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36 publications mentioning mmu-mir-709

Open access articles that are associated with the species Mus musculus and mention the gene name mir-709. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 195
However, there was no correlation in the number of predicted miR-709 binding sites in the mRNA and the degree of downregulation: an average of 1.87 ± 1.04 binding sites for the 36 genes downregulated >2-fold, versus 1.79 ± 1.35 for a subgroup of 36 genes downregulated <2-fold (−1.23 to −1.25-fold), p = 0.82. [score:10]
Similarly, genes expressed at extremely low levels in liver, were not affected by miR-709 [Egr2, Sox-2, Ctcfl, Ras-GRF1; Table 3. Genes that are not normally expressed in hepatocytes such as gastric inhibitory polypeptide (Gip; expressed in intestinal cells) and glucagon (Gcg; pancreas-specific), have log [2] probe signals of 4.8 and 3.4, respectively]. [score:9]
In hepatocytes (and most probably in other cell types) miR-709 regulates structural and cell adhesion target genes, where it is likely to contribute to maintain the appropriate level of its targets during cell proliferation, thereby tuning/buffering gene expression. [score:8]
miR-709 increases, repressing target gene expression, and miR-138 decreases, de-repressing expression 20. [score:7]
Despite its ubiquitous expression, miR-709 has distinctive targets during particular cellular processes, which underscores the complexity of gene regulation. [score:6]
Similarly, miR-709 targets that are involved in cytoskeleton function and attachment to the extracellular matrix, Rab11b, Dync1li1 and Timp3, were upregulated in tumors relative to adjacent non-tumor liver and livers from control mice (Fig. 5B). [score:6]
To verify that the genes identified by microarray are direct targets of miR-709, we looked for predicted miR-709 binding sites on the 3′ UTR of three target genes using the miRanda database 24. [score:6]
Among genes downregulated, 36 were significantly decreased >2-fold in the miR-709 group compared to Cel-239b -treated control cells (Table 1), while only 4 were upregulated >2-fold (Table 2). [score:6]
However, other targets, including Akt and Gsk3β, may only be regulated by miR-709 in specific tissues and/or during oncogenic/developmental conditions. [score:5]
Protein changes did not correlate with target prediction in this group: Slc27a1 (Fatp1) and Gck were predicted miR-709 targets, while Ldlr was not. [score:5]
Computational analysis of predicted targets using miRanda 24 and miRWalk 25 suggested that miR-709 gene targets are associated with cytoskeleton functions. [score:5]
Indeed, half of the previously described miR-709 targets are abundantly expressed in liver [Jun, Gsk3β, Myc, Akt1; Table 3. As reference, albumin (Alb), fatty acid synthase (Fasn) and LDL receptor (Ldlr) have log [2] signals of 13.5, 9.1 and 10.5, respectively]. [score:5]
Overall, the data suggest that some miR-709 gene targets may be regulated by this miRNA in multiple tissues (Rab11b, Dync1li1). [score:4]
Remarkably, levels of mature miR-709 were significantly upregulated (5.3-fold) in liver tumors (Fig. 5A), indicating that this miRNA is associated with the genetic reprogramming that takes place in HCC. [score:4]
These data indicate that Rab11b, Pctp, and Ces1g are direct targets of miR-709, supporting the microarray results. [score:4]
Given that miR-709 is a ubiquitously expressed miRNA, we then questioned whether it regulates the same genes in separate tissues. [score:4]
miR-709 is upregulated in hepatocellular carcinoma. [score:4]
Genes significantly upregulated >2-fold in miR-709 -transfected primary hepatocytes (p < 0.01). [score:4]
Genes significantly downregulated >2-fold in miR-709 -transfected primary hepatocytes (p < 0.01). [score:4]
How to cite this article: Surendran, S. et al. Gene targets of mouse miR-709: regulation of distinct pools. [score:4]
To confirm that Rab11b, Ces1g and Pctp are direct targets of miR-709, 150–300 base pairs of the 3′ UTR containing the putative binding sites [microrna. [score:4]
It is possible that repression of a number of genes occurs at the translational level instead of the mRNA, and additional genes from those identified through our microarray might be regulated by miR-709. [score:4]
Therefore, we proceeded to identify miR-709 targets by transcriptome analysis. [score:3]
Likewise, miR-709 had no impact on Gsk3β protein, a target in adipocytes (Fig. 3). [score:3]
