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91 publications mentioning mmu-mir-25

Open access articles that are associated with the species Mus musculus and mention the gene name mir-25. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 227
Taken together, these finding demonstrate that RBM24 inhibits the expression of MALAT1 through upregulation of the expression of miR-25, which directly targets MALAT1 for degradation. [score:13]
To assess whether and how RBM24 expression inhibits MALAT1 expression, we found that MALAT1 expression was significantly increased (Figure 6a), while miR-25 expression was significantly decreased (Figure 6b), in RBM24 -induced cells following the knock down of RBM24 compared with that in the respective control cells. [score:11]
Moreover, we also observed that the increase or decrease in the expression of lncRNA XIST was consistent for the expression of MALAT1 when suppressing or overexpressing miR-25 expression in the 5-8 F and CNE-2 cells (Supplementary Figure S4). [score:11]
As shown in Figures 6d–f, RBM24 overexpression resulted in a significant increase in the miR-25 expression and reduction in the MALAT1 RNA level compared with control vector transfection in 5-8 F and CNE-2 cells, whereas deletion of the RRM of RBM24 abolished the effects of miR-25 upregulation and MALAT1 inhibition. [score:9]
On the basis of our findings, we propose a mo del in which RBM24 plays a role as a tumor suppressor through the upregulation of miR-25, which directly targets MALAT1 for degradation (Figure 7h). [score:9]
Conversely, suppression of endogenous miR-25 expression resulted in significant attenuation of the proliferative inhibitory effect of RBM24 expression. [score:9]
Tet-Off-inducible RBM24-stable cells were transfected with miR-25 mimics or inhibitor to overexpress or suppress miR-25 expression, respectively. [score:9]
RBM24 inhibits MALAT1 expression by upregulating the miR-25 level. [score:8]
RBM24 exerts its inhibitory effects, at least in part, by upregulating the level of miR-25, which in turn targets MALAT1 for degradation in an Ago2 -dependent manner. [score:8]
Taken together, these results suggest that the suppression of tumorigenicity and invasiveness by RBM24 depends, to a certain extent, on upregulation of the level of miR-25, which in turn targets MALAT1 for degradation. [score:8]
Furthermore, we observed that the knockdown of Ago2 expression, which is the only component of the human RNA -induced silencing complex to have slicer activity, [48] blocked the inhibitory effects of miR-25 on MALAT1-regulated processes. [score:7]
In contrast, the miR-25 inhibitor significantly attenuated the inhibitory effects of RBM24 expression on migration and invasion (Figure 4d). [score:7]
49, 50 This evidence also supports our finding that miR-25 downregulates MALAT1 expression in NPC. [score:6]
The observation that miR-25 expression was upregulated after the induction of RBM24 expression prompted us to further investigate the biological function of miR-25. [score:6]
RBM24 upregulates miR-25 expression in NPC cells. [score:6]
Thus, we conducted experiments to confirm that miR-25 can bind to and inhibit the expression of MALAT1 in NPC cells. [score:5]
Notably, the lncRNA MALAT1, an oncogenic lncRNA that is overexpressed in various human cancers, was the most common lncRNA target of miR-25 in all cancers according to the analysis results. [score:5]
As shown in Figure 7g, the RBM24 mRNA level was positively associated with miR-25 expression (P=0.0002, r=0.8026) and negatively associated with MALAT1 expression (P<0.0001, r=−0.8874). [score:5]
To gain insights into the mechanisms underlying the tumor suppressive function of miR-25, we next identified its target genes in NPC. [score:5]
Taken together, these data indicate that miR-25 can be considered a downstream effector molecule for the inhibitory effects of RBM24 expression in NPC cells. [score:4]
Moreover, the silencing of endogenous RBM24 in NPEC1 Bmi-1 cell line resulted in a significant reduction in the miR-25 expression and increase in the MALAT1 expression compared with scramble siRNAs (Figure 6c). [score:4]
To validate the predicted miR-25 -binding sites, luciferase reporter assay was performed, which showed that miR-25 overexpression resulted in a significant decrease in luciferase activity, whereas the opposite effect was observed when this miRNA was inhibited (Figure 5b). [score:4]
Next, we compared miR-25 and MALAT1 expression following transfection of NPC cells with an RBM24 overexpression vector versus a control vector. [score:4]
This increase may have been due to the inhibition of miR-25 function in the RBM24 -induced cells following Ago2 knockdown. [score:4]
These 23 miRNAs were sorted in descending order according to their fold changes, and miR-25 was ranked the highest out of all of the common upregulated genes. [score:4]
Transwell assays revealed that miR-25 overexpression suppressed the migration and invasion abilities of the 5-8 F and CNE-2 Tet-Off-inducible RBM24-stable cells (Figure 4d). [score:4]
[34] Based on these results, we used a miRNA-lncRNA interaction analysis program, starBase v2.0, which employs a database containing a large set of Ago and RBP binding sites derived from all available CLIP-Seq experimental techniques, to screen for potential lncRNAs targeted by miR-25. [score:3]
Altogether, these results suggest that MALAT1 is a target of miR-25. [score:3]
[46] Similarly, an elevated miR-25 level in NPC cells has been associated with the significant inhibition of cell proliferation, migration and invasion. [score:3]
The results showed that 33 lncRNAs were possible targets of miR-25 (Supplementary Table S2). [score:3]
In addition, similar results were obtained from correlation analysis among the expression levels of RBM24, miR-25, and MALAT1 in the primary NPC fresh tumor tissues (Supplementary Figure S5). [score:3]
We also observed a negative association between miR-25 and MALAT1 expression (P=0.005, r=−0.6647). [score:3]
The siRNAs, miR-25 mimic, miR-25 inhibitor and scrambled negative control were purchased from Ribobio Co (Guangzhou, China). [score:3]
[41] Previous reports have demonstrated that miR-25 is overexpressed in a number of cancers, including gastric, lung, liver and ovarian cancers. [score:3]
Next, we investigated whether miR-25 overexpression has suppressive effects on migration and invasion. [score:3]
Further, qRT-PCR analysis of three Tet-Off-inducible RBM24-stable cells showed that the induction of RBM24 expression significantly increased the miR-25 level (Figure 4b). [score:3]
MiR-25 directly targets the lncRNA MALAT1. [score:3]
In contrast, miR-25 inhibitor significantly restored the MALAT1 RNA level in RBM24 -induced cells (Figure 5d). [score:3]
Briefly, pMIR-REPORT-MALAT1 or pMIR-REPORT-MALAT1-mut was cotransfected with miR-25 mimic, inhibitor, or the corresponding negative control into 5-8 F and CNE-2 cells by Lipofectamine -mediated gene transfer. [score:3]
Moreover, mutation of the predicted miR-25 -binding sites abolished this effect (Figure 5b). [score:2]
Furthermore, we found that MALAT1 expression was significantly reduced by transfection with miR-25 mimic compared with negative control miRNA mimic (NC mimic) (Figure 5c). [score:2]
As shown in Figure 4c, CCK8 assay revealed that the ectopic expression of miR-25 slowed the propagation of NPC cells. [score:2]
MiR-25 suppresses the proliferation, migration and invasion of NPC cells. [score:2]
In this study, we searched a database of miRNA-lncRNA interactions using starBase v2.0 [47] and found that miR-25 bound to numerous lncRNAs. [score:1]
Two putative miR-25 binding sites in the MALAT1 RNA were cloned downstream of the cytomegalovirus (CMV) promoter in a pMIR-REPORT vector (Ambion, Carlsbad, CA, USA). [score:1]
Interestingly, a well-known oncogenic lncRNA, MALAT1, was the most common among 33 lncRNAs that were bound by miR-25 in all cancers. [score:1]
Next, we used RNA hybrid programs to identify two putative binding sites for miR-25 in the MALAT1 sequence (NR_002819.2) at positions 640 and 2857 (Figure 5a and Supplementary Figure S3). [score:1]
The final tumor weights and photographs of the isolated tumors are shown in Figures 7e and f. To further investigate the correlations between RBM24, miR-25 and MALAT1 expression in vivo, we performed qRT-PCR to determine the RBM24, miR-25 and MALAT1 RNA levels in the xenografted tumors. [score:1]
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[+] score: 201
The only 7mers that were enriched within the 3′UTRs of these down-regulated genes correspond to words complementary to the miR-25 seed sequence, indicating that the experimental profile can be used to derive lists of genes enriched for direct targets of miR-25 (Fig. 5b). [score:7]
Moreover, through bioinformatics analysis and experimental validation, we identified that miR-25 directly regulated Wwp2, an E3 ubiquitin ligase that targets Oct4 for ubiquitination, and Fbxw7, which is known to regulate c-Myc, Klf5 and other important factors. [score:6]
To identify the direct target genes of miR-25, we introduced either a mimic version of miR-25 or a control miRNA (C. elegans miRNA, cel-miR-239b) (Fig. 5a) into the Dgcr8 -deficient ES cells and generated gene expression profiles using Illumina BeadChip microarrays. [score:6]
We observed that these miR-25 candidate targets were down-regulated in the 25-iPS cells (p value 9×10 [−4] by a Wilcoxon signed-rank test) (Fig. 5 C ). [score:6]
Thus, repression of Fbxw7 induced by over -expression of miR-25 might also contribute to improving reprogramming through upregulation of Klf5. [score:6]
Potential miR-25 target genes were expected to be down-regulated in cells with the miR-25 mimic but not in control cells. [score:6]
NC: negative control using a PB-Neo plasmid with no reprogramming factors; 4F-iPSC: iPSCs reprogramming by expressing OCKS (Dox inducible); 25-iPSC: iPSCs reprogramming by expressing OCKS (Dox inducible) and miR-25. [score:5]
We first used quantitative (real-time) (qRT-PCR) to examine the expression of two selected miR-25 targets, Wwp2 and Fbxw7, as well as the pluripotency markers Oct4 and Nanog in MEF, 4F-iPSCs, 25-iPSCs and mouse ES cells. [score:5]
The iPSCs produced by overexpressing miR-25 together with the four Yamanaka factors were pluripotent stem cells, based on their gene expression profiles, and on their ability to contribute to both the somatic lineages and the germline in chimeras. [score:5]
The expression results were thus consistent with the predictions of Wwp2, and to a certain degree Fbxw7, as the potential targets of miR-25. [score:5]
miR-25 expression was normalized against expression of Sno202 (Applied Biosystems). [score:5]
In order to determine a list of transcripts down-regulated by miR-25 a linear mo del was fitted across a large set of similar experiments prior to the comparison of the relevant samples (Davis et al in preparation); these include arrays considering a transfection time series and the transfection of alternative miRNAs. [score:4]
From this experiment we obtained a list of 72 transcripts, which were down-regulated after transfection of the miR-25 mimic, with a fold change of at least 1.2 and with an estimated false discovery rate less than 10%. [score:4]
The 3′UTR sequences of all the transcripts profiled on the microarrays were sorted starting with the most down-regulated in the miR-25 transfection experiment. [score:4]
We introduced a point mutation into this target site, which would abolish miR-25 binding based on computational prediction. [score:4]
These data thus confirmed Fbxw7 as another direct target of miR-25. [score:4]
In this study, we identified a different set of miR-25 targets in Dgcr8 -deficient mouse ES cells. [score:3]
The wild type 3′ UTR of Wwp2 carries one miR-25 target site. [score:3]
To confirm the effects of miR-25 over -expression on reprogramming, we transfected 1×10 [6] MEFs with PB-TRE-OCKS, PB-CAG-rtTA and PB-CAG-mir25 (Fig. 1a). [score:3]
We found that over -expressing miR-25 or introducing miR-25 mimics enhanced production of iPSCs. [score:3]
Table S4 Candidate target genes of miR-25. [score:3]
While this manuscript was under preparation, miR-25 was shown to directly regulate p53 in tumour cells, and possibly p21 and Tgfβ signalling in MEFs [64], [65]. [score:3]
Validation of wwp2 and fbxw7 as miR-25 targets. [score:3]
We next proceeded to validate the experimentally predicted miR-25 targets. [score:3]
Again expression of miR-25 substantially increased the number of Puro [r] iPSCs (Fig. 2c–d). [score:3]
From this screen, we found that overexpressing miR-25 substantially improved reprogramming, which was confirmed by introducing miR-25 mimics. [score:3]
Identification of potential miR-25 targets. [score:3]
The fold-changes for all genes are indicated by the black curve; the green curve represents the 54 miR-25 targets from Table S4. [score:3]
Of these genes, 54 possessed at least one seed-matching site for miR-25 in their 3′UTR and constitute the initial set of experimentally derived miR-25 targets (Table S4). [score:3]
Validation of miR-25 targets. [score:3]
Identification of miR-25 targets. [score:3]
The table lists 54 genes based on microarray expression and Sylamer analysis following transfection of miR-25 mimic to the Dgcr8 -deficient ES cells. [score:3]
We identified a number of miR-25 candidate gene targets. [score:3]
d. Luciferase reporter assays for validating Wwp2 and Fbxw7 as direct targets of miR-25. [score:3]
Once the miR-25 binding target site was mutated, the repressing effect of the miR-25 mimic was lost (Fig. 6d). [score:3]
