MEF2, and in a self-regulatory manner, it suppresses YY1 and HDAC4 translation by targeting their 3′-UTRs [48, 49]; miR-146a is another positive regulator of myogenesis, since it modulates the activity of NUMB protein, which promotes satellite cell differentiation towards muscle cells by inhibiting Notch signaling [55, 56]; miR-181 is involved in skeletal muscle differentiation and regeneration after injury and one of its targets is Hox-A11, which in turn represses transcription of MyoD [54]; miR-214 was identified in zebrafish as regulating the muscle development. [score:18]
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[+] score: 17
In order to mitigate the observed off- target transgene expression in ganglion cells following intravitreal delivery of hGRK1-containing AAV vectors, we incorporated a target sequence for miR181, an miRNA shown to be expressed exclusively in ganglion cells and inner retina into our AAV vectors (Atlas of miRNA distribution: http://mirneye. [score:9]
Similar to methods previously described, [32] we further restricted transgene expression to PRs by incorporating multiple target sequences for miR181, an miRNA endogenously expressed in cells of the inner and middle retina. [score:7]
A hGRK1-GFP-miR181c construct was also generated and packaged in AAV2(quad Y−F+T−V) by inserting four tandem copies of complementary sequence for mature miR-181 (5′ ACTCACCGACAGGTTGAA 3′) (Atlas of miRNA distribution: http://mirneye. [score:1]
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[+] score: 17
The striking up-regulation of all the members of the miR-181 family upon lt-NES cell differentiation (Figure 1E right panel) points to potential roles of these miRNAs in human neuronal lineage. [score:4]
Expression of miR-181 family members can be detected in a variety of tissues, with the highest levels found in the brain [37]– [39]. [score:3]
Figure S2 Expression of miR-181 family members in hES cells, lt-NES cells and derived differentiating cultures. [score:3]
The other members of the miR-181 family showed comparable expression patterns (Figure S2). [score:3]
Northern blot analyses showing expression of mature miR-181b, miR-181c and miR-181d in human ES cells (ES), lt-NES cells (NES) and lt-NES cells differentiated for 15 days (ND15) and 30 days (ND30) from the I3 and H9.2 cell lines. [score:3]
Among these, we found miR-153, miR-324-5p/3p and the miR-181 family (Figure 1E right panel), for which evidence from other studies points to potential roles in the nervous system. [score:1]
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[+] score: 17
Similarly, major product, miR-181 was strongly up-regulated during RA treatment while the minor product, miR-181* was not detected in any cell type. [score:4]
Similarly, miR-181 family members, which are located in three genomic clusters: mir-181a-1 and mir-181b-1 on chromosome 1; mir-181a-2 and mir-181b-2 on chromosome 9; and mir-181c and mir-181d on chromosome 19, were all up-regulated during the RA time-course, but miR-181a* and miR-181d had log2 intensity below threshold at 28 days RA (Fig. 3B). [score:4]
The expression levels of the same miR-302 (A; bottom left panel) and miR-181 (B; bottom right panel) genomic clusters in NT2-undiff and NT2-28D plotted as yellow and blue bars, respectively. [score:3]
The expression levels of the members of the miR-302 (A) and the miR-181 (B) genomic clusters during neural differentiation plotted as heatmaps (top panels). [score:3]
0011109.g003 Figure 3The expression levels of the members of the miR-302 (A) and the miR-181 (B) genomic clusters during neural differentiation plotted as heatmaps (top panels). [score:3]
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35
[+] score: 17
For example, miR-181 upregulates expression of let-7 by effectively repressing Lin28 expression, and eventually promoting megakaryocytic differentiation, thus providing insight into future development of miRNA-oriented therapeutics [33]. [score:9]
It has been reported that Lin28 mRNA expression can be depressed by several other miRNAs including miR-125, miR-9, and miR-30 [39] and miR-181 [33], and Lin28 expression can be modulated by proteasome inhibitors such as MG132 [40]. [score:7]
Li X. Zhang J. Gao L. McClellan S. Finan M. A. Butler T. W. Owen L. B. Piazza G. A. Xi Y. MiR-181 mediates cell differentiation by interrupting the Lin28 and let-7 feedback circuit Cell Death Differ. [score:1]
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36
[+] score: 17
Additional data showing a miR-181d down-regulation in human gliomas, confirmed that miR-181d acted as a tumor suppressor by directly targeting KRAS mRNA [61]. [score:9]
Other members of the miR-181 family (with a similar seed sequence) have also been described to target KRAS mRNA. [score:3]
In addition, KRAS was shown to be targeted by miR-181a in oral squamous cell carcinoma, by miR-181c in gastric carcinoma, and by miR-181d in glioma. [score:3]
These observations emphasized the role of miR-181 family as a major negative regulator of the RAS-MAPK pathway in cancer. [score:2]
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37
[+] score: 16
Value Targets INTERACTION EFFECT miR-205 +2.44 CDH1, ZEB1/2, ERRB3, AKTCarraway et al., 1997 miR-155 +1.90 Inhibits negative regulators of inflammation (SHIP1, SOCS)Elton et al., 2013 miR-10b +1.48 HOXA1 and NFKBFang et al., 2010; Tonja, 2012 miR-31 +1.38 ICAM1, E-SelectinSuárez et al., 2010 miR-181 −1.60 Zeb2, MCL1, BCL2L11, BCL2,PTEN, DUSP6, PTPN11Pati et al., 2014 miR-17 −1.83 APP, TGFBRII, SMAD2, SMAD4, p21, BIM (BCL2L11), PTEN. [score:6]