miR-709 expression in an animal mo del of hepatocellular carcinoma. [score:3]
These data suggest that the overall level of expression of these genes is influenced by the simultaneous action of multiple miRNA, some of which increase (like miR-709), while others decrease in HCC, as described in PNS injury 20. [score:3]
This indicates that miR-709 is expressed in hepatocytes and that the 3p strand is used for gene silencing. [score:3]
Targets of miR-709. [score:3]
Based on signal intensity, mmu-miR-709 (miR-709) is expressed at high levels in this tissue, at approximately one-fourth of the most abundant miRNA, miR-122, and ~2-fold higher than let-7a (Supplementary Table 1). [score:3]
A total of 556 genes were downregulated and 848 were increased in miR-709 -treated cells compared to Cel-239b (p < 0.01). [score:3]
Previously validated miR-709 gene targets are not considerably modified in hepatocytes. [score:3]
The degree of luciferase repression was ~3-fold below the level observed with a tough decoy containing a target site for miR-122, the most abundant miRNA in liver, which is consistent with the amount of miR-709 relative to miR-122 (Supplementary Table 1). [score:3]
We used luciferase reporter plasmids containing the complementary sequence to miR-709 (tough decoys), to confirm that in primary hepatocytes the 3p strand of miR-709 is used to repress its targets (Fig. 1A). [score:3]
Insr is a predicted target, and neither the mRNA or protein were changed by miR-709. [score:3]
All three are predicted targets of miR-709. [score:3]
Eight genes have been previously shown to be validated targets of miR-709 in non-hepatic tissues (Table 3). [score:3]
Construct p. miR-709 was generated by cloning an oligonucleotide with a sequence perfectly complementary to the 3′ strand of miR-709 (based on the sequence published in TargetScan), downstream of the renilla luciferase gene in psiCHECK [TM]-2 (Promega, Madison, WI). [score:3]
To validate the newly identified miR-709 targets in other cell types, 3T3-L1 fibroblasts and C2C12 myoblasts were transfected with miR-709 mimic (Fig. 4). [score:3]
Pctp, Ces1g, and Rab11b are directly repressed by miR-709. [score:2]
We questioned whether miR-709 would be dysregulated in this process, as occurs in PNS injury 20. [score:2]
miR-709 regulates a distinct set of genes in liver. [score:2]
Thus, despite being a ubiquitous miRNA, miR-709 appears to control different gene networks in specific cellular processes and tissues, influencing distinct genetic programs. [score:1]
miR-709 levels are lower in T cell acute lymphoblastic leukemia and during adipocyte differentiation, and this decrease is needed for the oncogenic and the differentiation process to occur 15 22. [score:1]
Increasing cytoplasmic levels of miR-709 has no impact on cell viability or proliferation (Supplementary Fig. 4). [score:1]
Neither one was significantly silenced by miR-709 in this tissue. [score:1]
Four replicates for miR-709 and three replicates for Cel-239b were used. [score:1]
Primary hepatocytes were transfected with miR-709 or Cel-239b and cells were harvested 48 hours or 96 hours later. [score:1]
In addition, a portion of the 3′ UTR without miR-709 binding sites was cloned into psiCHECK [TM]-2 and used as negative controls (p. NC-Rab11b, p. NC-Ces1g, and p. NC-Pctp). [score:1]
Gsk3α does not have binding sites for miR-709 (miRanda database 24). [score:1]
Tough decoys (TuDs) binding miR-709 or miR-122 were generated by cloning 8 copies of the sequence complementary to the 3p strand of miR-709 or the 5p strand of miR-122, downstream from the luciferase gene in psiCHECK [TM]-2. The sequence inserted was synthesized with XhoI and NotI sites at the ends to facilitate cloning (GenScript, NJ, and Genewiz, NJ). [score:1]
In peripheral nerve system (PNS) injury, miR-709 and miR-138 have opposing roles. [score:1]
Furthermore, luciferase was lower only when miR-709 mimic –but not Cel-239b– was used. [score:1]
miR-709 does not repress Akt and GSK3β in primary hepatocytes. [score:1]
The experiment was repeated in a separate hepatocyte isolation, with similar results; p-values (**p < 0.01) are relative to cells treated with the same plasmid plus Cel-239b; p. 709: plasmid containing the sequence perfectly complementary to miR-709-3p strand; p. Pc, p. Ce and p. Ra: plasmids containing a fragment of the 3′ UTR with miR-709 binding sites of Pctp, Ces1g and Rab11b, respectively; p. NC-Pc, p. NC-Ce and p. NC-Ra: plasmids with a fragment of the 3′ UTR without miR-709 binding sites. [score:1]