b. qPCR analysis of the mature form of miR-25 expression. [score:3]
The x-axis represents the 3′UTR sequences of all transcripts, sorted from the most down-regulated after miR-25 transfection compared to the cel-miR-239b transfection. [score:3]
Candidate target genes of miR-25. [score:3]
To test if these targets are being actively repressed by miR-25 in our iPSCs, we compared the 25-iPS microarray samples against the 4F-iPS samples. [score:2]
Given the conservation of miR-25 mature sequence during evolution and its role in regulating pluripotency genes, it will be interesting to determine whether its role is conserved in reprogramming human cells. [score:2]
Further experiments designed to elucidate the contribution of miR-25 to this process combining computational prediction and experimental analysis using Dgcr8 -deficient ES cells, demonstrated that miR-25 regulates a number of genes in mouse ES cells. [score:2]
We chose Wwp2 and Fbxw7 for further analysis and confirmed that miR-25 directly regulated Wwp2 and Fbxw7 in the luciferase reporter assay. [score:2]
To demonstrate that miR-25 directly regulates Wwp2 and Fbxw7, we performed the luciferase reporter assay based on pmirGLO Dual-Luciferase system where the full-length 3′ UTR of either Wwp2 or Fbxw7 was inserted into the 3′ side of the firefly luciferase gene (luc2) (Fig. 6b–c). [score:2]
These results thus confirmed the critical role of the miR-25 binding site in regulating the luciferase activity in the reporter plasmid and thus Wwp2. [score:2]
However, compared to MEFs and 4F-iPSCs, 25-iPSCs expressed higher levels of miR-25 (Fig. 2b). [score:2]
These results thus reveal a mechanism for miR-25 to regulate pluripotency genes and provide new information for efficient reprogramming. [score:2]
240 pmoles of miRNA control mimic (miRIDIAN Negative Control #2 (Dharmacon CN-002000-01-05) or miRIDIAN mmu-miR-25 mimic (Dharmacon C-310564-01-0005)) were added to 240 µl OptiMEM I (Gibco). [score:1]
Other miR-25 targets identified in this study still remain to be characterised for their role in reprogramming. [score:1]
We therefore chose initially to further characterize miR-25 since it was found to be expressed in ES cells (Fig. 2b), and its mature sequence is conserved across all vertebrate genomes examined (Table S3). [score:1]
Mimic: Transfection used a miR-25 mimic instead of the PB-CAG-mir25. [score:1]
The reporter plasmids carrying either the wild type or the mutant 3′ UTR of Wwp2 were co -transfected with the miR-25 mimics or the negative control mimics into HeLa S3 cells. [score:1]
To further examine the specific effect of miR-25 on reprogramming, we repeated the above reprogramming experiments using a miR-25 mimic instead of the genomic DNA containing miR-25. [score:1]
Four out of the 52 tested miRNAs or miRNA clusters: the miR-302 cluster, miR-25, miR-290 and miR-298, gave substantially more Puro [r] iPSC colonies (2–4 fold) than the control where only the four factors were used (PB-CAG-OCKS) (Fig. 2a). [score:1]
0040938.g005 Figure 5. a. Timeline of miR-25 mimic transfection into the Dgcr8 -deficient ES cells for discovering transcripts that were repressed by miR-25. [score:1]
The 3′ UTR of Wwp2 has one miR-25 binding site, whereas Fbxw7 has two. [score:1]
a. Timeline of miR-25 mimic transfection into the Dgcr8 -deficient ES cells for discovering transcripts that were repressed by miR-25. [score:1]
However, the miR-25 mimic significantly repressed luciferase activity from the wild type reporter plasmid (Fig. 6d). [score:1]
Adding miR-25 mimic increased AP [+] colony number similar to using PB-CAG-mir-25/93 (Fig. 2C) a. Schematic diagrams of the PB transposon constructs. [score:1]
Our results, together with the other studies, show that, miR-25 promotes reprogramming by several mechanisms and possibly at distinct reprogramming stages. [score:1]
a. Four microRNAs: miR302 (cluster), miR-25/93, miR-290 and miR-298 were able to improve reprogramming. [score:1]
Wwp2, an E3 ubiquitin ligase, promotes Oct4 degradation by ubiquitination in both mouse and human ES cells [55], [56], thus suggesting a potential mechanism for improving reprogramming efficiency by miR-25. [score:1]
We used Sylamer to further characterise the effect of miR-25 expression [54]. [score:1]
The other two miRNAs identified in this screen, miR-25 and miR-298, were not previously reported for their role in ES cells or in reprogramming when the project started. [score:1]
The wild type and mutated miR-25 binding sites (highlighted in red) were indicated. [score:1]
Again, we co -transfected the reporter plasmids with the miR-25 mimics and the negative control mimic into HeLa S3 cells. [score:1]
iPSCs produced from using either the 4 Yamanaka factors (4F-iPSC) or 4F plus miR-25 (25-iPSC) proliferated well in the 2i medium. [score:1]
Two candidates, miR-25 and miR-298, were found to substantially improve reprogramming with the four Yamanaka factors. [score:1]
We focused on characterizing miR-25 in this study as miR-25 had a strong phenotype in promoting reprogramming, is highly conserved during evolution and is expressed in ES cells. [score:1]
d. A primary iPSC colony reprogrammed with the four Yamanaka factors and miR-25. [score:1]
Sylamer [54] was used to count the number of miRNA seed sequences associated with miR-25 in the 3′UTR of the annotated transcripts. [score:1]
MEF cells were transfected with 2.0 µg of PB-CAG-OCKS plasmid, together with 16 nM of miRNA-25 mimic (Dharmacon) using the Amaxa transfection device. [score:1]
Adding miR-25 mimic increased AP [+] colony number similar to using PB-CAG-mir-25/93 (Fig. 2C) Dox induced iPSCs of both 4F-iPSC and 25-iPSC were expanded for over 20 passages in the 2i medium without Dox. [score:1]
A miR-25 mimic (Dharmacon) was added at a concentration of 20 nM. [score:1]
The negative control mimic did not show any effect on the reporter activity, whereas the miRNA-25 mimics caused significant repression on the luciferase activity from the wild type reporter but not the mutated reporter (Fig. 6d). [score:1]
The miR-25 genomic DNA cloned in the PB also contains miR-93 (Table S2). [score:1]
At 3, 6 and 9 days post initial transfection, these cells were transiently transfected with 16 nM of miRNA-25 mimic (Dharmacon) with Lipofectamin 2000 (Invitrogen) according to manufacture's instructions. [score:1]
Transfection of the miR-25 mimics in reprogramming. [score:1]
Words matching the mmu-miR-25 and cel-miR-293b seeds are highlighted. [score:1]
Characterization of iPSCs produced by over -expressing miR-25. [score:1]
The 3′ UTR of Fbxw7 has two miR-25 binding sites. [score:1]
Table S3 Conservation of miR-25 and miR-298 mature sequences. [score:1]
0040938.g002 Figure 2 a. Four microRNAs: miR302 (cluster), miR-25/93, miR-290 and miR-298 were able to improve reprogramming. [score:1]
All mature sequences of miR-25 and miR-298 are obtained from miRBase database. [score:1]
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[+] score: 178
To examine miR-25 targets through multiple bioinformatics approaches, we first used the TargetScan program [68] to predict the conserved mRNA targets of miR-25 (~600 targets) and then used the gene classification programs PANTHER [69, 70] (Figure 6A) or GSEA [71] (Figure 6B) to associate biological processes and gene sets with these targets. [score:11]
However, FoxO3 -null NSPCs did not display decreased expression of the mature forms of miR-106b, miR-93, and miR-25, suggesting that FoxO3 does not directly upregulate miR-106b~25 and might even indirectly repress the expression of this cluster. [score:10]
Two signaling pathways in particular stood out from this target analysis: transforming growth factor β (TGFβ)/bone morphogenic protein (BMP) signaling, which was enriched for miR-25 targets in all three bioinformatics approaches, and insulin/IGF signaling, which was enriched for miR-25 targets in the TargetScan-PANTHER analysis (Figure 6D). [score:9]
Figure 6. (A) The PANTHER gene classification program was used to analyze TargetScan-predicted conserved targets for mouse miR-25 (~600 targets total). [score:7]
Given that PTEN can be a major inhibitor of insulin/IGF signaling [99, 100] and is a known target of miR-25 in prostate cancer cells [101], miR-25 may target PTEN to increase insulin/IGF signaling and repress FoxO activity. [score:7]
We found that miR-25 knockdown decreases NSPC proliferation, miR-25 or miR-106b~25 overexpression increases adult NSPC proliferation, and miR-106b~25 overexpression promotes neuronal differentiation. [score:6]
Knockdown of miR-106b or miR-93, which shares the same mRNA -targeting seed sequence, did not affect proliferation, while knockdown of miR-25, which has a different seed sequence, reduced proliferation. [score:5]
While inhibitory Smads (Smad6 and Smad7) are also predicted miR-25 targets, Smad7 -deficient mice have increased adult NSPC proliferation and numbers, which may be due to TGFβ-independent mechanisms [98]. [score:5]
Figure 3. NSPCs were infected with an empty control retrovirus (expressing a GFP marker only) or a retrovirus expressing miR-25. [score:5]
NSPCs were infected with an empty control retrovirus (expressing a GFP marker only) or a retrovirus expressing miR-106b, miR-93, and miR-25 simultaneously (miR-106b~25). [score:5]
Figure 4. NSPCs were infected with an empty control retrovirus (expressing a GFP marker only) or a retrovirus expressing miR-106b, miR-93, and miR-25 simultaneously (miR-106b~25). [score:5]
The effects of miR-106b~25 on adult NSPC proliferation are modest: miR-106b~25 or miR-25 overexpression increased NSPC proliferation by about 1.2-fold, miR-25 knockdown reduced proliferation by about 1.4-fold, and individual miR-106b and miR-93 knockdowns did not affect NSPC proliferation. [score:5]
NSPCs were infected with an empty control retrovirus (expressing a GFP marker only) or a retrovirus expressing miR-25. [score:5]
The net functional effect of miR-25 regulation of TGFβ signaling in NSPCs will depend on the relative expression, degree of miR-25 repression, and network connections of each member of the TGFβ pathway in NSPCs. [score:4]
Knocking down miR-25 decreases NSPC proliferation, and ectopically expressing miR-25 or the entire miR-106b~25 cluster increases proliferation. [score:4]
In a parallel approach, we used the DIANA-miRPath program [72] to predict miR-25 targets (~150) with the DIANA-microT-3.0-Strict algorithm [73] followed by comparison with the Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathways [74] (Figure 6C). [score:3]
miR-25 has a number of predicted targets in the TGFβ and insulin/IGF-FoxO pathways. [score:3]
To test if miR-25 could promote proliferation in adult NSPCs, we ectopically expressed miR-25 in NSPCs using a retroviral vector containing the miR-25 precursor and green fluorescent protein (GFP). [score:3]
Analyzing candidate targets of miR-25 revealed that miR-25 might modulate TGFβ or insulin/IGF signaling at multiple points in each pathway. [score:3]
We examined the expression levels of the miR-106b~25 cluster members (miR-106b, miR-93, and miR-25; Figure 1A) in self-renewing or differentiating NSPCs isolated from young adult (3 month-old) mice. [score:3]
miR-106b, miR-93, and miR-25 are expressed in adult NSPC cultures. [score:3]
gr/pathways/) using DIANA-microT-3.0-Strict was used to predict and analyze conserved targets for mouse miR-25 in the KEGG database. [score:3]
Expression of miR-25 enhances adult NSPC proliferation. [score:3]
The observation that the insulin/IGF-FoxO pathway is enriched for miR-25 targets is especially pertinent because the genomic locus of miR-106b~25 contains a conserved FoxO binding sequence (Figure 7A). [score:3]
To inhibit miR-106b~25, we transfected NSPCs with locked nucleic acid (LNA) -modified oligonucleotides antisense to miR-106b, miR-93, or miR-25, or with a scrambled control LNA oligonucleotide. [score:3]
TGFβ signaling has been shown to inhibit adult NSC proliferation and neurogenesis [78, 79], suggesting that miR-25 might promote NSC proliferation and neuronal differentiation by repressing TGFβ signaling. [score:3]
We found that miR-25 knockdown decreased EdU incorporation in NSPCs by 45% (p=0.005), whereas miR-106b or miR-93 knockdown did not significantly affect EdU incorporation in NSPCs (Figure 2). [score:3]
We found that miR-106b, miR-93, and miR-25 were all expressed in self-renewing NSPCs. [score:3]
We verified by that miR-25 was overexpressed, on average by 8-fold, in NSPCs after miR-25 retrovirus infection (Figure 3A). [score:3]
miR-25 targets genes involved in TGFβ and insulin/IGF signaling. [score:3]
We find that potential miR-25 target mRNAs are overrepresented in insulin/IGF signaling. [score:3]
Within the miR-17 family, members of the miR-106b~25 cluster (miR-106b, miR-93, and miR-25) appear to be the most strongly expressed in the adult brain [27, 52]. [score:3]
There may even be crosstalk between the different pathways targeted by miR-25. [score:3]
A number of interesting molecular networks were enriched for miR-25 targets, including p53 signaling, hypoxia signaling, and nitric oxide signaling, which are all important for NSC maintenance and activity [75- 77]. [score:3]
org, version 5.1) was used to predict all conserved targets for mouse miR-25. [score:3]
Ectopic expression of miR-25 promotes proliferation in adult NSPCs. [score:3]
We cannot exclude the possibility, however, that miR-25 negatively regulates insulin/IGF signaling under some circum-stances, such as by repressing Akt or PI3K. [score:2]
We found that ectopic miR-25 expression increased NSPC incorporation of EdU by 18% compared to the GFP-only control (p=0.04; Figure 3B,C). [score:2]