In fact, miR-181 is induced by LIF, a cytokine which inhibits the proliferation of stem cells, and hence, it inhibits neurogenesis (Pati et al., 2014). [score:5]
One of the target of miR-181 is MCL1, which however, has two isoforms: while the isoform 1 is anti-apoptotic, the isoform 2 is pro-apoptotic. [score:3]
The evaluation of miR-181 effects according to its targets, suggests that Older Men Group could have higher levels than Older Women Group of the following activities: more cell adhesion (i. e., more CdhE due to low ZEB2), viability (more PI3K/AKT due to low PTEN), more MAPK signaling (i. e., potentially more ERK [*], JUN [*], p38 [*]), more pro-apoptotic activity (less Bcl2), and low cytoskeleton organization (less RhoA activation due to the loss of PTPN11 effect on Rock2). [score:1]
The negative super-ratio observed with miR-181 (interaction = −1.60) is also consistent with the miR-17 finding. [score:1]
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38
[+] score: 15
Together, these results demonstrate that a 400-bp region of the GARP 3’ UTR, that is directly targeted by miR-142-3p, miR-185 and the four miR-181, controls GARP protein levels and the amounts of TGF-β1 that are processed and secreted by human CD4 [+] T cells. [score:4]
Mutation of the miR-142-3p binding site, but not that of the miR-181 site, suppressed the ability of the miR-142-3p mimic to decrease reporter activity in 293 cells (Figure 6D). [score:4]
Conversely, mutation of the miR-181 site, but not that of the miR-142-3p site, suppressed the ability of the four m iR-181 family members to decrease reporter activity (Figure 6D). [score:4]
Others have reported a reduced expression of miR-142-3p and miR-181 b and d in murine or human Tregs by comparison to Th cells [37, 38, 44, 46]. [score:3]
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39
[+] score: 15
Intriguingly, several of the differentially expressed miRNAs have been shown in previous studies to regulate host cell death: miR-145 modulates the expression of KLF4 (Davis-Dusenbery et al., 2011), a transcription factor for TP53, which regulates apoptosis (Rowland et al., 2005); miR-15b and miR-29b are known to be pro-apoptotic in leukemia cells (Cimmino et al., 2005; Garzon et al., 2009); miR-148a promotes apoptosis by targeting BCL2 in colorectal cancer cells (Zhang et al., 2011); miR-181d also targets BCL-2 and promotes apoptosis in glioma cells (Wang et al., 2012). [score:11]
MiR-181d acts as a tumor suppressor in glioma by targeting K-ras and Bcl-2. J. Cancer Res. [score:4]
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40
[+] score: 15
For example, miR-181 and miR-153 promote apoptosis by directly targeting B-cell chronic lymphocytic leukemia/lymphoma 2 (Bcl-2) mRNA and repressing its translation, thereby inhibiting gliomagenesis [84]. [score:8]
Moreover, miR-181 downregulation is more prominent in grade III and IV glioma than that in lower grades [84, 87]. [score:4]
Both miR-181 and miR-153 expression is decreased in glioma cell lines and a subset of clinical glioma specimens, suggesting roles of the two miRNAs in glioma progression. [score:3]
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41
[+] score: 14
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-105-1, hsa-mir-105-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-205, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-141, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-188, hsa-mir-320a, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-302a, hsa-mir-34c, hsa-mir-30e, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-372, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-383, hsa-mir-339, hsa-mir-133b, hsa-mir-345, hsa-mir-425, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-193b, hsa-mir-498, hsa-mir-518f, hsa-mir-518b, hsa-mir-520c, hsa-mir-518c, hsa-mir-518e, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-503, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-376a-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-645, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-744, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-302e, hsa-mir-302f, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-371b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
With the mouse mo del, it has been shown that a minimal uterine expression of miR-181 is essential for the onset of embryo implantation and that it is regulated by the leukemia inhibitory factor (LIF) [80]. [score:6]
Also miRNA precursors are present in human sperm, such as pri-miR-181, whose targets might have a function in early embryonic development and globally decrease at the 4–8-cell stage of human embryo development [8]. [score:5]
A specific target of pri-miRNA-181 is the embryonic stem cell pluripotency factor, termed coactivator -associated arginine methyltransferase I (CARM1). [score:3]
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[+] score: 14
Interestingly, mutation of the miR181 site also decreased of luciferase in pMirTarget 3′ UTR hGRβ, but this was not observed in the UMUC-3. Total RNA was extracted from the UMUC-3 and T24 cells to measure the miRNA expression that may target the 3′ UTR of human GRβ (Figure 5C). [score:6]
Insulin did not significantly change expression of miR33a, miR144, miR181a, miR181b, miR181c, or miR181d in the T24 cells. [score:3]