Mouse primary hepatocytes or Hepa1c1c7 cells were co -transfected with plasmids (1.5 μg) and miR-709 or the control miRNA Cel-239b (1 μg) (Dharmacon, Lafayette, CO), or with these miRNAs alone (1 μg). [score:1]
Based on information available from the miRBase, the 3p strand of miR-709 is used for silencing (http://www. [score:1]
miR-709 induces transcriptional silencing of cytoskeleton genes. [score:1]
miR-709 is highly abundant in mouse liver. [score:1]
Remarkably, none of these genes were considerably reduced by miR-709 in hepatocytes (Table 3). [score:1]
This resulted in a 3.8-fold increase in cytoplasmic levels of miR-709 (Supplementary Fig. 1). [score:1]
Mouse primary hepatocytes were transfected with miR-709 mimic or a control miRNA, Cel-239b, and harvested 24 hour later. [score:1]
To quantify the level of mature miR-709, cDNA was generated from 10 ng of total RNA sample using the TaqMan MicroRNA Reverse Transcription Kit (Applied Biosystems, Foster City, CA). [score:1]
miR-709 does not repress Akt and GSK3β in 3T3-L1 fibroblasts and C2C12 myoblasts. [score:1]
In this study we have shown that the mRNAs of hundreds of genes are changed upon increasing miR-709 in hepatocytes. [score:1]
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2
[+] score: 130
Other miRNAs from this paper: mmu-mir-138-2, mmu-mir-140, mmu-mir-338, mmu-mir-138-1, mmu-mir-146b
Overexpression of miR-709 and/or an inhibitor of miR-138 (antimiR-138) lead to down-regulation of Egr2 protein expression in Schwann cells. [score:10]
In addition, we wanted to use two miRNAs with opposing function in PNS injury (miR-138 is down-regulated while miR-709 is up-regulated) to emphasize that the final outcome of gene expression is molded by a synchronized action of opposing signals. [score:9]
Finally, to show that the addition of the CMV-miR vector has no effect on luciferase expression in the empty sensor vector we analyzed the effect of the pCMV-miRNA expressing vectors, as well as miR-709 and miR-138 on the expression of luciferase from pMIR-report vector. [score:7]
In conclusion, our Luciferase expression data demonstrate that miR-138 and miR-709 can efficiently bind and regulate the expression of Sox-2, c-Jun and Egr2 in the context of an in vitro experiment. [score:6]
MiR-138 and miR-709 show the highest affinity for binding and regulation of Egr2, c-Jun and Sox-2 expression, which are the main gene regulators of the transition between differentiation and dedifferentiation following PNS injury [14]. [score:5]
The data was normalized with GAPDH RNA C [T] value as internal control and fold difference (2 [-ΔΔC] [T]) between miR709 and control miR treated Egr2 expression in Schwann cells was plotted as log 2 median ratios and error is expressed as s. d. Sciatic Nerve In vivo CHIPSciatic nerves (5 per condition) from control and axotomized (distal nerves from 48 h post-injury) mice were isolated and snap frozen in methanol/dry ice bath and stored at -80°C. [score:5]
The data was normalized with GAPDH RNA C [T] value as internal control and fold difference (2 [-ΔΔC] [T]) between miR709 and control miR treated Egr2 expression in Schwann cells was plotted as log 2 median ratios and error is expressed as s. d. Sciatic nerves (5 per condition) from control and axotomized (distal nerves from 48 h post-injury) mice were isolated and snap frozen in methanol/dry ice bath and stored at -80°C. [score:5]
miRNAs Form Functional Complexes with Their Targeted mRNAs in Association with Ago-2 in vivo Our results show that the protein expression pattern during peripheral nerve injury response (Fig. 1A) is a result of the synchronous and concerted action of miRNAs with similar or opposing roles (e. g. miR-138 and miR-709). [score:5]
miR-138 and miR-709 Bind and Regulate the Expression of Sox-2, c-Jun and Egr2. [score:4]
Egr2 protein expression in Schwann cells transfected with miR-709, antimiR-138 or non -targeting control miRNA and compared with non -transfected Schwann cells. [score:4]
Rat Schwann cells (1×10 [6]) were nucleofected (Amaxa/Lonza) with 100 nM miR-709 or AntimiR-138 or both to confirm that these miRNA do indeed regulate Egr2 expression in Schwann cells. [score:4]