Figure 2. NSPCs were transfected to knock down miR-106b, miR-93, or miR-25 or were transfected with a scrambled control oligonucleotide. [score:2]
NSPCs were transfected to knock down miR-106b, miR-93, or miR-25 or were transfected with a scrambled control oligonucleotide. [score:2]
Thus, it is possible that miR-25 regulate NSPCs by coordinately modulating insulin/IGF and TGFβ networks. [score:2]
Potential signaling pathways regulated by miR-25. [score:2]
For miRNA overexpression, the 725-bp segment of the mouse Mcm7 gene containing the miR-106b, miR-93, and miR-25 precursors was cloned between the XhoI and PmeI sites of the MDH1-PGK-GFP 2.0 vector [105] using the primers F: 5' -AAACTCGAGCCTGCTGGCCATTCTCCGACTTTC C-3' and R: 5' -AAAGTTTAAACGGATCTTTCTTTGCTCCAGCTTCAAGC-3'. [score:2]
Thus, another way miR-25 might increase NSPC proliferation is by de-repressing insulin/IGF signaling. [score:1]
We next sought to identify the molecular networks involving miR-25, the main miR-106b~25 member controlling NSPC proliferation. [score:1]
miR-25 is important for adult NSPC proliferation. [score:1]
miR-25 is necessary for adult NSPC prolifer-ation. [score:1]
Thus, FoxO3 might transcriptionally activate miR-106b~25/Mcm7, but act to repress miR-106b, miR-93, and miR-25 at a different promoter or at posttranscriptional steps like precursor cleavage, nuclear export, base editing, and degradation. [score:1]
Taken together, these results suggest that modulation of the TGFβ and insulin/IGF signaling pathways may mediate part of the effects of miR-25 in NSPCs. [score:1]
These results indicate that within the miR-106b~25 cluster, miR-25 is the most important for NSPC proliferation. [score:1]
The miR-17 family consists of three paralogous polycistronic clusters on different chromosomes: miR-17~92 (miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1), miR-106b~25 (miR-106b, miR-93, and miR-25), and miR-106a~363 (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2, and miR-363). [score:1]
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[+] score: 159
These results suggest that initial step of miRNA processing may be inhibited by diabetic conditions because, although primary miR-25 expression is upregulated, precursor and mature miR-25 expressions are downregulated in mesangial cells under diabetic milieu in vivo and in vitro. [score:13]
Nox4 mRNA and primary miR-25 expression levels are upregulated, while Siah1 expression as well as precursor and mature miR-25 expression levels are downregulated in glomeruli from diabetic mice. [score:13]
Primary miR-25 expression is upregulated, while precursor and mature miR-25 expressions are downregulated in HG and TGF-β treated MMCs. [score:11]
Consequently, NOX4, a target of miR-25 and an inducer of oxidative stress, can be upregulated due to downregulation of miR-25. [score:9]
In this study, we showed for the first time that miR-25 expression can be downregulated under diabetic conditions due to the inhibition of the first step of miR-25 processing by p-MeCP2. [score:8]
Among these miRNAs and also decreased miRNAs identified by small RNA sequencing in glomeruli from STZ diabetic mice 22, we confirmed that miR-25 and miR-93 expressions were significantly downregulated in TGF-β treated mouse mesangial cells (MMCs), but the expression of only miR-25 was consistently and significantly decreased even in HG -treated MMCs relative to control. [score:8]
The expression of primary miR-25 was significantly upregulated in the glomeruli of diabetic mice compared with that in the control (Fig. 2E), whereas precursor and mature miR-25 levels were significantly downregulated in the diabetic mice compared to control (Fig. 2F and G). [score:7]
Uncropped scans are presented in Supplementary Fig. 3. Abbreviations; NTC, nontargeting control siRNA; HIPK2, homeo-domain interacting protein kinase 2; MeCP2, methyl-CpG binding protein 2; NOX4, NADPH oxidase 4; SIAH1, seven in absentia homolog 1; p-MeCP2, phosphorylated methyl-CpG binding protein 2; t-MeCP2, total methyl-CpG binding protein 2. The expression of primary miR-25 was significantly increased, but expressions of precursor and mature miR-25 were significantly decreased after HG (A to C) and 24 hr TGF-β treatment (D to F) in NTC transfected MMCs. [score:7]
Increased primary miR-25 expression, but decreased precursor and mature miR-25 expression levels are attenuated by knockdown of Hipk2 in HG and TGF-β treated MMCs. [score:6]
In summary, these data demonstrate that MeCP2 regulated by HIPK2 stabilized by decreases in SIAH1 under diabetic conditions plays an important role in suppressing miR-25 processing and expression. [score:6]
Importantly, since NOX4 is a direct target of miR-25 37, the resultant decreases in miR-25 can lead to enhance NOX4 expression (and related oxidative stress) as seen in diabetes. [score:6]
As a consequence, NOX4, a target of miR-25, can be upregulated and this leads to oxidant stress associated with the pathology of DN (Fig. 8G). [score:6]
Increased primary miR-25 expression, but decreased precursor and mature miR-25 expression levels are also attenuated by knockdown of HIPK2 even in HG and TGF-β treated MMCs. [score:6]
The primary miR-25 was significantly upregulated, but expressions of precursor and mature miR-25 were significantly decreased after HG and 24 hr TGF-β treatment in NTC transfected MMCs. [score:6]
Primary miR-25 expression is increased, while precursor and mature miR-25 expressions are decreased in diabetic conditions. [score:5]
Primary miR-25 expression is increased, while precursor and mature miR-25 expressions are decreased in HG and TGF-β treated MMCs. [score:5]
All data were expressed as means ± S. E. How to cite this article: Oh, H. J. et al. Inhibition of the processing of miR-25 by HIPK2-Phosphorylated-MeCP2 induces NOX4 in early diabetic nephropathy. [score:5]
Our results revealed associations between SIAH1, HIPK2 and p-MeCP2 levels and processing of miRNAs, such as miR-25 which are downregulated by factors related to DN. [score:4]
Since we previously showed that let-7 family (lin28 -mediated) 35 and miR-130b 44 were downregulated under diabetic conditions by mechanisms not involving p-MeCP2, we focused on miR-25 in this study. [score:4]
The expression levels of primary miR-25 were significantly increased in the HG and 24 hr TGF-β treated MMCs compared with those in the control, while the expressions of precursor and mature miR-25 were significantly decreased in the treated group compared to the control (Fig. 5A to F). [score:3]
The expression of primary miR-25 was significantly increased in the glomeruli of diabetic mice compared with that in control mice (E), whereas precursor and mature miR-25 expressions were significantly decreased in the diabetic mice compared to control (F and G). [score:3]
NOX4 is one of the most relevant targets of miR-25 that is related to DN pathology. [score:3]
We also observed that the expression levels of mature and precursor miR-25 were decreased, but primary miR-25 levels were increased in vivo in the diabetic mice. [score:3]
Based on these findings, a schematic mo del for miR-25 processing and NOX4 expression in the early stage of DN is depicted in Fig. 8G. [score:3]
Conversely, knockdown of Hipk2 can prevent the induction of NOX4 by restoring miR-25 processing and mature miR-25 levels. [score:2]
Next, we investigated the effect of siRNA mediated knockdown of Hipk2 on MeCP2 phosphorylation, miR-25 processing, and NOX4 expression. [score:2]
Uncropped scans are presented in Supplementary Fig. 2. Abbreviations; MeCP2, methyl-CpG binding protein 2; HIPK2, homeo-domain interacting protein kinase 2; NOX4, NADPH oxidase 4; SIAH1, seven in absentia homolog 1; p-MeCP2, phosphorylated methyl-CpG binding protein 2; t-MeCP2, total methyl-CpG binding protein 2. Levels of primary miR-25 were significantly increased in the HG and 24 hr TGF-β treated MMCs compared to respective controls (A and D), while the expressions of precursor and mature miR-25 were significantly decreased in the treated group compared to the respective controls (B and C, E and F). [score:1]
Our studies do not fully address the functional in vivo role of this pathway from SIAH1 to miR-25 and NOX4 via HIPK2 and p-MeCP2. [score:1]
These results suggest that MeCP2 phosphorylated by HIPK2 stabilized under diabetic conditions can block the first step of miR-25 processing and thus reduce the levels of precursor and mature miR-25. [score:1]
These data further substantiate the role of HIPK2 as a critical kinase of MeCP2 as reported 33 and that increased p-MeCP2 mediated by HIPK2 stabilized under the diabetic conditions can block miR-25 processing from the primary to precursor conversion steps. [score:1]
Alterations in processing of miRNAs such as miR-25 by p-MeCP2 could be one such mechanism. [score:1]
[1 to 20 of 31 sentences]
5
[+] score: 149
Other miRNAs from this paper: hsa-mir-25, hsa-mir-451a, mmu-mir-451a, hsa-mir-451b, mmu-mir-451b
Further, downregulation of microRNA-25-5p (“miR-25-5p”), a PKCζ -targeting miRNA [24], could be the cause of PKCζ upregulation in CRC cells. [score:9]
We here showed that expression of miR-25-5p inhibited CRC cell proliferation possibly via downregulating PKCζ. [score:8]
In the current study, we showed that miR-25-5p, an anti-PKCζ miRNA [24], was downregulated in human colon cancer tissues and CRC cells, which could be the cause of PKCζ upregulation. [score:7]
miR-25-5p downregulation could therefore be the cause of PKCζ upregulation. [score:7]
On the other hand, PKCζ silence, by targeted-shRNA or miR-25-5p expression, activates AMPK and inhibits HT-29 cell proliferation. [score:7]
Notably, PKCζ mRNA upregulation and miR-25-5p downregulation were also noticed in other established CRC cell lines, including HCT-116, Lovo, SW403 and SW48 (Supplementary Figure 1). [score:7]
HT-29 xenograft growth in SCID mice is inhibited after expressing or miR-25-5p. [score:5]
HT-29 xenograft growth in mice is inhibited after expressing or miR-25-5p. [score:5]
Remarkably, forced exogenous expression of miR-25-5p silenced PKCζ, activated AMPK and inhibited HT-29 cell proliferation. [score:5]
Exogenous expression of miR-25-5p silences PKCζ and inhibits HT-29 cell proliferation. [score:5]
More importantly, in vivo growth of HT-29 xenografts was largely suppressed after expressing miR-25-5p. [score:5]
Weekly tumor growth curve result in Figure 4A demonstrated that the in vivo growth of HT-29 xenografts was significantly inhibited after expressing the or miR-25-5p. [score:5]
As demonstrated, miR-25-5p level was dramatically downregulated in colon cancer tissues (Figure 1C), and its level was relatively high in the surrounding normal tissues (Figure 1C). [score:4]
These results indicate that PKCζ could be the direct and primary target of miR-25-5p in HT-29 cells. [score:4]
Meanwhile, downregulation of PCNA (a proliferation marker) and induction of cleaved-PARP (an apoptosis marker) were observed in tumor tissues with or miR-25-5p (Figure 4C) Therefore, the in vivo signaling changes were in line with the in vitro findings. [score:4]
It is certainly possible that other targets of miR-25-5p could also be involved in above actions. [score:3]
To support this hypothesis, the pre-miR-25 -expressing vector (“miR-25-Vec”, a gift from Dr. [score:3]
For instance, several potential miR-25’s targeted genes have been identified thus far in cancer cells, including the apoptosis protein Bim [48] and mitochondrial calcium uniporter [49]. [score:3]
miR-25-5p -mediated silence of PKCζ, on the other hand, resulted in LKB1 activation and sustained/intensified AMPK activation, which should inhibit CRC cell proliferation. [score:3]
Forced miR-25 expression. [score:3]
In line with previous findings [24], expression of miR-25-5p was significantly elevated in the two lines (Figure 3A). [score:3]
Expressions of above signaling proteins and miR-25-5p were also examined in human CRC cancer cells. [score:3]
The pSuper-neo pre-miR-25 expression vector (“miR-25-Vec”) was provided by Dr. [score:3]
Via selection, two stable HT-29 cell lines expressing miR-25-Vec were established, named as “miR-25-Vec-L1” and “miR-25-Vec-L2”. [score:3]
Exogenous expression of miR-25-5p led to a dramatic reduction of PKCζ mRNA UTR luciferase activity (Figure 3B). [score:3]
We thus tested miR-25-5p expression in above human tissues. [score:3]
Expressions of listed genes and miR-25-5p in fresh tissue lysates were examined. [score:3]
miR-25-5p is a recently-indentified PKCζ -targeting miRNA [24], its level was negatively correlated with PKCζ level in human colon cancer tissues and CRC cells (Figure 1). [score:3]
Collectively, we confirmed, which was correlated with AMPK inhibition, mTORC1 activation and miR-25-5p depletion. [score:3]
Further studies will be needed to identify possible other targets of miR-25-5p in CRC cells. [score:3]
Mature miR-25-5p expression in the stable cells was always tested by the qRT-PCR assay (Method was descried early [50]). [score:2]
Stable HT-29 cells, expressing pre-miR-25 -expressing vector (“miR-25-Vec”, “L1/L2”) or empty vector (“Vec”), as well as the parental control HT-29 cells (“Par”) were subjected to qRT-PCR (A and C) assay, PKCζ mRNA UTR luciferase activity assay (B) and (D); proliferation of above cells was tested by viable cell counting assay (E) and BrdU ELISA assay (F). [score:1]
miR-25-5p level was also decreased in the CRC cells (Figure 1F). [score:1]
The potential effect of or miR-25-5p on CRC cell growth in vivo was tested next. [score:1]
miR-25-3p level was not changed in these cells (Data not shown), suggesting that miR-25-5p could be the primary product of the vector (reported in [24]). [score:1]