Next, we wanted to determine if miR33a, miR144, miR181a, miR181b, miR181c, or miR181d changed during a scratch assay and if this affected the human GRβ or GRα expression. [score:2]
The T24 and UMUC-3 bladder cancer cells were transfected with the 3′UTR GRβ-Luc expression construct with mutation in the miRNA binding site for miR181, miR144, or miR33a and was measured by a luciferase assay, and normalized to renilla (B). [score:1]
Interestingly, miR33a, miR144, miR181a, miR181b, miR181c, and miR181d were all increased in the T24 cells. [score:1]
Three miRNAs were predicted to bind the 3′UTR of human GRβ (miR33a, miR181-a/b/c/d, and miR144). [score:1]
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[+] score: 14
After determining the expression levels of these miRNAs in the same 7 pairs of NSCLC tissues and normal adjacent tissues, we observed that 8 miRNAs (miR-203, miR-30, let-7, miR-132, miR-181, miR-212, miR-101 and miR-9) were downregulated in the NSCLC tissues, while the other 5 miRNAs (miR-125, miR-98, miR-196, miR-23 and miR-499) were upregulated (Fig. S1). [score:9]
In addition to let-7, miR-181 26, miR-30 29, miR-9 27 28, miR-132 32 33, miR-101 30 and miR-212 31 have also been shown to directly bind the 3′-UTR of LIN28B and repress the translation of this protein. [score:4]
A total of 13 miRNAs, including miR-203, miR-30, let-7, miR-132, miR-181, miR-212, miR-101, miR-9, miR-125, miR-98, miR-196, miR-23 and miR-499, were identified as candidate miRNAs by all three computational algorithms (Table S2). [score:1]
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[+] score: 14
miRNAs (e. g. miR-146a[49], miR-34[50], miR-181[51]) that downregulate protective genes against AD (e. g., complement factor H)/upregulate “pro-AD” genes (e. g. p53, SIRT1)/are correlated with amount of Aβ plaque and NFTs, exhibit upregulated in the brain and/or peripheral circulation of AD patients. [score:10]
Addition of Aβ peptides to primary neuronal cell cultures/primary human astrocytes cultures has been shown to downregulate miR-9/miR-181[51]. [score:4]
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45
[+] score: 14
All the isoforms and combined sum of expression of isoforms showed the same pattern in plots created using our tool as shown in the paper, with poor overall survival observed in the group having low expression of miR-181 isoforms. [score:5]
In another study, Chen et al [61], have demonstrated down-regulation of several isoforms of miR-181 (miR-181-a, miR-181-b, miR-181-c and miR-181-d) being correlated with poor overall survival in acute myeloid leukemia (AML). [score:4]
Prognostic plot for sum of expression of hsa-mir-181 isoforms a,b,c and d in TCGA AML data. [score:3]
Additional file 1: Figures S1-S4 provided in supplementary data show prognostic plots for miR-181 isoforms in AML data. [score:1]
Prognostic plot created using PROGmiR for isoforms a, b, c and d of miRNA hsa-miR-181 identified as prognostically important biomarker in Acute Myeloid Leukemia (AML) by Chen et al, using TCGA data. [score:1]
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46
[+] score: 14
Suppression of miR-181-a/-b produced a significant delay in tumour development in a mouse mo del of MM, confirming that this miRNA nourishes MM tumour growth. [score:4]
Pichiorri et al. [25] have shown that miR-181-a/-b, miR-106b~25 and miR-32 are up-regulated in MGUS, MM primary cells and cell lines. [score:4]
Moreover, miR-21, as well as miR-181-a/-b, is upregulated in two drug resistant MM cell lines when compared with parental line [31]. [score:3]
Finally, miR-181-a/-b were significantly upregulated in two drug resistant MM cell lines when compared with parental line [31]. [score:3]
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47
[+] score: 13
As a critical regulator of tumor cell migration and invasion and breast cancer progression in vitro, miR-181 could potentially be an important therapeutic target [243]. [score:4]
We and others have demonstrated the mir-181 family of microRNAs to be up-regulated by TGF β and activin, a closely related TGF β family member [243, 247, 249]. [score:4]
In hepatocellular carcinoma, TGF β -induced miR-181 targets TIMP3 for degradation, thereby increasing invasiveness of the cells [247]. [score:3]
We also found miR-181 to be a downstream regulator of activin/TGF β -induced cellular migration and invasion in breast cancer (Figure 4). [score:2]
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48
[+] score: 13
miR-181d belongs to the miR-181 family, which mediates inflammatory responses through the regulation of PI3K and NF-κB signaling [47], and it has been shown to be upregulated in dendritic cells upon infection with MTB [48]. [score:5]
Central within the cluster, and up-regulated in both MAB-S and MAB-R-infected cells at 24 hpi, is miR-181d, with 57 predicted interactions (Fig.   6). [score:4]
Central to this network is miR-181d, which is regulated at 24 hpi in response to both MAB-R and MAB-S, and is predicted to interact with 57 core mRNAs showing inverse expression patterns. [score:4]
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49
[+] score: 13
miR-138 is upregulated in glioma cells with acquired TMZ resistance and in recurrent glioblastomas in vivoMicroarray -based miRNA expression profiling of parental and TMZ-resistant (TMZR) LN-18, LN-229 and LN-308 cells revealed several differentially expressed MiRNAs (Figure 1A), including several miRNAs previously implicated in TMZ resistance, such as mir-125b [10], miR-181 [12] or miR-221/222 [13]. [score:8]