Down-regulation of Egr2 protein expression in Schwann cells transfected with miR-709 (Fig. 5C) is consistent with the post-transcriptional and transcriptional silencing observed with luciferase assays and nuclear run-on assays respectively. [score:4]
The data was normalized with miR-709 C [T] value as internal control and fold difference (2 [-ΔΔC] [T]) between injured and uninjured control nerves for each microRNA was plotted as log 2 median ratios and error is expressed as s. d. SDS Protein lysates isolated from control and Injured (48h-post injury) mouse sciatic nerves (n = 4) were separated on SDS-PAGE and probed with antibodies for Egr2 (Covance), Sox-2, c-Jun (cell signaling), ID-2 (Cell signaling), Nanog (R&D) and QKI-6 (Millipore), P75NTR (Abcam), Ago1, Ago2 and Dicer (Cell Signaling). [score:3]
Figure S3 Cos-7 cells were transfected with empty pmiR-Report luciferase vector (50 ng) in presence of pCMV-vectors expressing miR-709 or miR-138 or empty pCMV vector and β-Gal report vector (25 ng each). [score:3]
As shown in Fig. S3, when pMIR-luciferase vector was co -transfected with either pCMV-empty vector, or pCMV-miR-709 or pCMV-miR-138 and b-gal transfection control vector the expression of luciferase was not significantly affected. [score:3]
We also demonstrate that miR-709 is involved in regulating transcriptional gene silencing of Egr2, a master regulator of the dedifferentiation/myelination switch [15]. [score:3]
Rat Schwann cells were nucleofected with control or miR-709 duplexes (Ambion) at 50 nm following pre-treatment with Ascorbic acid (50 µg/ml) for 48 h to activate Egr2 expression. [score:3]
We selected miR-138 and miR-709 for exogenous expression as Sox-2, c-Jun and Egr2 had multiple sites for these two miRNAs (Fig. 2, Table 1). [score:3]
The fold difference (2 [-ΔΔCT]) in the association of MSE and miR-709 with H3K27Me3 complex between injured and control nerves, was plotted as a log-2 median ratio and the error is expressed as standard deviation. [score:3]
Our results show that the protein expression pattern during peripheral nerve injury response (Fig. 1A) is a result of the synchronous and concerted action of miRNAs with similar or opposing roles (e. g. miR-138 and miR-709). [score:3]
Sox-2, which lacks highly accessible sites for miR-138 and miR-709 show comparable expression to control (A & D, first two bars), while c-Jun (C, first two bars) and Egr2 (B & E, first two bars) that have multiple highly accessible sites for both miR-138 and 709 (Table 1 & Table S2) are highly de-repressed (c-Jun) or highly repressed (Egr2) by endogenous miRNAs. [score:3]
Cos-7 cells were transfected with individual vectors containing gene of interest with multiple predicted miRNA binding sites in the 3′-UTR of the luciferase gene in the pmiR-Report (50 ng) in presence or absence of 5 nM microRNA oligonucleotides, (anti-miR miRNA-138 or anti-miR miRNA-709, or a negative control oligo, Ambion or 25 ng of pCMV-vectors expressing miR-709 or miR-138). [score:3]
The transcriptional silencing is accomplished through direct interaction of miR-709 with the myelin specific element (MSE) of the Egr-2 promoter, which affects nascent transcription of Egr2 and through the formation of epigenetic silencing complexes comprised of the repressive histone mark H3K27me3, Ago-1 and miR-709 on Egr2 promoter. [score:2]
RNase H treatment of lysates from injured and control nerves resulted in a decrease in the co-precipitation of miR-709 with the H3K27me3-MSE complex (Fig. 5F) while the association was unaffected by RNase A treatment (data not shown) indicating a direct interaction between miR-709 and the MSE promoter DNA. [score:2]
Since miR-709 regulates nascent transcription of Egr2 we hypothesized that miR-709 contributes to the formation of epigenetic silencing complexes on Egr2 promoter with the repressive histone H3K27Me3 and Ago-1 to induce transcriptional silencing. [score:2]
We next performed nuclear “run-on” assay by transfecting miR-709 into rat Schwann cells activated for Egr2 expression with ascorbic acid. [score:2]
miR-138 and miR-709 bind and regulate Sox-2, c-Jun and Egr2. [score:2]
It is beyond doubt however, that miR-709 interacts directly with the MSE-promoter DNA as indicated by the susceptibility of the complex to RNase H treatment (Fig. 5F). [score:2]
Selected miRNA (miR-138 and miR-709) binding regions of the genes of interest were amplified from mouse sciatic nerve RNA or from vectors (Sox-2 expression vector from Origene) cloned downstream of Luciferase gene in pmiR-report vector (Ambion) using the following primers. [score:2]