A very recent study by Fan et al., has characterized a PKCζ -targeting miRNA, miR-25-5p [24]. [score:1]
The UTR reporter vector that contains the 3′-UTR of PKCζ carrying the miR-25-5p site was provided again by Dr. [score:1]
Figure 3Stable HT-29 cells, expressing pre-miR-25 -expressing vector (“miR-25-Vec”, “L1/L2”) or empty vector (“Vec”), as well as the parental control HT-29 cells (“Par”) were subjected to qRT-PCR (A and C) assay, PKCζ mRNA UTR luciferase activity assay (B) and (D); proliferation of above cells was tested by viable cell counting assay (E) and BrdU ELISA assay (F). [score:1]
Expressions of protein kinase C ζ (PKCζ) mRNA (A and D, qRT-PCR assay), listed proteins (B and E,) and microRNA-25-5p (“miR-25-5p”, C and F, qRT-PCR assay) in fresh human colon cancer tissues (“Tum”, N=10) and surrounding normal colon tissues (“Nor”), as well as in the FHC colon epithelial cells (“Epi”) and human CRC cells (HT-29 and DLD-1) were shown. [score:1]
TaqMan microRNA assay system was applied to detect miR-25-5p expression using the described primer [53]. [score:1]
Figure 4Same amount (five million cells per mouse) of HT-29 cells, bearing (1#) or miR-25-5p (“L1”) as well as the parental control HT-29 cells (“Par”) were inoculated s. c. to the SCID mice. [score:1]
These results imply that miR-25-5p could be an anti-cancer miRNA in CRC cells. [score:1]
The construct was then co -transfected with miR-25 vector into HT-29 cells. [score:1]
Same amount of HT-29 cells, bearing (“1#”, see Figure 2), miR-25-5p (“L1”, see Figure 3) or the parental control HT-29 cells (“Par”, or control tumors) were inoculated to the SCID mice via s. c. injection. [score:1]
Figure 1Expressions of protein kinase C ζ (PKCζ) mRNA (A and D, qRT-PCR assay), listed proteins (B and E,) and microRNA-25-5p (“miR-25-5p”, C and F, qRT-PCR assay) in fresh human colon cancer tissues (“Tum”, N=10) and surrounding normal colon tissues (“Nor”), as well as in the FHC colon epithelial cells (“Epi”) and human CRC cells (HT-29 and DLD-1) were shown. [score:1]
Same amount (five million cells per mouse) of HT-29 cells, bearing (1#) or miR-25-5p (“L1”) as well as the parental control HT-29 cells (“Par”) were inoculated s. c. to the SCID mice. [score:1]
[1 to 20 of 46 sentences]
6
[+] score: 120
Upstream inhibitors like miR-1 besides downstream inhibitors like miR-25 thus show interesting properties for anti-cancer treatments in Wnt -dependent cancers and further support current findings that upstream components of the Wnt pathway are also valid and rational targets for cancer-therapies, even in cells with downstream mutations [15], [54], [55]. [score:8]
Curiously the effect of hsa-miR-25 on β-catenin seems to be more effective under conditions of high pathway and low destruction complex activity, when translational differences preponderate and come into play due to strongly reduced post-translational regulation of β-cat. [score:6]
Deregulated miR expression profiles might also contribute to oncogenesis by repressing the tumor suppressors, p21/p53 (miR-25 [42], [43], miR-504 [44]) which in turn might affect Wnt signaling. [score:6]
Analyses of miR-25 function in the regulation of the Wnt pathway suggests a potential function in the translational inhibition of β-catenin via its binding to the β-catenin coding sequence and not its 3′-UTR. [score:6]
Additionally, expression of Pri-miR-25 in SW480 colon cancer cells, that exhibit high Wnt/β-catenin activity due to an APC truncation, significantly inhibited both the STF Wnt-reporter activity by ∼40% (Fig. 3D) and β-catenin protein levels by 20% (Fig. 3C). [score:5]
Intriguingly, miR-32, that inherits the same seed as miR-25 also targets Pcaf [52] but instead, upregulates the Wnt-reporter in our reporter assays (Fig. S4). [score:5]
Recent evidence also suggests that miR-25 may inhibit Wnt/β-catenin dependent cancer viability by targeting Pcaf [52] which binds, acetylates, stabilizes and activates β-cat [53], thereby corroborating our observation that the influence of miR-25 is likely at the level of β-cat. [score:5]
Epistasis experiments revealed that miR-1 and miR-613 target the pathway upstream of Axin or active β-catenin, and that miR-25 acts downstream, at the level of β-cat, likely by targeting β-cat's coding sequence. [score:5]
Importantly, overexpression of miR-25 and miR-1 inhibited proliferation/viability of human colon cancer cells that are known to be dependent on sustained β-cat signaling for their survival [22], [24]. [score:5]
All miRs down-regulated Wnt3a-CM and LiCl induced Wnt pathway activity, while only Pre-miR-25 was able to repress Axin1+2-siRNAs or β-catenin-S37A induced activity. [score:4]
These observations suggest that the coding sequence of β-catenin itself may be the primary and direct target of miR-25. [score:4]
To test whether miR-25 could directly target the β-catenin cDNA, a fragment of the β-catenin coding sequence (CDS) containing the potential miR-25 binding sites was cloned into the psi-check-2 reporter. [score:4]
Elevated reporter activity by simultaneous siRNA mediated knockdown of Axin1 and Axin2 could be strongly inhibited by transfection of Pre-miR-25 (P<0.05; unpaired t-test), while miR-1 and miR-613 showed no significant influences (P>0.05). [score:4]
As experiments revealed no significant change in β-catenin transcript levels for all three miRs (Fig. S7), one remaining possibility is that miR-25 represses translation of β-catenin but not its transcript level. [score:3]
A downstream role of miR-25 is also in agreement with a Drosophila miR-25/92 evolutionarily related cluster (Fig. S2) that can target the Wnt/Wg pathway (Pancratov and DasGupta, unpublished data). [score:3]
Secondary validation and functional testing of 3 candidate miRs, namely miR-1, miR-25 and miR-613 confirmed their inhibitory effect on the activity of the Wnt pathway. [score:3]
The coding region of human β-catenin (S37A mutant; transcript nt position 307–1874 NcoI-Klenow; NotI) was subcloned into the 3′UTR of the Renilla gene (NotI, SpeI-Klenow) within a psi-check-2 reporter vector with modified MCS to monitor the influence of miR-25 on its transcript stability and translation. [score:3]
Notably, not only synthetic Pre-miR-25 but also over -expression of Pri-miR-25 could reduce a normalized Renilla gene activity with the β-catenin-CDS-fragment-3′UTR but to a lesser degree. [score:3]
Intriguingly the most stringent RNAhybrid predictions that allow non-canonical seed sequences indicated some potential binding sites of miR-25 in the β-catenin cDNA (Fig. S5), while other target prediction algorithms (PicTar, EMBL-Microcosm, etc. ) [score:3]
While miR-1 and miR-613 could slightly reduce Wnt3a-CM mediated induction of β-catenin protein levels in HEK293 cells, miR-25 and miR-613 expression resulted in a moderate (∼20%) reduction in LiCl induced total β-catenin protein level, (Fig. 3B). [score:3]
Expression of miR-25 repressed the psi-check2 sensor containing the miR-25 binding site, and moderately reduced β-catenin protein levels, while β-catenin transcript levels remained unchanged. [score:3]
This was particularly evident in HT-29 cells where despite several attempts we could not generate HT29-pcDNA3.1(-)-hsa-miR-25 expressing stable cell lines, although a few pcDNA3.1(-) empty vector transfected clones survived the selection procedure (Fig. 3F). [score:3]
Additionally, only miR-25 inhibited the activity of degradation-resistant S37A β-catenin mutant on the STF reporter (Fig. 3 A). [score:3]
Taken together, these data suggest that miR-25 represses the Wnt pathway downstream of GSK3β, Axin1/2 and stabilized β-catenin, while miR-1 and miR-613 act upstream of Axin1/2 and stabilized β-catenin but probably downstream of LiCl -mediated inhibition of GSK3β. [score:3]
Relative amount of cells obtained after the selection procedure to establish HCT116, SW480, and HT29 colorectal cancer cell lines expressing Pri-miR-25-pcDNA3.1(-)-Neomycin compared to empty vector control cells. [score:2]
Upon transfection of colon cancer cells (HCT116, HT29, SW480) with Pri-miR-25 expressing vector, the number of Pri-miR-25 stable cell-colonies was markedly reduced compared to empty vector controls (Fig. 3F). [score:2]
HPLC grade human synthetic Pre-miR™ precursor miRNAs that are strand-selection optimized/approved and chemically modified siRNA-like precursor miRs (Pre-miR-1™ #AM17100; Pre-miR-25™ #AM17100; Pre-miR-613™ #AM17100) were purchased from Ambion. [score:1]
3 out of 38 candidate miRs (miR-1, miR-25, miR-613) were further characterized in Wnt-responsive cultured cells and all were validated for their Wnt -inhibitory properties identified in the initial screen. [score:1]
Pre-mir-1 may function most upstream, followed by miR-613 and then miR-25, which seems to influence the most downstream activity at the level of β-catenin. [score:1]
Renilla gene activity with an inserted β-catenin CDS in the 3′UTR indicated a significant miR-25 -dependent reduction while control siRNAs, miR-1 or miR-613 had no effect (Fig. 3E). [score:1]
Phylogenetic analysis support the miR-base classification that miR-1 belongs to the miR-1/206 family including hsa-miR-206 and the Drosophila dme-miR-1, an indication of the high evolutionary conservation of this family (shown in Supplementary, Fig. S2A by alignments and phylogenetic quartette puzzling trees); hsa-miR-25 belongs to the evolutionary conserved miR-25/92 family [39] including Drosophila miR-92a+b/310/311/312/313, shown in Fig. S2B, and shares only the seed sequence with other miRs like miR-4325 or miR-367. [score:1]
Additionally, the opposite effects of miR-25 and miR-32 on the Wnt reporter may imply an important and distinguishing role for the co-seed sequence of miR-25, which is strongly divergent between miR-25 and miR-32 (Fig. S4). [score:1]
On the other hand miRs like miR-32 or 367 that shares the seed with the miR-25/92 family could not repress Wnt reporter activity (Fig. S4). [score:1]
Figure S4 Screening results and alignment of studied miRs (miR-1/206 and miR-25/92 family) and miRs with a similar seed sequence. [score:1]
Secondary validation of miR-1, miR-25 and miR-613. [score:1]
0026257.g003 Figure 3 (A) Epistasis experiments with synthetic human Pre-miR-1, Pre-miR-25 and Pre-miR-613. [score:1]
In order to investigate the function of miR-25 in Wnt-responsive cell lines we cloned a human unprocessed Pri-miR-25 into the pcDNA3.1(-) expression vector with a selectable neomycin marker. [score:1]
Selection media for cells transfected with linearized empty pcDNA3.1(-) or Pri-hsa-miR-25 pcDNA3.1(-) using Lipofectamine2000 contained increasing amounts of active G418 sulfate (Cellgro #30-234-CR) for 7–16 days. [score:1]
The epistasis experiments indicated that miR-25 may act in parallel or downstream of β-catenin itself. [score:1]
Figure S5 Possible miR-25 binding sites in β-catenin CDS (543–1874) predicted with RNAhybrid and without seed sequence constraints to include non-canonical seed identification. [score:1]
After sub-cloning the hsa-Pri-miR-25 amplicon that contains endogenous 5′- and 3′-flanking sequences was finally cloned into the pcDNA3.1(-) vector (Invitrogen) via BamHI (vector and insert) and NheI (vector) XbaI (insert). [score:1]
This could indicate that some miRs or miR-families may repress the Wnt pathway components/activity mainly with the seed sequence (miR-1/613 -family), while others may require the coordinated action of the seed and co-seed (miR-25/92 -family). [score:1]
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7
[+] score: 75
Considering the signaling pathway which induces the miRNA transcription directly upon LPS stimulation and suitable number of miRNA targets for biomarkers, expression of miRNAs in whole blood following LPS injection was quantified using real-time RT-PCR to verify selected up-regulated, but not down-regulated, miRNA targets with at least 4-fold increase in expression (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451). [score:16]
Upregulated expression of the miRNA targets (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) following LPS injection on real-time RT-PCR was dose- and time -dependent. [score:8]
With a dose- and time -dependentupregulated expression of the miRNA targets (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) following LPS injection, these whole blood-derived miRNAs are promising as biomarkers for LPS exposure. [score:8]
Expression of representative up-regulated miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) identified using miRNA microarray of whole blood using real-time RT-PCR. [score:6]
In TLR4 receptor knockout mice, significantly lower expression of let-7d, miR-25, miR-92a, miR-103 and miR-107 was observed following LPS treatment (Figure 4). [score:4]
Additionally, following exposure to LPS, expression of only 5 miRNAs (let-7d, miR-25, miR-92a, miR-103, and miR-107) was significantly lower in TLR4 receptor knockout mice. [score:4]
miR-25 were significantly upregulated in the serum of patients with hepatitis B virus (HBV) -positive hepatocellular carcinoma [30]. [score:4]
In contrast, upon 100 ug and 1000 ug of LPS injection, all these 8 miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) had a significant expression than the control (Figure 2A). [score:3]
Figure 3 Expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 from whole blood of C57BL/6 mice based on real-time RT-PCR experiments 6 h after exposure to 100 μg LPS originating from different bacteria, including Escherichia coli serotype 026:B6, Klebsiella pneumonia, Pseudomonas aeruginosa, Salmonella enterica, serotype Enteritidis, and Serratia marcescens. [score:3]