Microarray -based miRNA expression profiling of parental and TMZ-resistant (TMZR) LN-18, LN-229 and LN-308 cells revealed several differentially expressed MiRNAs (Figure 1A), including several miRNAs previously implicated in TMZ resistance, such as mir-125b [10], miR-181 [12] or miR-221/222 [13]. [score:5]
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50
[+] score: 12
Six miRNAs (miRNA181-b, miRNA-181d, miRNA-605, has-let-7a, has-let-7b, and has-let-7f) were predicted to be related to stroke based on the targetgenes network (Fig. 5). [score:3]
ESM1, KRAS, miR-181d, miR-181b-3p, miR-605-3p and miR-605-5p were highly expressed in the blood of stroke patients compare to healthy people. [score:3]
In our study, miR-605 and miR-181d were predicted to be related to stroke for the first time and we validated the prediction, which were highly expressed in the blood of stroke patients. [score:3]
Finally, ESM1, KRAS, miR-181d, miR-181b-3p, miR-605-3p and miR-605-5p were highly expressed in the blood of stroke patients compared to healthy people (Fig. 6). [score:2]
miR-181b, miR-181d and miR-605 are predicted based on the genes from miRanda database. [score:1]
[1 to 20 of 5 sentences]
51
[+] score: 12
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-139, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-190a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-190b, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
Polycyclic aromatic hydrocarbon (PAH) -mediated upregulation of hepatic microRNA-181 family promotes cancer cell migration by targeting MAPK phosphatase-5, regulating the activation of p38 MAPK. [score:7]
Zhang and Pan (2009) have evaluated the effects of Hexahydro-1, 3, 5-trinitro-1, 3, 5-triazine (also known as hexogen or cyclonite) (RDX) on miRNA expression in mouse brain and liver, most of the miRNAs that showed altered expression, including let-7, miR-17-92, miR-10b, miR-15, miR-16, miR-26, and miR-181, were related to toxicant-metabolizing enzymes, and genes related to carcinogenesis, and neurotoxicity, in addition, consistent with the known neurotoxic effects of RDX, the authors documented significant changes in miRNA expression in the brains of RDX -treated animals, such as miR-206, miR-30a, miR-30c, miR-30d, and miR-195. [score:5]
[1 to 20 of 2 sentences]
52
[+] score: 11
The miR-181 family has been shown to exert oncogenic effects via suppression of the apoptosis gene Bcl-2. Therefore, the sequestration of miR-181a by MEG3 results in upregulation of Bcl-2, and suppresses gastric carcinogenesis [22]. [score:8]
LncRNA MEG3 was also found to be capable of inhibiting gastric cancer cell proliferation, migration, and invasion by competitively binding with members of the miR-181 family such as MEG3 sequestering oncogenic miR-181a (Table 1 and Figure 1). [score:3]
[1 to 20 of 2 sentences]
53
[+] score: 11
A primary regulator of exercise -induced SIRT1 expression is NAD [+] availability through AMPK (White and Schenk, 2012) and it seems plausible that AMPK, rather than miR-133b or miR-181, may be the primary regulator of post-exercise changes in SIRT1 expression. [score:7]
The expression of miR-181 increased at 4 h post-exercise with PRO (~80%, P < 0.05) that resulted in higher miR-181 with PRO compared to PLA at 4 h (~76%, P < 0.05; Figure 2A). [score:2]
We also found greater miR-133b and miR-181 abundance with post-exercise protein ingestion. [score:1]
Figure 2(A) mir-181-5p, (B) miR-378-5p, (C) miR-486-5p, and (D) miR-494-3p abundance at rest and at 4 h post-exercise recovery following a concurrent exercise session of resistance (8 sets of 5 leg extension at 80% 1-RM) and endurance (30 min cycling at 70% VO [2peak]) exercise and ingestion of either 500-mL PLA or PRO beverage immediately after exercise. [score:1]
[1 to 20 of 4 sentences]
54
[+] score: 11
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-31, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-221, hsa-mir-23b, hsa-mir-27b, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-200c, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-30e, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-10b-1, dre-mir-181b-1, dre-mir-181b-2, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-204-1, dre-mir-181a-1, dre-mir-221, dre-mir-222a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7e, dre-mir-7a-3, dre-mir-10b-2, dre-mir-20a, dre-mir-21-1, dre-mir-21-2, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-26b, dre-mir-27a, dre-mir-27b, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-30e-2, dre-mir-101b, dre-mir-103, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-148, dre-mir-181c, dre-mir-200a, dre-mir-200c, dre-mir-203b, dre-mir-204-2, dre-mir-338-1, dre-mir-338-2, dre-mir-454b, dre-mir-212, dre-mir-181a-2, hsa-mir-551a, hsa-mir-551b, dre-mir-31, dre-mir-722, dre-mir-724, dre-mir-725, dre-mir-735, dre-mir-740, hsa-mir-103b-1, hsa-mir-103b-2, dre-mir-2184, hsa-mir-203b, dre-mir-7146, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-204-3, dre-mir-24b, dre-mir-7133, dre-mir-128-3, dre-mir-7132, dre-mir-338-3
Morphological and histological studies of miR-21, miR-31 and/or miR-181 inhibition combined with identification of target genes would demonstrate their roles in blastema formation. [score:5]
STRING interactions with 11 common blastema -associated genes, miR-21, miR-31, miR-181, and 50 additional common differentially expressed genes with common predicted miRNAs binding sites. [score:3]
Next, we established a gene network for common miRNA target genes for miR-21, miR-31 and miR-181. [score:3]