In addition, it is possible that miR-709 binds in trans and regulates the antisense strand of Egr2 promoter since MSE shows miRNA binding sites in both strands. [score:2]
We also show that miR-709 orchestrates transcriptional gene silencing of Egr2 through direct interaction with the Egr2 promoter that guides the promoter to associate with H3K27me3 -mediated silencing complexes in vivo. [score:2]
Supporting our prediction, exogenously added miR-709 leads to transcriptional gene silencing of Egr2 as indicated by the decrease in the nascent transcripts of Egr2 (Fig. 5B), suggesting a trans-regulatory role for miR-709 to induce transcriptional silencing in injury in addition to the observed post-transcriptional gene silencing (Fig. 1A & 4C & D). [score:2]
Values for the MSE and miR-709 were normalized to input DNA and miRNA respectively. [score:1]
Despite this, the fact that miR-709 represses the transcription of nascent Egr2 transcripts (Fig. 5B) means that there is a mechanism to recruit miRNAs to accessible promoter sequences. [score:1]
Real-time quantitative PCR to assess the presence of the MSE region of the Egr2 promoter (left bars) and miR-709 (right bars) in the H3K27me3 immunoprecipitated chromatin. [score:1]
The association of miR-709 with Ago2 was unperturbed suggesting that miR-709 may act on different subset of genes in normal and injured nerves to mediate post-transcriptional gene silencing or that miR-709 functions independent of Ago-2 association. [score:1]
Note the significant increase in the association of miR-709 and MSE with H3K27me3 silencing complexes following in vivo nerve injury. [score:1]
* miR-709 shows the most efficient binding sites in the MSE region of the Egr2 promoter. [score:1]
This showed that the MSE has efficient binding sites for miR-709, 468, 146b, 711 and 690 (Table 2). [score:1]
We selected miR-709 for our subsequent studies regarding the transcriptional gene silencing of Egr2 since STarMir predicted the highest total energy for miRNA 709 - MSE interaction (Table 2) indicating the possibility of a functional interplay. [score:1]
These repressive complexes contain miR-709 (Figure 5F) and associate with the MSE of the Egr2 promoter in vivo (Figure 5F). [score:1]
The combinatorial effect of miR-138 and miR-709 was validated as shown in Fig. 3A-E (last bar). [score:1]
miR-709 Induces Transcriptional Gene Silencing of Egr2. [score:1]
To verify our hypothesis for the role of miR-709 in transcriptional silencing of Egr2 following peripheral nerve injury we performed in vivo ChIP with H3K27Me3 antibody using chromatin from mouse sciatic nerves. [score:1]
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3
[+] score: 113
Other miRNAs from this paper: mmu-mir-705
Co-transduction of the cells with the Wnt1 3’UTR sensor vector and miR-709 or miR-705 should result in a reduction of luciferase protein levels, relative to an “empty” control vector (that does not contain any Wnt1 3’UTR sequences), if and only if these miRNAs bind to their target sites within the Wnt1 3’UTR and post-transcriptionally inhibit the expression of luciferase protein in these cells. [score:7]
However, it did not yield insight into the detailed interactions or the necessity of miR-709 for MHB development, which would require the establishment of a knock-out, knock-down and/or over -expression mouse mo del for miR-709. [score:6]
Beyond the complete verification of the miRNA -based regulation of Wnt1 expression in vivo, another question that arises about the mechanism behind the formation of the observed gradient of miR-709 expression across the MHB. [score:6]
Possible mechanisms include the regulation of miR-709 expression by external factors or by a direct feedback regulated by Fgf8 or other factors involved in the formation of the MHB. [score:6]
These results indicated that only miR-709 is expressed within the MHR and around the MHB in a pattern as predicted by the mo del and consistent with a possible regulatory function of miR-709 on Wnt1 expression at the MHB. [score:6]
miR-709 regulates Wnt1 mRNA expression in vitroUp to this point, hypotheses about a possible regulation of Wnt1 by miRNAs was based on available knowledge about miRNA-mRNA interaction [30, 35] and simulation studies of the MHB mo del. [score:5]
mmu-miR-709 is expressed in the MHR close to the MHB of the developing mouse embryo and targets the Wnt1 3’UTR in vitro. [score:5]