Additionally, significantly lower expression levels of let-7d, miR-25, miR-92a, miR-103, and miR-107 were observed in whole blood of Tlr4 [−/−] mice. [score:3]
In this study, we demonstrated that expression of multiple miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) is significantly altered in the whole blood of mice after exposure to LPS in a dose- and time -dependent fashion. [score:3]
To investigate the role of the TLR4 receptor in inducing expression of the miRNA targets, expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 in the whole blood of Tlr4 [−/−] mice 6 h after intraperitoneal injection of 100 μg LPS (L3755) was measured against that from the whole blood of Tlr4 [−/−] mice injected with PBS. [score:3]
Figure 5 Expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 of whole blood from C57BL/6 mice using real-time RT-PCR experiment 6 h after exposure to 10, 100, and 1000 μg LTA originating from Staphylococcus aureus ; *, P  < 0.05 vs. [score:3]
At 24 h, only miR-25 and miR-92a continued to be significantly expressed in the blood. [score:3]
Figure 4 Expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451 of whole blood from C57BL/6 and Tlr4 [−/−] (C57BL/10ScNJ) mice from real-time RT-PCR experiments 6 h after exposure to 100 μg LPS; **, P  < 0.01 vs. [score:3]
To investigate that whether lipoteichoic acid (LTA) originating from gram -positive bacteria induces expression of let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451, whole blood was drawn at 6 h following intraperitoneal injections of 10, 100, or 1000 μg LTA from S. aureus for real-time PCR. [score:1]
[1 to 20 of 16 sentences]
8
[+] score: 36
Other miRNAs from this paper: mmu-mir-133a-1, mmu-mir-133a-2, mmu-mir-133b, mmu-mir-133c
The increase in the expression of NOX-4 expression is associated with a decrease in the expression of miR-25, a known regulator of NOX-4, (47, 48), in smooth muscle of ob/ob mice and smooth muscle of WT mice treated with HG (Fig 5E and 5F), suggesting that NOX-4 expression is negatively regulated by miR-25 and hyperglycemia -induced decrease in miR-25 expression caused an increase in NOX-4 expression. [score:15]
Downregulation of miR-25 was shown to induce NOX-4 expression in diabetic rat kidney [67]. [score:6]
The increase in NOX-4 expression and ROS levels observed in smooth muscle of ob/ob mice or in smooth muscle treated with HG could be due to a decrease in miR-25 expression in diabetes. [score:5]
miR-133a and miR-25 expression by qRT-PCR. [score:3]
Expression of NOX-4 and microRNA-25 in diabetes and hyperglycemia. [score:3]
The expression levels of miR-133a and miR-25 were detected by qRT-PCR assay. [score:2]
Smooth muscle of the fundus from WT and ob/ob mice, and smooth muscle of the fundus from WT mice treated with NG or HG for 48 h were used to measure the expression of NOX-4 and microRNA-25 (miR-25). [score:1]
0178574.g005 Fig 5 Smooth muscle of the fundus from WT and ob/ob mice, and smooth muscle of the fundus from WT mice treated with NG or HG for 48 h were used to measure the expression of NOX-4 and microRNA-25 (miR-25). [score:1]
[1 to 20 of 8 sentences]
9
[+] score: 34
Other miRNAs from this paper: hsa-mir-25
This result strongly suggests that the strong up-regulation of miR-25 expression might be responsible for the down-regulation of TOB1 expression in cancer cells. [score:11]
A recent study reported that miR-25, which is highly expressed in the plasma and primary tumor tissues from patients with gastric cancer, repressed TOB1 mRNA expression through direct interaction with its 3′-untranslated region (3′-UTR), thereby increasing the proliferation, metastasis, and invasion of gastric cancer cells [27]. [score:8]
miR25 represses TOB1 mRNA expression by binding to its 3′-untranslated region (3′-UTR) directly. [score:6]
Interestingly, we found that the miR-25 locus was highly amplified in these TCGA human clinical cancer samples and miR-25 expression was highly up-regulated in TCGA stomach cancer samples, showing its gain and amplification at the genomic level (Figure 3E–G). [score:6]
Figure 3Genomic copy number alteration and expression of AURKA, SAMD4, and miR-25 in TCGA human clinical cancer samples across a variety of cancer types. [score:3]
[1 to 20 of 5 sentences]
10
[+] score: 33
The miR-25 target list contains a single gene within the cell cycle pathway, Cdkn1c, a confirmed miR-25 target [35]. [score:5]
Briefly, 1500 ng of biotinylated cRNA was hybridised to Illumina expression BeadChips (Mouse-6 v1.1 for mmu-miR-291-3p and mmu-miR-25 mimics and cell line expression profiles, and Mouse-6 v2 for mmu-miR-302, mmu-miR-292-5p, mmu-miR-106a, mmu-miR-21 and mmu-miR-298 mimics. [score:5]
The signal to noise ratio varied form 11.8∶1 for the miR-25 target list to 2.2∶1 for the miR-292-5p target list (Table S2). [score:5]
In addition, we have recently demonstrated that miR-25 directly targets two significant ubiquitin ligases and may influence the core ES transcriptional network as a consequence [49]. [score:4]
A: Sylamer plots comparing the expression profiles of Dgcr8 [gt1/tm1] cells transfected with a miRNA mimic (miR-25, miR-291a-3p, miR-292-5p or miR-298) and a cel-miR-239b control miRNA. [score:3]
For a full description see Figure 3. B: GSEA enrichment plots [29] judging the enrichment of the transcripts within the miRNA target lists for miR-25, miR-291a-3p, miR-292-5p or miR-298 within regions of a list of transcripts ordered according to log fold change following the depletion of Dgcr8 in homozygous mutant cell lines. [score:3]
For a more complete description of miR-25 targets please see D. Lu et al. [49]. [score:3]
miRIDIAN Negative Control #2 (Dharmacon CN-002000-01-05) miRIDIAN mmu-miR-291-3p mimic (Dharmacon C-310470-01-0005) miRIDIAN mmu-miR-25 mimic (Dharmacon C-310564-01-0005) miRIDIAN mmu-miR-302 mimic (Dharmacon C-310483-05-0005) miRIDIAN mmu-miR-292-5p mimic (Dharmacon C-310471-03-0005) miRIDIAN mmu-miR-106a mimic (Dharmacon C-310488-07-0005) miRIDIAN mmu-miR-21 mimic (Dharmacon C-310515-05-0005) miRIDIAN mmu-miR-298 mimic (Dharmacon C-310479-07-0005) Trizol purified RNA was cleaned up with an RNeasy MiniElute Cleanup Kit (Qiagen). [score:1]
This large overlap is contrasted with the much lower overlap (0–11%) seen between these two miRNAs and miR-298, miR-21, miR-25 and miR-292-5p (Figure S8). [score:1]
Initially, miR-291a-3p and miR-25 were transfected into the Dgcr8 [gt1/tm1] cells. [score:1]
miRIDIAN Negative Control #2 (Dharmacon CN-002000-01-05) miRIDIAN mmu-miR-291-3p mimic (Dharmacon C-310470-01-0005) miRIDIAN mmu-miR-25 mimic (Dharmacon C-310564-01-0005) miRIDIAN mmu-miR-302 mimic (Dharmacon C-310483-05-0005) miRIDIAN mmu-miR-292-5p mimic (Dharmacon C-310471-03-0005) miRIDIAN mmu-miR-106a mimic (Dharmacon C-310488-07-0005) miRIDIAN mmu-miR-21 mimic (Dharmacon C-310515-05-0005) miRIDIAN mmu-miR-298 mimic (Dharmacon C-310479-07-0005) Trizol purified RNA was cleaned up with an RNeasy MiniElute Cleanup Kit (Qiagen). [score:1]
A set of miRNAs was transfected including miR-25, miR-291a-3p, miR-292-5p, miR-106a, miR-21, miR-302a and miR-298. [score:1]
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[+] score: 27
In particular, we identified 10 over-expressed miRNAs (miR-17-5p, miR-221-3p, miR-93-5p, miR-25-3p, miR-181b-5p, miR-106b-5p, miR-186-5p, miR-222-3p, miR-15b-5p, and miR-223-3p; Figure 2A) that are involved in the activation of major liver carcinogenesis-related gene expression networks, especially the TGF-β- and Wnt/β-catenin signaling pathways, the roles of which are well-established in hepatocarcinogenesis [14]. [score:5]
Among the miRNAs distinctively over-expressed in NASH-derived HCC, miR-221-3p and miR-222-3p, which exhibited a carcinogenesis stage -dependent increase in expression, and miR-25-3p, miR-93-5p, and miR-106b-5p, which are members of the oncogenic miR-106b∼25 cluster, are of special interest. [score:5]
Mechanistically, the over -expression of miR-25-3p, miR-93-5p, and miR-106b-5p in NASH-derived HCC may be attributed to an increased expression of the Mcm7 gene, which harbors the miR-106b∼25 cluster [16– 18]. [score:5]
We also demonstrated that over -expression of miR-25-3p, miR-93-5p, miR-106b-5p, miR-221-3p, and miR-222-3p was accompanied by the reduced protein levels of their targets, including E2F1, PTEN, and CDKN1A. [score:5]
Among these miRNAs, the over -expression of ten miRNAs (miR-15b-5p, miR-17-5p, miR-25-3p, miR-93-5p, miR-106b-5p, miR-181b-5p, miR-186-5p, miR-221-3p, miR-222-3p, and miR-223-3p) was associated with the activation of major hepatocarcinogenesis-related pathways, including the TGF-β, Wnt/β-catenin, ERK1/2, mTOR, and EGF signaling. [score:3]
Among the differentially expressed miRNAs in NASH-derived HCC, three miRNAs, miR-106b, miR-93, and miR-25, are members of the oncogenic miR-106b∼25 intragenic cluster [15, 16]. [score:3]
To investigate the functional consequences of the miR-106b∼25 cluster over -expression with respect to the hepatocarcinogenic process, the levels of E2F1, PTEN, and CDKN1A proteins, experimentally confirmed targets of miR-106b, miR-93-5p, and miR-25, were evaluated. [score:1]
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12
[+] score: 24
It has been reported that the miR-25 is a direct regulator of p53 gene (encoded by TP53) and negatively regulate the p53 function [25]. [score:4]
The possibility cannot be ignored that the miR-25 is an initial key regulator of p53 an important tumor suppressor altered during UVR-carcinogenesis. [score:4]
Our profiling study shows that the miR-25-5p was down-regulated due to acute UVR exposure in UVR-sensitive SKH1 mice. [score:4]
In this communication, differential expression (log fold change>1) of miR-25-5p was observed between untreated and acute UVR treated SKH1 mice skin. [score:3]
A comparison between acute and chronically affected miRNAs indicates that the miR-25-5p was up-regulated (LogFC = 1.58) in chronically treated skin compared to acute UVR. [score:3]
Global miRNA profiling revealed down-regulation of miR-25-5p in acutely UVR treated SKH1 mice skin compared to their untreated littermates. [score:3]
However, miR-25-5p was the only up-regulated miRNAs in chronically treated SKH1 mice compared to acute UVR treatment (Table 1). [score:3]
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13
[+] score: 19
Taken together with our later observations that targeting of the liver-specific miR-122-5p or poorly abundant miR-195-5p, miR-25-3p, miR-200a/b/c-3p, miR182-5p and the mutant miR-224-5p mut2 by 2′OMe AMOs (but not their LNA/DNA AMO counterparts) also resulted in significant inhibition of immunostimulatory ssRNA sensing, our work establishes sequence -dependent and miRNA-independent off-target inhibitory activity of 2′OMe AMOs on the immune sensing of pathogenic RNA by human and mouse phagocytes. [score:9]
The sequence-specific and miRNA-independent significant inhibition of immunostimulatory ssRNA sensing by 2′OMe AMOs targeting miR-195-5p, miR-25-3p, miR-122-5p, miR-200a/b/c-3p and miR182-5p (Figure 2B) was supported by the lack of inhibitory activity with LNA/DNA AMOs (Figure 2C), and the low abundance of these miRNAs (less than 100-fold the level of the most abundant miRNA in BMMs) (Figure 2A). [score:7]
Critically, this core sequence overlapped with a significantly enriched motif found in all the inhibitory sequences of Class 2 AMOs previously identified, in 5′-3′ orientation (for miR-200a/b-3p, and miR-25-3p) or 3′-5′ orientation (for AMO-NC1, miR-182-5p, miR-122-5p and miR-195-5p) (Figure 4C and Supplementary Table S2). [score:3]
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14
[+] score: 18
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-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-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-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
We have recently shown that HDI downregulated the expression of AID and Blimp-1 by upregulating miR-155, miR-181b, and miR-361, which silence Aicda mRNA, and miR-23b, miR-30a, and miR-125b, which silence Prdm1 mRNA, but not miR-19a/b, miR-20a, and miR-25, which are not known to regulate Aicda, Prdm1, or Xbp1 (16). [score:10]
The selectivity of HDI -mediated silencing of AICDA/Aicda and PRDM1/Prdm1 was emphasized by unchanged expression of HoxC4 and Irf4 (important inducers/modulators of AICDA/Aicda), Rev1 and Ung (central elements for CSR/SHM), and Bcl6, Bach2, or Pax5 (repressors of PRDM1/Prdm1 expression), as well as unchanged expression of miR-19a/b, miR-20a, and miR-25, which are not known to regulate AICDA/Aicda or PRDM1/Prdm1. [score:8]
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15
[+] score: 14
In fact, growing evidence of indirect p53 deregulation in MM through MDM2 overexpression, TP53 promoter hypermethylation and alterations in certain miRNAs that directly or indirectly affect p53 expression, such as miR-25, miR-30d, miR-125a-5p and miR-214, have been reported. [score:9]
Two miRNAs, miR-25 and miR-30d, which directly interact with the 3′-UTR of the human TP53 mRNA [107] are downregulated in MM and their levels are inversely correlated to TP53 mRNA. [score:5]
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[+] score: 14
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
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[+] score: 14
Recently, we also identified a novel cross-talk mechanism, by which pharmacologic or genetic inhibition of MEK restores PTEN expression, thus leading to cross -inhibition of downstream signaling through AKT and mTOR: more specifically, ERK -dependent upregulation of c-Jun and miR-25 leads to suppression of PTEN expression (Figure 2) [77]. [score:14]