[1 to 20 of 3 sentences]
55
[+] score: 10
miR-181a, miR-181c and miR-181d were downregulated in two normal aging mouse mo dels, C57BL/6J and CBA/J [82], implying that aging can lead to decreased levels of miR-181, which then inhibits proliferation. [score:6]
MiR-181 is known to cause proliferation of hair cells in the chicken inner ear and inhibition of miR-181a reduces proliferation [85]. [score:3]
This suggests that during the early post-natal growth of the inner ear, miR-181 is required, but may not be necessary during the adult stage. [score:1]
[1 to 20 of 3 sentences]
56
[+] score: 9
In hematopoietic stem cells, miR-181a-2*, a member of the miR-181 family and deregulated in both 2102Ep and NTera-2 cells, can directly target NANOG [101]. [score:5]
The expression of the miR-181 family increases during early hESC differentiation and has previously been identified as regulators of stem cell differentiation, including that of hESCs and CSCs [102– 105]. [score:4]
[1 to 20 of 2 sentences]
57
[+] score: 9
Of the most up-expressed miRNA (miRNA-181a-3p) in HepG2/DOX, one target gene RBM22 supported by three softwares (Mireap, miRDB and PicTar), was expected to be the common targets of seven other significantly differentially expressed miRNAs including miR-21, miR-101, miR-217, miR-590-5p, miR-181b, miR-181c, and miR-181d. [score:9]
[1 to 20 of 1 sentences]
58
[+] score: 9
Since miR-181b-abundant glioma cells is more sensitive to temozolomide (TMZ) [21], aplysin enhances TMZ action through increasing the expression of miR-181 in TMZ-resistant glioma cells, which results in MEK1 (mitogen-activated protein kinase kinase 1) downregulation [22]. [score:6]
For example, in human pancreatic cancer cells treated with circumin, miR-181d is significantly changed, but miR-181c (chr19:13874699-13874808), which is close to miR-181d (chr19:13874875-13875011) in the genome, is not changed [48]. [score:1]
For example, miR-181 is related to TMZ-resistance of glioma, and interestingly, aplysin can also enhance the sensitivity of glioma cells to TMZ. [score:1]
Thus, researchers investigated their association and found aplysin exerts its function through increasing the expression of miR-181. [score:1]
[1 to 20 of 4 sentences]
59
[+] score: 9
Consistently, we previously demonstrated that CBX7 negatively regulates the expression of miR-181 that has among its targets CBX7, creating a synergistic loop that contributes to breast cancer progression [11]. [score:6]
The results presented in Fig.   1 confirm a drastic overexpression of miR-181, miR-137, miR-199, miR-706 and miR-719 and repression of miR-155 in Cbx7 KO MEFs in comparison with the WT ones. [score:3]
[1 to 20 of 2 sentences]
60
[+] score: 9
miR-181 downregulation enhanced by ~ 60% ALX/FPR2 protein expression in CFBE41o-cells (Fig.   2D), although it did not change ALX/FPR2 mRNA expression (results not shown). [score:8]
Along these lines, the downstream signaling leading to the enhanced LXA [4] -induced phagocytic activity, observed when miR-181 was inhibited, requires further investigation. [score:1]
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61
[+] score: 9
Although in most instances miR-181a-1 attenuates inflammatory responses, in some cases miR-181 family members are upregulated by inflammatory signals and have been reported to be pro-inflammatory, which may explain its reported dual roles as a tumor suppressor-miR or onco-miR in different types of cancers. [score:6]
It should also be noted that miR-181 is an important regulator of hematopoiesis, therefore, decreased miR-181a-1 may impact hematopoietic lineage development during aging [36]. [score:3]
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62
[+] score: 9
Indeed, miRNA inhibitors were designed to inhibit individual members of miRNA families, and, for example, miR-181, a miRNA essential for differentiation [15] was below the threshold of detection in this screen, likely due to the high redundancy of the miR-181 family. [score:5]
The positive control was a miR-181 LNA inhibiting the whole miR-181family (Exiqon) and the negative controls were a mutant of this oligonucleotide ([15] or mock transfected cells. [score:3]
Thus, a few miRNAs, miR-133, miR-1, miR-206, miR-181 and miR-27a, have previously been shown to be important in skeletal muscle cell terminal differentiation [5]. [score:1]
[1 to 20 of 3 sentences]
63
[+] score: 9
miR-1236 was a negative regulator of VEGFR-3 in lymphangiogenesis [28] and miR-181 was found to be an important regulator of angiogenesis and lymphangiogenesis via Prox-1 inhibition [29]. [score:5]
Prox1 expression is negatively regulated by miR-181 in endothelial cells. [score:4]
[1 to 20 of 2 sentences]
64
[+] score: 9
MicroRNAs that function as oncogenes, including miR-17, miR-21, and miR-106a, were upregulated, whereas microRNAs that function as tumor suppressors, such as miR-101, miR-181, miR-449, miR-486, and let-7a, were downregulated in gastric cancer [42, 43]. [score:9]
[1 to 20 of 1 sentences]
65
[+] score: 9
In PB NK, highly expressed miRNAs included has-let-7a, has-let-7g, has-mir-133b, has-mir-181b, and has-mir-181d that target the anti-apoptotic genes Bcl-2 and Bcl-2L, which may indicate that PB NK cells are closer to reaching the limit of cell expansion than pNK cells. [score:5]
Cutting edge: microRNA-181 promotes human NK cell development by regulating Notch signaling. [score:3]
Furthermore, we identified a has-mir-181 group (has-mir-181b, has-mir-181c, has-mir-181d) that was threefold higher in PB NK. [score:1]