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[+] score: 13
There were four up-regulated miRNAs (mmu-miR-709, mmu-miR-467a-3p, mmu-miR-182-5p and mmu-miR-25-5p) and seven down-regulated miRNAs (mmu-miR-615-3p, mmu-miR-409-3p, mmu-miR-680, mmu-miR-129-5p, mmu-miR-151-5p, mmu-miR-142-5p and mmu-miR-30b-5p), as the values presented in Table 1. Then we performed unsupervised hierarchical clustering of the eleven miRNAs. [score:7]
Control) P -valuemmu-miR-25-5p2.210.04mmu-miR-7091.980.02mmu-miR-467a-3p1.820.04mmu-miR-182-5p1.540.05mmu-miR-129-5p0.290.02mmu-miR-6800.340.02mmu-miR-615-3p0.360.00mmu-miR-409-3p0.440.02mmu-miR-30b-5p0.510.05mmu-miR-151-5p0.610.03 mmu-miR-142-5p 0.63 0.04By TargetScan, we found that mmu-miR-25-5p, mmu-miR-615-3p, mmu-miR-151-5p and mmu-miR-680 had few target genes directly relating with Tregs in MeSH database, so we excluded the four miRNAs for further exploration. [score:6]
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[+] score: 13
Previously, we had identified a specific whole blood–derived miRNA signature in mice exposed to LPS as there was a dose- and time -dependent upregulated expression of the miRNA targets (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) follo-wing in vivo LPS injection [14]. [score:8]
In previous study, we had demonstrated that expression of multiple miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) is significantly altered in the whole blood of mice after exposure to LPS in a dose- and time -dependent fashion [14]. [score:3]
In our previous work, in TLR4 receptor knockout mice, five of eight miRNAs (i. e. let-7d, miR-25, miR-92a, miR-103, and miR-107) was significantly lower following exposure to LPS, with unchanged levels of the other three miRNAs [14]. [score:2]
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[+] score: 12
MicroRNAs associated with the basal breast cancer subtype, including four members of the miR-17~92 family, miR-25 and miR-150, showed a distinctly different pattern, being equally distributed among clusters 1 and 2. Of particular interest was cluster 4, which in contrast to the global decrease in miRNA expression during lactation and involution showed a specific increase in expression during these stages, paralleled by a decrease in the expression of predicted targets for one of the cluster members, miR-429 (Additional file 7). [score:9]
In contrast, miRNAs overexpressed in the basal breast cancer subtype (four members of the miR-17~92 family, miR-25 and miR-150) were distributed equally among clusters 1 and 2 (Figure 3b). [score:3]
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[+] score: 12
The circulating miRNA targets that were up-regulated following CLP belong not only to the miR-17∼92 cluster but also to its evolutionary paralogs, miR-106a∼363 (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2, and miR-363) and miR-106b∼93 (miR-106b, miR-93, miR-25). [score:6]
Previously, we had demonstrated a dose- and time -dependent up-regulation of 8 (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107, and miR-451) and 4 (miR-451, miR-668, miR-1902, and miR-1904) circulating miRNA targets in mice following injection of LPS [11] and LTA [12], respectively. [score:6]
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[+] score: 12
MiR-25 and miR-92a show a high expression correlation (PCC = 0.798), whereas miR-92b has distinct expression patterns with miR-25 and miR-92a. [score:5]
The expression correlation between miR-92a and miR-92b is 0.2, and the expression correlation between miR-25 and miR-92b is 0.172. [score:5]
For example, three miRNAs including miR-25, miR-92a and miR-92b are from the miR-25 family. [score:1]
Both miR-25 and miR-92a were found to play roles in cell proliferation [31], [47]. [score:1]
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[+] score: 12
Highest-ranking miRNAs included miR-16/15a (46 targets), miR-27b (44 targets), let-7f (35 targets), miR-26b (33 targets), and miR-25 (30 targets). [score:11]
These observations were validated by qRT-PCR on “positive” miRNAs (i. e., miR-16, miR-15a, and miR-25) (Fig. 4D) in an independent set of animals (n = 3 per group). [score:1]
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24
[+] score: 11
Recently, it was reported that miR-25, an MCU -targeting miRNA, reduces MCU expression and [Ca [2+]] [m] uptake, thereby inducing resistance to apoptotic stimuli in and leading to increased survival of prostate and colon cancer cells [24]. [score:5]
Figure 3 (A-E) Expression of miR-17, miR-25, miR-124, miR-195 and miR-340 in a panel of four breast cancer cell lines by quantitative polymerase chain reaction analysis. [score:3]
The screening predicted five breast cancer-related miRNAs (miR-17, miR-25, miR-124, miR-195, and miR-340) to target MCU. [score:3]
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25
[+] score: 11
Regarding circulating miRNAs as potential biomarkers of diabetic cardiomyopathy, we found an association between differential miRNA expressions in myocardium and plasma at 16 months in 8 miRNAs (let-7f-5p, miR-10a-5p, miR-19b-3p, miR-25-3p, miR-140-5p, miR-146a-5p, miR-181b-5p, miR-499-5p). [score:3]
We found 8 circulating miRNAs that were less abundant in the obese mice than in normal mice, indicating an association between their gene expression in myocardium: let-7f-5p (FC: 5.4), miR-10a-5p (FC: 2.3), miRNA-19b-3p (FC: 2.5), miR-25-3p (FC: 3.4), miR-140-5p (FC: 4.5), miR-146a-5p (FC: 3.3), miR-181b-5p (FC: 5.2) and miR-499-5p (FC: 2.2). [score:3]
At 16 months, all 15 miRNAs were significantly downregulated in heart tissue of obese mice compared to heart tissue of normal mice: let-7f-5p (FC: 3.3), miR-10a-5p (FC: 2.6), miRNA-19b-3p (FC: 5.0), miR-25-3p (FC: 2.6), miR30e-5p (FC: 5.6), miR-140-5p (FC: 5.0), miR-155-5p (FC: 1.7), miR-146a-5p (FC: 4.0), miR-181b-5p (3.0), miR-199a-3p (FC: 3.6), miR-322 (FC: 1.5), miR-451 (FC: 1.9), miR-499-5p (FC: 5.4), miR-669m-5p (FC: 1.7) and miR-3473b (FC: 3.4). [score:3]
Based on previous pre-clinic studies, the miRNAs validated by RT-qPCR in our study are involved in alteration of glucose and lipid metabolism via insulin pathways (let-7f-5p, miR-10a-5p, miR-322) 20– 22, in cardiomyocytes apoptosis (miR-19b-3p, miR-25-3p, miR-30e-5p, miR-140-5p, miR-199a-3p, miR-499) 23– 28, in mitochondrial function (miR-181a/b) [29], in pro-inflammatory signalling (miR-146a-5p, miR-155, miR-181b-3p, miR-3473b) 30– 33, and in cardiac hypertrophy (miR-451) [34] and myocardial fibrosis process (miR-19b) 35, 36. [score:1]
At 12 months we observed a reduction of their abundance in 4 circulating miRNAs: miR-25-3p (FC: 1.5), let-7f-5p (FC: 5.2), miR-181b-5p (FC: 2.0) and miR-19b-3p (FC: 3.4); plasmatic levels were reduced in obese mice during the dietary treatment (Fig.   6). [score:1]
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[+] score: 10
For example, miR-106b, miR-21, miR- 22, miR-19b and miR-25 are known to regulate PTEN and miR-27 and miR-139 repress FoxO1 translation through direct binding to the 3′-UTR [31], [32], [33], [34], [35], [36], [37], [38]. [score:5]
Among the up-regulated miRNAs, miR-106b, miR-25 and miR-19b share the same primary transcripts, and miR-24 and miR-27 share primary transcripts. [score:4]
We have also noticed that miRNAs previously detected in neurites such as miR-134, miR-25 and miR-26a showed changes at 24 h after contextual conditioning [17], [19]. [score:1]
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[+] score: 10
Upregulation of miR-25, 93, and 106b was confirmed by qRT-PCR in sorted CD45 [–] BM cells and CD45 [–]CD140a [+]SCA-1 [+] mesenchymal progenitor cells, respectively (Figure 1B) [14]. [score:4]
n=7, * p<0.05 for miR-25/93/106b antagomir treatment versus control antagomir. [score:1]
C. In vitro invasion of BMC towards WT-MSC in the presence or absence of miR-25/93/106b antagomiR. [score:1]
E. In vitro invasion of BMC towards WT-MSC in the presence or absence of miR-25/93/106b antagomiR. [score:1]
Control groups are replicated from Figure 2C; n=7, * p<0.05 for miR-25/93/106b antagomir treatment versus control antagomir, ** p<0.05 for CXCR4 antagonist treatment versus PBS control. [score:1]
We found enhanced invasion/migration through the Matrigel™ layer for WT-MSC treated with antagomiR for miR-93 and 106b, but not for miR-25 (Figure 2C/Figure 5E). [score:1]
To validate individual cluster members as crucial for the observed phenotype, we studied the invasion of WT BMC towards CD45 [–] WT BM-derived mesenchymal stem cells (WT-MSC) that were pre -treated with control or antagomiR for miR-25, 93, and 106b. [score:1]
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28
[+] score: 10
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-21, hsa-mir-22, hsa-mir-25, hsa-mir-33a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-141, mmu-mir-155, mmu-mir-10b, mmu-mir-129-1, mmu-mir-181a-2, mmu-mir-183, mmu-mir-184, hsa-mir-192, mmu-mir-200b, hsa-mir-129-1, mmu-mir-122, 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-183, hsa-mir-210, hsa-mir-181a-1, hsa-mir-216a, hsa-mir-217, hsa-mir-223, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-129-2, hsa-mir-184, mmu-mir-192, mmu-mir-200a, 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-21a, mmu-mir-22, mmu-mir-96, mmu-mir-34a, mmu-mir-129-2, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-210, mmu-mir-181a-1, mmu-mir-216a, mmu-mir-223, mmu-mir-33, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, mmu-mir-217, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-375, mmu-mir-375, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-33b, mmu-mir-216b, hsa-mir-216b, mmu-mir-1b, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-129b, mmu-mir-216c, bbe-let-7a-1, bbe-let-7a-2, bbe-mir-10a, bbe-mir-10b, bbe-mir-10c, bbe-mir-125a, bbe-mir-125b, bbe-mir-129a, bbe-mir-129b, bbe-mir-133, bbe-mir-1, bbe-mir-183, bbe-mir-184, bbe-mir-200a, bbe-mir-200b, bbe-mir-210, bbe-mir-216, bbe-mir-217, bbe-mir-22, bbe-mir-252a, bbe-mir-252b, bbe-mir-278, bbe-mir-281, bbe-mir-33-1, bbe-mir-33-2, bbe-mir-34a, bbe-mir-34b, bbe-mir-34c, bbe-mir-34d, bbe-mir-34f, bbe-mir-375, bbe-mir-7, bbe-mir-71, bbe-mir-9, bbe-mir-96, bbe-mir-34g, bbe-mir-34h, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The sequencing frequency of the four most abundantly expressed miRNAs (miR-22, miR-1, let-7a and miR-25) constituted 78.82% of the total miRNA sequencing reads, suggesting that they might be ubiquitously expressed in amphioxus. [score:5]
As shown in the figure, bbe-miR-1, bbe-let-7, bbe-miR-25, bbe-miR-22, and so on were clearly expressed in amphioxus. [score:3]
In contrast, many phylogenetically conserved miRNAs, as well as miRNAs present in both chordates and vertebrates (for example, miR-216, miR-217, miR-22, miR-25, and miR-96), could be reliably traced back to B. belcheri (Gray). [score:1]
Based on the available nematode, fruitfly, zebrafish, frog, chicken, mouse, rat and human miRNA information [18], 45 conserved amphioxus miRNAs could be classified into three distinct groups: 23 miRNAs (let-7a, miR-1, miR-7, miR-9, and so on) were conserved throughout the Bilateria; 5 miRNAs (miR-252a, miR-252b, miR-278, miR-281 and miR-71) were homologous to invertebrate miRNAs; and 17 miRNAs (miR-141, miR-200a, miR-200b, miR-183, miR-216, miR-217, miR-25, miR-22, miR-96, and so on) were present both in chordates and vertebrates (Table S9 in). [score:1]
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[+] score: 9
Bone morphogenetic protein receptor 2 (BMPR2) is known to be targeted by miR-19a, −20a and miR-25 [28] and predicted to be targeted by miR-455. [score:5]
These 10 miRNAs and their predicted regulatory network are presented in Fig.   5. Bone morphogenetic protein 2 (BMP2) and BMP7 are predicted to be targeted by miR-20a,-140 and miR-25, −30b, respectively. [score:4]
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[+] score: 9
107.5.1919 2460471 2. Zhu Z. He J. Jia X. Jiang J. Bai R. Yu X. Lv L. Fan R. He X. Geng J. MicroRNA-25 functions in regulation of pigmentation by targeting the transcription factor MITF in Alpaca (Lama pacos) skin melanocytes Domest. [score:3]
Over -expression of miR-25 in melanocytes reduced Mitf mRNA and protein abundance [2]. [score:3]
Furthermore, over -expression of miR-25 reduced Mitf, Tyr and Tyrp1 mRNA and protein abundance in cultured melanocytes [2]. [score:3]
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[+] score: 9
The first, Pten, was upregulated (1.38-fold change and P=2.5E–03) and the three miRNAs (mir-369-5p, mir-25 and mir-495) predicted to target it were downregulated, with mir-369-5p belonging to the Dlk1-Dio3 cluster (Fig. 7). [score:9]
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[+] score: 9
In general, the rank order differences that we observed correlate well with analog miRNA abundance, expressed as DCt in the median normalized data or DDCt in the sno135/miR-25 normalized (Statminer) analyses. [score:3]
A comparison of the changes in rank order of individual miRNAs (Rank Difference AC-Con) and the log2 fold change from median normalized data [Median Normalized DCt (AC-Con)] is shown in Figure 1A, whereas a similar comparison of log2 fold change after Limma normalization to sno135 and miR-25 [DDCt(AC-Con)] is shown in Figure 1B. [score:1]
MicroRNA abundance in the four different sample cohorts was normalized using Statminer and sno135/miR-25 as endogenous controls. [score:1]