[1 to 20 of 3 sentences]
66
[+] score: 8
miR-181 and miR-29 could down-regulate TCL1, Mcl1, Bcl2 and Bcl2L11 [46- 48]. [score:4]
From our analyses, miR-181b appeared to be the strongest TCL1 inhibitor among members of the miR-181 or miR-29 families. [score:3]
Following transfection of miRNA mimics of the miR-181 and miR-29 families, we assessed the TCL1 protein level. [score:1]
[1 to 20 of 3 sentences]
67
[+] score: 8
miR-181 expression was also enhanced in SPARC expressed medulloblastoma cells compared to controls. [score:4]
miR-181 expression was shown to enhance radio and chemo sensitivity [61– 63]. [score:3]
Taken together, these findings support the hypothesis that mir-181 may be involved in enhancing radio response in medulloblastoma. [score:1]
[1 to 20 of 3 sentences]
68
[+] score: 8
However, there was no significant difference in the expression of miR-181d, miR-3185 and miR-4763. [score:3]
We validated the expression of leucine -dependent microRNAs in HepG2 cells, including miR-143, miR-92b*, miR-335, miR-181d, miR-3185 and miR-4763 by real-time PCR (qPCR) (Table  1). [score:3]
The cDNA synthesis was carried out with 2 μg total RNA using a miScript II RT Kit (Qiagen, Hilden, Germany), and expression of the miR-143, miR-92b*, miR-335, miR-181d, miR-3185 and miR-4763 was assayed with a a miScript SYBR Green PCR kit (Qiagen, Hilden, Germany). [score:2]
[1 to 20 of 3 sentences]
69
[+] score: 8
We previously demonstrated that the expression of five microRNAs (miR-181d, miR-518b, miR-524-5p, miR-566 and miR-1227) were correlated with the survival of glioblastoma patients [12]. [score:3]
Additionally, we demonstrated that the expression profile of miR-566 as well as that of four other miRNAs (miR-181d, miR-518b, miR-524-5p and miR-1227) correlated with the prognosis of glioblastoma patients [12]. [score:3]
Previous studies have clarified the functions of the miR-181 family, miR-518b, miR-524-5p and miR-1227. [score:1]
The function of miR-181d, miR-518, and miR-1227 have been reported in glioma or in other cancer types [13- 15], however, there are no reports about miR-566 function till now. [score:1]
[1 to 20 of 4 sentences]
70
[+] score: 8
For instance, Zhang et al. confirmed that downregulation of miRNA-181d, probably through reverse regulation on a microRNA-181d gene (Na+/K+ transporting ATPase interacting 2), could suppress the development of pancreatic cancer cell lines [17]. [score:8]
[1 to 20 of 1 sentences]
71
[+] score: 8
A previous study from our institution had predicted eleven of these fourteen (79%) miRNAs (hsa-miR-454, has-miR-582-5p, has-miR-181d, has-miR-500, has-miR-181c, has-miR-411, has-miR-363, has-miR-381, has-miR-302c*, has-miR-652 and has-miR-452), to target CYP3A4/5/7 3’-UTR using in silico approach [29]. [score:3]
We found several combinations of miRNAs including miRNA-155, miRNA-181 and miRNA-652 as well as miRNA-363, miRNA-532 and miRNA-582 which clustered or overlapped in their binding locations on these UTRs, suggesting possible competition for binding to control gene expression in a combinatorial fashion. [score:3]
Among the miRNAs, miR-155, miR-454, miR-582-5p, let-7f-1*, miR-181d, and miR-500 had > 1.2-fold increase in cirrhotic liver samples (Table 2 ). [score:1]
Six microRNAs (miR-155, miR-454, miR-582-5p, let-7f-1*, miR-181d, and miR-500) had >1.2-fold increase in cirrhotic livers and also had significant negative correlation with hepatic CYP3A activity (range of r = -0.44 to -0.52, P <0.05). [score:1]
[1 to 20 of 4 sentences]
72
[+] score: 8
Based on a miRNA profiling study that identified the miR-17 and miR-181 family members as the most downregulated miRNAs during neutrophil differentiation of NB4 APL cells [52], and our study identifying ULK1 as a novel target of the miR-17 family member miR-106a in lung cancer therapy [53], we hypothesized that this miRNA also targets ULK1 in AML. [score:8]
[1 to 20 of 1 sentences]
73
[+] score: 8
Dai et al. have correlated a miRNA signature (downregulation of miR-100, miR-130a, and miR-197 and upregulation of miR-181b, miR-181d, miR-101, and miR-195) in HNSCC cells with multiple drug resistance phenotypes in vitro [84]. [score:7]
miR-31, miR-17/20a, miR-125b, miR-155, miR-181, miR-375 and miR-491-5p, miR-205, and miR-let7d were found to be associated with lymph node metastasis and poor OSCC patient survival [38, 59, 60, 65, 72, 77– 80]. [score:1]
[1 to 20 of 2 sentences]
74
[+] score: 8
Pekarsky et al. discovered that the expression levels of miR-29 and miR-181 were inversely correlated with Tcl1 expression in CLL. [score:5]
Their results showed that miR-29 and miR-181 might be candidates for therapeutic agents in CLL overexpressing Tcl1 [30]. [score:3]
[1 to 20 of 2 sentences]
75
[+] score: 8
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-204, hsa-mir-205, hsa-mir-181a-1, hsa-mir-216a, hsa-mir-217, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-149, hsa-mir-150, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-370, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-335, hsa-mir-133b, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-92b, hsa-mir-574, hsa-mir-605, hsa-mir-33b, hsa-mir-378d-2, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-378j
Pekarsky Y. Santanam U. Cimmino A. Palamarchuk A. Efanov A. Maximov V. Volinia S. Alder H. Liu C. G. Rassenti L. Tcl1 expression in chronic lymphocytic leukemia is regulated by miR-29 and miR-181 Cancer Res. [score:4]