However, changes in rank order are not informative in terms of absolute (or more precisely analog) miRNA abundance, so we relied on Limma to calculate normalized abundance, expressed as DDCt, which corresponds to −log2 fold change normalized to sno135b/miR-25. [score:1]
In our case the least variant endogenous controls were sno135 and miR-25, and these were used to normalize the data. [score:1]
We selected sno135 and miR-25 as normalizers since both had M functions <0.15 individually and a combined M function of <0.1. [score:1]
We used Statminer normalization (against sno135 and miR-25) to extract relative miRNA abundance. [score:1]
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[+] score: 9
To address this issue, we first screened the miRNAs whose expressions are modulated in 4T1 cells by miRNA microarray analysis using both total cellular miRNA and exosomal miRNA after treatment with 100 μM of EGCG for 24 h. In brief, a set of miRNAs including let-7, miR-16, miR-18b, miR-20a, miR-25, miR-92, miR-93, miR-221, and miR-320 were up-regulated, and dozens of miRNAs including miR-10a, miR-18a, miR-19a, miR-26b, miR-29b, miR-34b, miR-98, miR-129, miR-181d were down-regulated in both total cellular and exosomal fraction by EGCG treatment (data not shown). [score:9]
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[+] score: 8
Cyclin E2 is also over-expressed in several small lung cancer cell lines [24], and ectopic over -expression of cyclin E2 reversed the G0/G1 cell cycle arrest induced by miR-25 down-regulation [29]. [score:8]
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[+] score: 8
reported here are in line with those reported in the literature describing miR-25, miR-221 and miR-222 as direct regulators of CDKN1C expression in a wide variety of solid tumours, showing a new mechanism responsible for CDKN1C downregulation in carcinogenesis [43– 45]. [score:8]
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[+] score: 8
This study confirmed that miR-25 was frequently over-expressed in OS, and up-regulation of miR-25 promoted cell proliferation in vitro and tumor growth in a xenograftmouse mo del. [score:6]
One of the 2 studies reported that miR-25 was transfected into OS cells directly [49]. [score:2]
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[+] score: 8
The expression of each individual miRNA corresponded broadly with its predicted effects upon target gene expression (e. g. miR-25 highest at P4 and miR-124 absent in CE-RSCs but present in P4 and adult mouse retina). [score:7]
A range of other candidates with p-values < 0.05 in at least one experimental condition (miR-128, miR-150, miR-204, miR-25, miR-27, miR-326 miR-34, miR-370, miR-378 and miR-485-5p) were selected to represent different predicted patterns of activity or for their lack of previous association with neural tissue. [score:1]
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[+] score: 8
Cofilin 2 is a target of miR-25, miR-363, miR-92a, and miR-92b. [score:3]
Cdc42 is a target of miR-92a and miR-92b and miR-25 and miR-363. [score:3]
As shown in Table 4, eight miRNAs were observed to belong to the miR-17 family; three miRNAs were identified to belong to the miR-19 family and three miRNAs to the miR-25 family; the miR-363-5p was found to belong to the miR-363 family, but its sequence was similar in part to that of miR-25 family members (Table 3). [score:1]
The miR-106b, miR-93, and miR-25 from miR-106b-25 cluster were decreased in response to high glucose while increased in response to low glucose treatment. [score:1]
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[+] score: 7
Other miRNAs tested, miR-27 and miR-25/32/92/363/367 have highly conserved binding sites but did not have an effect on reporter gene expression in HEK293 or 501mel cells. [score:3]
All Mitf 3′UTR sequences in 11 vertebrate species analysed contain the miR-27, miR-25/32/92/363/367 and the miR-101/144 binding sites (Fig. 1B). [score:1]
Black bars: miR-124/506 binding sites, dark grey bars: binding sites, light grey bars: miR-148/152 binding sites, white bars: miR-27, miR-25/32/92/363/367 and miR-101/144. [score:1]
A. The line indicates the 3′ UTR region of the mouse Mitf gene, including the coding region of exon 9. Potential binding sites for miR-27, miR-124/506, miR-25/32/92/363/367, miR-148/152, and miR-101/144 in the mMitf 3′UTR sequence are indicated below the line and potential PAS sites above. [score:1]
We tested the effects of microRNAs which have conserved binding sites in the 3′UTR region of Mitf, including miR-27a (located at 229–235 in the mouse Mitf 3′UTR sequence), miR-25/32/92/363/367 (1491–1497), miR-101/144 (3023–3029), miR-124/506 (1639–1646) and miR-148/152 (1674–1680 and 2931–2937) (Fig. 1A and 1B). [score:1]
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[+] 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-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-99a, mmu-mir-140, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-192, hsa-mir-148a, hsa-mir-30d, mmu-mir-122, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-122, hsa-mir-140, hsa-mir-191, hsa-mir-320a, mmu-mir-30d, 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-21a, mmu-mir-22, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-92a-2, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-92a-1, hsa-mir-26a-2, hsa-mir-423, hsa-mir-451a, mmu-mir-451a, hsa-mir-486-1, mmu-mir-486a, mmu-mir-423, bta-mir-26a-2, bta-let-7f-2, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-320a-2, bta-mir-99a, bta-mir-181a-2, bta-mir-27b, bta-mir-140, bta-mir-92a-2, bta-let-7d, bta-mir-191, bta-mir-192, bta-mir-22, bta-mir-423, bta-let-7g, bta-mir-10b, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, hsa-mir-1246, bta-mir-24-1, bta-mir-26a-1, bta-mir-451, bta-mir-486, bta-mir-92a-1, bta-mir-181a-1, bta-mir-320a-1, mmu-mir-486b, hsa-mir-451b, bta-mir-1246, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2
There were eight microRNAs (bta-miR-27b, bta-miR-191, bta-miR-30d, bta-miR-451, bta-miR-25, bta-miR-140, bta-miR-24-3p, and bta-miR-122), that were upregulated in older animals in the present study, and upregulated in fetal muscle tissue of the study. [score:7]
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[+] score: 7
We observed a similar trend of expression of miR-106b and miR-25, the other two miRNAs in the cluster (Figure 1F ) even though their absolute expression is lower with respect to miR-93 (see Figure 1B ). [score:5]
TaqMan quantitative real-time PCR was performed with hsa-miR-16, hsa-let7a, hsa-miR-125b, mmu-miR93, mmu-miR-124a, hsa-miR-23a, hsa-miR-106b, hsa-miR-25 and hsa-miR-9 specific probes (Life Technologies-Applied Biosystems) on ABI7900 thermal cycler. [score:1]
On the other hand, the high activity of miR-93 in SVZ neuroblasts and in Ki67 [+]nestin [+] cells in NSC cultures strongly points to the association between miR-93 and the proliferative state (as previously suggested for miR-25) [42], possibly linked to the capacity of immature progenitors to reactivate proliferation and acquire stem-like functional attributes. [score:1]
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[+] score: 7
The 50 highest expressed miRNAs in the mice ovaries are represented in a heatmap in Fig 1 and for miRNA expression levels in Fig 2. The top five most expressed miRNAs in the ovary (all samples combined) were mmu-miR-92a-3p (miR-25 family), mmu-let-7c-5p (let-7 family), mmu-miR-143-3p (miR-143 family), mmu-miR-26a-5p (miR-26 family) and mmu-miR-145a-5p (miR-145 family). [score:7]
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[+] score: 6
miR-25, miR-32, miR-661 and miR-339–5p target MDM2 to up-regulate p53 protein levels and function [27– 30]. [score:6]
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[+] score: 6
VSELs also express several miRNAs that attenuate Igf-1/Igf-2 signaling in these cells (mir681, mir470, mir669b) as well as up regulate expression of p57 (mir25.1, mir19b, mir92). [score:6]
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[+] score: 6
In addition, the results seemed to contrast to our previous report that LPS injection induced up-regulation of the miRNAs (let-7d, miR-15b, miR-16, miR-25, miR-92a, miR-103, miR-107 and miR-451) of the whole blood in a dose- and time -dependent manner [19]. [score:4]
Small RNA deep sequencing and qPCR results of five selected miRNAs (mir-133a-1-3p, mir-127-3p, mir-25-3p, mir-191-5p, and mir-215-5p) were generally in agreement, with a Pearson correlation value of 0.921 (Additional file 2). [score:1]
Among them, there were 52 mature miRNAs with sequence reads ≥ 400 (Additional file 1: Table S4) and 10 mature miRNAs (mir-10b-5p, mir-133a-1-3p, mir-133a-2-3p, mir-191-5p, mir-22-3p, mir-25-3p, mir-3107-5p, mir-486-5p, mir-92a-1-3p, mir-92a-2-3p) with sequence reads ≧ 4000 in at least 1 of the 12 twelve libraries (Additional file 1: Table S5). [score:1]
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[+] score: 6
In this study, five miRNAs (miR-29a, miR-29b, miR-126*, miR-127-3p, miR324-3p) were found upregulated and four (miR-188-5p, miR-25, miR-320a, miR-346) downregulated in both quiescent and active UC compared to healthy controls (Fasseu et al., 2010). [score:6]
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[+] score: 6
Among which we found that three miRNAs (miR-363, miR-367, miR-25) were commonly upregulated while six (miR-33a, miR-33b, miR-92a, miR-92b, miR-137, miR-32) were downregulated in IL-6 -treated GBC-SD cell line samples compared to the representative controls (Figure 4A and Figure 4B). [score:6]
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[+] score: 6
MicroRNAs targeting MDM2: miR-192, miR-194, miR-215, miR-221, miR-605, miR-17-3p, miR-193a, miR-25, miR-32, miR-143, miR-145, miR-18b, miR-661 [reviewed in Ref. [score:3]
Figure 1 MicroRNAs targeting p53: miR-125b, miR-504, miR-1285, miR-92, miR-141, miR-380-5p, miR-15a, miR-16, miR-25, miR-30d, miR-200a [reviewed in Ref. [score:3]
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[+] score: 4
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-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, 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-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The prospect that a similar function may extend to other miRNAs is suggested by the conservation of several miRNAs (e. g. miR-25, miR-34a/b/c, miR-135a/b, miR-194, and miR-200a) that are capable of directly targeting the Wnt/β-catenin, a signaling pathway that has been wi dely implicated in the control of oncogenic hallmarks such as cell proliferation, metastasis, angiogenesis, telomerase activity, and apoptosis (reviewed by [49]). [score:4]
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[+] score: 4
Differential expression of six miRNAs (miR-142-3p, miR-505*, miR-1248, miR-181a-2*, miR-25* and miR-340*) was found to accurately discriminate between tumors from BRCA1/2 mutation carriers and noncarriers [12]. [score:4]
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[+] score: 4
With ≥5,000 reads, the following four miRNAs were dominantly expressed in all these six libraries: miR-25-3p, miR-486-5p, miR-3107-5p, and miR-92a-3p (Supplementary File 1: Table S5). [score:3]
In addition to miR-486-5p and miR-3107-5p, which have ≥200000 sequence reads in all six libraries, miR-92a-3p and miR-25-3p were the third and fourth most abundant miRNA in (F)7d (22068 and 13644 reads, resp. [score:1]
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[+] score: 4
Mmu-miR-31, mmu-miR-351, mmu-miR-672, mmu-miR-339-3p, mmu-miR-138, mmu-miR-210, mmu-miR-25, and mmu-miR-322 were found to be more prominent and may play crucial roles in the regulatory network for their degree were more than 5. 10.1371/journal. [score:2]
Mmu-miR-31, mmu-miR-351, mmu-miR-672, mmu-miR-339-3p, mmu-miR-138, mmu-miR-210, mmu-miR-25, and mmu-miR-322 were found to be more prominent and may play crucial roles in the regulatory network for their degree were more than 5. 10.1371/journal. [score:2]
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53
[+] score: 4
Expression levels of miR-92a paralog miRNAs miR-25 (C) and miR-363 (D) in heart of WT and miR-92a [−/−] mice. [score:3]
All other cluster members and the paralog microRNAs miR-25 and miR-363 were not changed in miR-92a [−/−] mice (Figure S1C/D). [score:1]
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54
[+] score: 4
For example, overexpression of the putative oncogenic miR-25-106b-93 cluster in mice showed no tumor development. [score:4]
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55
[+] score: 3
However, exosomes derived from pleural fluid expressed much higher levels of the miR-17-92 and miR-106b-25 cluster members, with the exception of miR-25 and miR-92a (Figure 5B). [score:3]
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56
[+] score: 3
Here, by sequence matching using bioinformatics analyses, we found quite a few of candidate miRNAs that target Bcl-2, including miR-429, miR-30, miR-22, miR-25, miR-32, miR-92, miR-363, miR-367, miR-99, miR-27, miR-128, etc. [score:3]
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57
[+] score: 3
Other miRNAs from this paper: hsa-mir-25
Wahlquist C, Jeong D, Rojas-Muñoz A, Kho C, Lee A, Mitsuyama S, van Mil A, Jin Park W, Sluijter JPG, Doevendans PAF, Hajjar RJ, Mercola M: Inhibition of miR-25 improves cardiac contractility in the failing heart. [score:3]
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58
[+] score: 3
Further, ILF-3 and ILF-2 are targeted by miR-181b/c and miR-25, respectively [Table S2]. [score:3]
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59
[+] score: 3