In particular, miR-181 and miR-155, which are known to regulate B cell differentiation [48, 105, 106], are present in high concentrations in HM [44, 48], suggesting a function in the development of the infant’s immune system. [score:3]
HM is rich in B cell-related microRNAs, such as miR-181 and miR-155, which potentially induce B cell differentiation [108, 110]. [score:1]
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76
[+] score: 8
Responses to ischemia in mouse brain also showed increased expression of miR-181 in the core, where cells die, and decreased expression of miR-181 in the penumbra, where cells survive (69). [score:5]
by manipulation of miRNA-related pathways are also found in astrocyte-rich miRNAs, including miR-181 and families, and miR-146a, and their validated targets, GRP78, and Bcl-2 family members (114). [score:3]
[1 to 20 of 2 sentences]
77
[+] score: 8
MiRNA-181 interacts with the 3′ UTR region of the tumor suppressor KLF gene and have ability to inhibit the apoptosis of tumor cells (Zabaleta, 2012). [score:4]
MiRNA-181 targets 3′UTR region of tumor suppressor Krüppel-Like Factor (KLF) encoding gene during Helicobacter pylori infection (Zabaleta, 2012). [score:4]
[1 to 20 of 2 sentences]
78
[+] score: 8
Since we have previously shown that HMGA1 is able to negatively regulate CBX7 expression (Mansueto et al., 2010) and that HMGA1 positively regulates miR-181 that has CBX7 as target, we can envisage a HMGA1-CBX7 network that operates in the regulation of tumour progression and adipocyte cell growth and differentiation. [score:8]
[1 to 20 of 1 sentences]
79
[+] score: 8
In this respect, there is a long list of predicted miRNAs (i. e. from DIANA-microT, miRanda, TargetScanS algorithms) that may target the 3'UTR of APP, including let-7i, miR-15, -26, -29, -93, -101, -106, and miR-181 which are reportedly down-regulated in AD brain [96, 99]. [score:8]
[1 to 20 of 1 sentences]
80
[+] score: 8
In addition to let-7, the miRNAs miR-26a, miR-181, miR-9, miR-30, miR-125, miR-212 and miR-27 have also been shown to directly bind the 3′UTR of LIN28A/LIN28B and repress translation of the protein, and as these miRNAs are frequently under-expressed in malignant tumors, higher levels of LIN28 expression are seen [31– 34]. [score:8]
[1 to 20 of 1 sentences]
81
[+] score: 7
Moreover, miR-181 targets TIMP3 that is an inhibitor of metalloprotease, inductor of apoptosis and inhibits angiogenesis, cell migration and invasion [174]. [score:7]
[1 to 20 of 1 sentences]
82
[+] score: 7
Interestingly, members of the miR-181 family consistently upregulated the reporter in the Keklikoglou et al. study, while all four members downregulated reporter activity in our study to varying degrees (see Additional file 1, Table S2). [score:7]
[1 to 20 of 1 sentences]
83
[+] score: 7
We verified that coexpression of TCL1 with miR-29 and miR-181 decreased its expression and found inverse correlation between miR-29b, miR-181b, and Tcl1 expression in CLL samples [35]. [score:7]
[1 to 20 of 1 sentences]
84
[+] score: 7
In glioma cancer, miR-181d upregulation may correspond to a better response to temozolomide, while upregulation of miR-21 may predict poor response caused by temozolomide resistance [30]. [score:7]
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85
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Similarly, downregulation of miR-181 was responsible for resistance to imatinib by directly targeting the Bcl-2 family member Mcl-1 in chronic myelogenous leukemia cells [16]. [score:7]
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86
[+] score: 7
miRNAs of the miR-125 and miR-181 families contribute to the downregulation of Cbx7 during mESC differentiation by directly targeting its 3′UTR [100]. [score:7]
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87
[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-21, hsa-mir-29a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-194-1, mmu-mir-200b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-140, hsa-mir-194-1, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-21a, mmu-mir-29a, mmu-mir-96, mmu-mir-34a, mmu-mir-135b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-376c, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-135b, mmu-mir-181b-2, mmu-mir-376b, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-29a, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-140, dre-mir-181c, dre-mir-194a, dre-mir-194b, dre-mir-200b, dre-mir-200c, hsa-mir-376b, hsa-mir-507, dre-let-7j, dre-mir-135b, dre-mir-181a-2, hsa-mir-376a-2, mmu-mir-376c, dre-mir-34b, dre-mir-34c, mmu-mir-181d, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, mmu-mir-124b
The data verified that two miRNAs, miR-29a and -34a, which have been implicated in apoptotic pathways, are up-regulated and the two miRNAs, miR-181 and -183, which have been shown to have roles in proliferation and differentiation, are down-regulated While it is believed that a major cause of ARHL is the death of hair cells, other age-related changes in the central auditory pathways cannot be ruled out. [score:7]
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88
[+] score: 7
In cellular or animal mo dels, PAHs down-regulate miR-34c 31, miR-21, miR-221, miR-222, and miR-429 32, and up-regulate miR-34a 33 34, miR-181a, miR-181b, and miR-181d 35. [score:7]
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89
[+] score: 7
Among the up regulated miRNAs in AMLs, a number were already known to be haematopoietic tissue-specific, i. e. miR-142-5p, miR-155, and miR-181 [10], [41], [42], and/or reported highly expressed in a variety of haematological malignancies and solid tumours, i. e. miR-221, and miR-222. [score:4]
MiR-181 regulates the expression of TCL1 (X82240) in CLL [45]. [score:3]
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90
[+] score: 7
For the miRNA family, the upregulated miRNAs and downregulated miRNAs are enriched in miR-17 family (P = 4.03 × 10 [-3]) and miR-181 family (P = 1.64 × 10 [-3]), respectively. [score:7]
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91
[+] score: 7
Interestingly, miR-125b inhibitor boosts the chemosensitivity of glioblastoma stem cells to TMZ by targeting Bak1 [9], whereas the miR-128, miR-149 and miR-181 families enhance the chemosensitivity of glioblastoma cells to TMZ by targeting Rap1B [10, 11]. [score:7]
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92
[+] score: 7
microRNAs downregulated in quiescent cells included miR-18, miR-20, miR-29, and miR-7, and microRNAs upregulated with quiescence included let-7b, miR-125a, miR-30, miR-181, miR-26, and miR-199. [score:7]
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93
[+] score: 7
Overexpression of the miR-17-92 cluster and miR-181 enhanced B-cell proliferation, while miR-150 regulated B-cell differentiation (61– 64). [score:4]
When overexpressed, miR-181 has been shown to decrease T-cell numbers (61), but enhance T-cell receptor signaling (65). [score:3]
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94
[+] score: 7
In an ischemia -induced mo del of retinal neovascularization, seven miRNAs (miR-106a, miR-146, miR-181, miR-199a, miR-214, miR-424, and miR-451) were upregulated, and three miRNAs (miR-31, miR-150, and miR-184) were downregulated. [score:7]
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95
[+] score: 6
MiR-181c-5p is a known tumor suppressor in neuroblastoma: it belongs to the miR-181 family, whose members are known to be upregulated after MYCN silencing [26, 27]. [score:6]
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96
[+] score: 6
In addition, miRNA-181 expression was found to be elevated in response to acute endurance training in murine quadriceps femoris muscles, indicating a possible regulatory function in the adaptive processes to endurance exercise (Safdar et al., 2009) and also rises in circulating levels of miRNA-181b - but not of miRNA-181a - were detected with peaks directly after an uphill course, probably as an immediate consequence of hypoxia (Banzet et al., 2013). [score:5]
All of this suggests that members of the miRNA-181 family might be important for both contributing to an anti-inflammatory environment and inducing adaptations in response to exercise. [score:1]
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97
[+] score: 6
miR-181 is reported to be very strongly expressed in the brain [41- 43], downregulation of which contributes to accelerated HIV -associated dementia [51], and miR-155 is reportedly absent from latently infected cells [30]. [score:6]
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98
[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-27a, hsa-mir-29a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-146a, hsa-mir-150, hsa-mir-155, hsa-mir-181b-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-301a, hsa-mir-378a, hsa-mir-381, hsa-mir-340, hsa-mir-146b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-590, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-378c, hsa-mir-23c, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Cutting edge: microRNA-181 promotes human NK cell development by regulating Notch signaling. [score:3]
The results showed that four additional miRNAs were altered by HHV-6A and 6B infection (Figure 3), as both viruses, although to a different extent, induced a significant decrease (up to 12-fold compared to controls; p ≤ 0.001) of miR-155 and miR-181, which are respectively involved in cytotoxicity and maturation of NK cells, and a concomitant significant increase (up to 14-fold; p ≤ 0.001) in the expression of miR-146 and miR-223, which are associated to NK cell effector functions, including IFNγ and TNFα production. [score:2]
Notably, however, both species significantly decreased miR-155, important in the effector functions of NK cells as it stimulates IFNγ production in activated NK cells (Trotta et al., 2012), and miR-181, essential for the correct maturation of NK cells (Cichocki et al., 2011). [score:1]
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99
[+] score: 6
Table 1. The 30 most enriched miRNAs in human neural progenitorsWe found that members of the miR-181 family and miR-9-5p were highly expressed and considerably enriched in human neural progenitors (Fig.  3C-E), which is in line with other studies (Stappert et al., 2013; Yoo et al., 2011). [score:3]
Table 1. The 30 most enriched miRNAs in human neural progenitors We found that members of the miR-181 family and miR-9-5p were highly expressed and considerably enriched in human neural progenitors (Fig.  3C-E), which is in line with other studies (Stappert et al., 2013; Yoo et al., 2011). [score:3]
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100
[+] score: 6
Host miRNAs were previously shown to directly target viral genomic RNAs; for example, miR-122 facilitates hepatitis C virus replication [44], while miR-130b and miR-181 suppress the porcine reproductive and respiratory syndrome virus (PRRSV) [19, 45]. [score:6]
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