Nielsen LB Wang C Sørensen K Bang-Berthelsen CH Hansen L Andersen ML Hougaard P Juul A Zhang CY Pociot F Mortensen HB Circulating levels of microRNA from children with newly diagnosed type 1 diabetes and healthy controls: evidence that miR-25 associates to residual beta-cell function and glycaemic control during disease progressionExp Diabetes Res. [score:3]
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60
[+] score: 3
Included as controls were two miRNAs, miR-103 and miR-25, whose microarray expression levels were not statistically different in cell lines with different phenotypes. [score:3]
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61
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As a control, the total list of miRNAs profiled was randomized in order and 9 miRNAs were selected (miR-452, miR-7, miR-205, miR-15a, miR-144, miR-183, miR-463, miR-25, miR-99a), targets and pathway ontology was analyzed as for the candidate list. [score:3]
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62
[+] score: 3
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-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-31, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-9-2, mmu-mir-141, mmu-mir-145a, mmu-mir-155, mmu-mir-10b, mmu-mir-24-1, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10b, hsa-mir-34a, hsa-mir-205, hsa-mir-221, mmu-mir-290a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-21a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-31, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-322, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-200c, mmu-mir-221, mmu-mir-29b-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-373, hsa-mir-20b, hsa-mir-520c, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-126b, mmu-mir-290b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The Cip/Kip family CKIs are targeted by miR-17-92, miR-106b, the miR-221 family and miR-25 in many different carcinomas [136]. [score:3]
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63
[+] score: 3
It is known to be expressed from a conserved cluster including three miRNAs (mir-106b, mir-93 and miR-25) that are involved in cancer [72] and adult neural stem cell proliferation and differentiation [73]. [score:3]
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64
[+] score: 3
In cells with an activated MAPK/ERK pathway, the expression levels of let-7a, miR-10, miR-22, miR-26, miR-34, and miR-125a were lower, and those of miR-20, miR-25, and miR-135b, were higher (Supplementary Table 1). [score:3]
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65
[+] score: 3
Additionally, miR-25 expression was also related to radiotherapy sensitivity. [score:3]
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66
[+] score: 3
During superovulation, mmu-mir-351, mmu-mir-30c, mmu-miR-26a, mmu-mir-25 expressed extensively as already reported by Fiedler et al. using microarray technology [50]. [score:3]
[1 to 20 of 1 sentences]
67
[+] score: 3
107.5.1919 2460471 3. Zhu Z. He J. Jia X. Jiang J. Bai R. Yu X. Lv L. Fan R. He X. Geng J. MicroRNA-25 functions in regulation of pigmentation by targeting the transcription factor MITF in alpaca (Lama pacos) skin melanocytes Domest. [score:3]
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68
[+] score: 3
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-mir-208a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-328, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, mmu-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-744, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, mmu-mir-208b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, mmu-mir-299b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
The absorbance at 414 nm had a significant effect on the expression of eca-miR-25 (FDR = 4.15e-4) and eca-miR-486-5p (FDR = 0.066) that was previously reported as haemolysis dependant [27]. [score:3]
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69
[+] score: 3
The miRNAs that contributed most prominently to PC1 (human - mouse split) were miR-93 and miR-19a, with a lesser contribution from miR-19b, miR-20a and miR-130b, while the miRNAs that contributed most significantly to PC2 (MYCN high versus low expression) were miR-17, miR-25, miR-20b and miR-15b. [score:3]
[1 to 20 of 1 sentences]
70
[+] score: 3
In addition, 7 microRNAs of the 17~92 and paralog 106b~25 clusters (namely miR-19a, miR-19b, miR-20a, miR-25, miR-92, miR-93 and miR-106b) were identified among the 53 most expressed microRNAs (groups A and B, see Table 1). [score:3]
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71
[+] score: 3
The mir106b-25 cluster is composed of the highly conserved miRNA106b (mir-106b), miRNA93 (mir-93) and miRNA25 (mir-25) that have been reported to be overexpressed in a number of cancers including gastric, prostate and pancreatic neural endocrine tumors, neuroblastoma and multiple myeloma [1], [2], [3]. [score:3]
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72
[+] score: 2
The cluster encodes three miRNAs: miR-106b, miR-93, and miR-25 [35, 39]. [score:1]
Both the evolutionary sequence analysis and the seed-sequence -based grouping partition these miRNAs into four families: the miR-106 family (miR-17, miR-20a/b, miR-106a/b, and miR-93), the miR-18 family (miR-18a/b), the miR-19 family (miR-19a/b-1/2), and the miR-92 family (miR-25, miR-92a-1/2, and miR-363). [score:1]
[1 to 20 of 2 sentences]
73
[+] score: 2
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-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, mmu-mir-200a, 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-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-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-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, 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-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
miR-25 forms part of the evolutionary conserved miR-106-25 cluster (Tanzer and Stadler, 2004) which is located within the thirteenth intron of the protein-coding gene Mcm7, a member of a DNA helicase family required for DNA replication. [score:1]
miR-25. [score:1]
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74
[+] score: 2
Furthermore, several novel mechanisms have been postulated to be involved in driving the differentiation process i. e. extracellular signal-regulated kinase (ERK)/β-catenin [5], dickkopf-related protein-3 (DKK-3) [2], reactive oxygen species [6], histone deacetylases 7 [7], microRNA (miRNA)-221 and miRNA-25 [3]. [score:2]
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75
[+] score: 2
Kumar et al. pointed out that the human TP53 gene can be negatively regulated by several miRNAs: miRNA-125b, miRNA-504, miRNA-25, and miRNA-30d [30]. [score:2]
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76
[+] score: 2
These include miRNA-25, miRNA-106b, let-7g and miRNA-93 (Figure 3), while the level of miRNA-23a was not increased in samples with higher levels of hemolysis. [score:1]
Samples with high levels of hemolysis observed visually or based on relative abundance of miRNA-451 (>23%), miRNA-16 (>13%) correlating with increase in miRNA-25, miRNA-106b, let-7 g and miRNA-93 were also excluded from analysis. [score:1]
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77
[+] score: 1
8) GCACUUU mmu-miR-25 (2.. [score:1]
[1 to 20 of 1 sentences]
78
[+] score: 1
Fortunately, miRNA microarrays showed that Res treatment in SW480 CRC cells significantly decreased miR-17, miR-21, miR-25, miR-92a-2, miR-103-1 and miR-103-2 which have been shown to behave as onco-miRNAs [13]. [score:1]
[1 to 20 of 1 sentences]
79
[+] score: 1
In human and mouse, two paralog clusters exist, i. e. the miR-106a-363 cluster comprising 6 miRNAS (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2 and miR-363) and the miR-106b-25 one with 3 members (miR-106b, miR-93 and miR-25). [score:1]
[1 to 20 of 1 sentences]
80
[+] score: 1
The miR-25 and miR-93 belong to the miR-106b-93-25 cluster that acts as oncomiRs (18). [score:1]
[1 to 20 of 1 sentences]
81
[+] score: 1
At 15 dpi, 17 miRNAs (let-7b,c, miR-10a, miR-21, miR-25, miR-26a, miR-29c, miR-30a,b,c,d, miR-99a, miR-103, miR-151, miR-195, and miR-200b,c) were identified to be important in the late repair phase. [score:1]
[1 to 20 of 1 sentences]
82
[+] score: 1
Other miRNAs from this paper: hsa-mir-25, hsa-mir-31, mmu-mir-31
Among these H5N1-derived small RNAs, FLU-vsRNA-1 had the highest copy number, which was in a similar range of functional endogenous miR-25-3p and miR-31-5p (Figure 1B). [score:1]
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83
[+] score: 1
Zhang J MicroRNA-25 Negatively Regulates Cerebral Ischemia/Reperfusion Injury-Induced Cell Apoptosis Through Fas/FasL PathwayJ Mol Neurosci. [score:1]
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84
[+] score: 1
Other miRNAs from this paper: mmu-mir-31, mmu-mir-93, mmu-mir-181b-1, mmu-mir-181b-2
It was publicized that restoration of LATS2 significantly attenuated the oncogenic effects of miR-25 [57]. [score:1]
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85
[+] score: 1
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-17, hsa-mir-25, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-105-1, hsa-mir-105-2, dme-mir-1, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-124-3, mmu-mir-134, mmu-mir-10b, hsa-mir-10a, hsa-mir-10b, dme-mir-92a, dme-mir-124, dme-mir-92b, mmu-let-7d, dme-let-7, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-134, 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-92a-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-92a-1, hsa-mir-379, mmu-mir-379, mmu-mir-412, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-92-1, gga-mir-17, gga-mir-1a-2, gga-mir-124a, gga-mir-10b, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-1a-1, gga-mir-124b, gga-mir-1b, gga-let-7a-2, gga-let-7j, gga-let-7k, dre-mir-10a, dre-mir-10b-1, dre-mir-430b-1, hsa-mir-449a, mmu-mir-449a, 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-1-2, dre-mir-1-1, dre-mir-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-17a-1, dre-mir-17a-2, dre-mir-25, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, 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-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, hsa-mir-412, hsa-mir-511, dre-let-7j, hsa-mir-92b, hsa-mir-449b, gga-mir-449a, hsa-mir-758, hsa-mir-767, hsa-mir-449c, hsa-mir-802, mmu-mir-758, mmu-mir-802, mmu-mir-449c, mmu-mir-105, mmu-mir-92b, mmu-mir-449b, mmu-mir-511, mmu-mir-1b, gga-mir-1c, gga-mir-449c, gga-mir-10a, gga-mir-449b, gga-mir-124a-2, mmu-mir-767, mmu-let-7j, mmu-let-7k, gga-mir-124c, gga-mir-92-2, gga-mir-449d, mmu-mir-124b, gga-mir-10c, gga-let-7l-1, gga-let-7l-2
One example is the mir-25, 92/mir-92b case, in which the mature sequences are almost identical while the rest of the sequences share little sequence similarity (See additional file 6). [score:1]
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86
[+] score: 1
Nonetheless, bioinformatic investigation of the 3' UTRs of TNF-α, KC and MIP-2 predicts that only TNF-α might contain MRE sites for miR-25 and miR-100 and implies that miRNAs are unlikely to regulate the LPS -induced response through direct action upon the mRNAs of these inflammatory mediators. [score:1]
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87
[+] score: 1
The human genome contains two paralogues of the miR-17-92 cluster: 1) the miR-106b/25 cluster (miR-106b, miR-93, miR-25) is located on chromosome 7 (7q22.1) in the 13th intron of the Mini-Chromosome Maintenance gene MCM7); 2) the miR-106a/363 cluster (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92-2, miR-363) is located on chromosome X (Xq26.2). [score:1]
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88
[+] score: 1
Similar to mir322, mir106b is the 5′ most microRNA within the mir106b-mir93-mir25 cluster, which is located within intron 13 of the Mcm7 gene. [score:1]
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89
[+] score: 1
A comprehensive study on a wide cohort of patients with HBV or HCV based HCC revealed that high miR-25, let7f and primary miR-375 profiles only occurred in HCC -positive patients. [score:1]
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90
[+] score: 1
For example, the probe mixture for the miR-17 subfamily contains probes for miR-17, miR-20a, miR-106a, miR-20b, miR-106b, and miR-93, the probe mixture for the miR-18 subfamily contains probes for miR-18a and miR-18b, the probe mixture for the miR-19 subfamily contains probes for miR-19a and miR-19b, and the probe mixture for the miR-92 subfamily contains probes for miR-92, miR-363, and miR-25. [score:1]
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91
[+] score: 1
Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, 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-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, 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, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, 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, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
The functional networks of miR-92b (PRdmiR, mir-25 family, derived from GC rich tandem repeats), miR-28 (RdmiR, mir-28 family, derived from LINE), miR-151 (RdmiR, mir-28 family, derived from LINE), miR-421 (RdmiR, mir-95 family, derived from LINE), miR-1271 (RdmiR, mir-1271 family, derived from LINE), miR-340 (RdmiR, mir-340 family, derived from DNA transportable element) and miR-378 (RdmiR, mir-378 family, derived from SINE) have been reconstructed (Figure 8). [score:1]
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