In the E10.5 mouse embryo, miR-705 is expressed only very weakly across the MHB and in the midbrain and rostralmost hindbrain, whereas miR-709 is expressed strongly and uniformly across the MHB and in the midbrain and rostral hindbrain (see Additional file 2: Figure S2 and Additional file 2: Figure S3). [score:5]
Next, we determined whether the post-transcriptional regulation of Wnt1 expression by miR-709 is indeed mediated by the predicted miR-709 BS within the Wnt1 3’UTR. [score:4]
Mutagenesis of the two predicted miR-709 BS within the Wnt1 3’UTR in fact abolished the negative regulation of luciferase expression from the sensor vector by miR-709. [score:4]
However, we noted a graded expression of miR-709 across the MHB in the ventral MHR (which is the region used to determine the expression profiles of the other IsO genes in the considered mo del) at this stage. [score:4]
miR-709 regulates Wnt1 mRNA expression in vitro. [score:4]
Site-directed mutagenesis of the predicted mmu-miR-709 seed sequences within the 857 bp Wnt1 3’UTR fragment was done using the Quick Change Multi-Site Directed Mutagenesis Kit (Stratagene, USA) according to the manufacturer’s instructions. [score:3]
At E10.5, miR-709 is expressed strongly in the anterior neural tube including hindbrain, midbrain and part of the forebrain (diencephalon), but sparing the major part of the forebrain. [score:3]
Figure 4 Analysis of the miR-709 expression in the MHR close to the MHB of the developing mouse embryo at E12.5. [score:3]
Therefore, the predicted BS sequences were changed such that they could not be bound anymore by miR-709 (see Additional file 4: Table S1) and consequently the expression levels of luciferase protein should not be affected relative to the control (“empty”) sensor vector. [score:3]
Site-directed mutagenesis of both seed sequences within the Wnt1 3’UTR sensor vector (Mt-Wnt1 3’UTR) abolished this negative regulation (Mt-Wnt1 3’UTR + miR-709:0.93 ± 0.067, mean ± sd) (single asterisk, p<0.05; double asterisk, p<0.01; student’s-T-test). [score:3]
To determine whether miR-709 and miR-705 can indeed regulate the expression of Wnt1 in a cellular context, we used the so-called luciferase “sensor assays”. [score:3]
This result indicated that miR-709, but not miR-705, indeed targets the Wnt13’UTR. [score:3]
At E12.5, miR-709 is strongly expressed in the ventral forebrain and midbrain and declines towards the ventral rostral hindbrain. [score:3]
The in situ hybridization (detection) experiments showed a promising qualitative expression profile for miR-709, which is in line with the predictions made by the mo del. [score:3]
At E12.5, miR-709 is strongly expressed in the dorsal telencephalon (cortex), diencephalon (thalamus), anterior midbrain and caudal hindbrain (rhombomere 1), and apparently weaker in the rostral rhombomere 1 and around the ventral MHB (B,D). [score:3]
In contrast to miR-709, did not show a refined and graded expression around the ventral MHB in the E12.5 mouse embryo (see Additional file 3: Figure S3). [score:3]
This graded miR-709 expression profile became even more evident when we calculated the grayscale profile of miR-709 expression across the MHR, i. e. from the anterior end of the midbrain to the posterior end of the rostral hindbrain, as shown in Figure  4B (see “Methods”). [score:3]
This result indicated that the negative post-transcriptional regulation of the Wnt1 mRNA by miR-709 is in fact mediated by the two predicted miR-709 BS within the Wnt1 3’UTR. [score:2]
In this experimental setup, a fragment of the Wnt1 3’UTR containing the predicted miR-709 and miR-705 binding sites (BS) was cloned at the 3’ end of a sequence encoding the Firefly luciferase protein. [score:1]
The miRNA miR-709 was identified as a potential regulator of Wnt1 mRNA, which was validated by luciferase sensor assays. [score:1]
This Wnt1 3’UTR fragment contains two putative BS each for mmu-miR-709 and for mmu-miR-705 as predicted by miRBase (microCosm). [score:1]
We also neglect iii) as we had no experimental evidence for a diffusion of miR-709 in the neural tube. [score:1]
23% (Wnt1 3’UTR + miR-709:0.771 ± 0.037, mean ± sd) relative to the empty vector control. [score:1]
The LNA -modified mmu-miR-709 and mmu-miR-705 detection probes were labeled with [α [35] S]-dATP (GE Healthcare, USA), using the Terminal Transferase Labeling Kit (Roche, Germany) according to the manufacturer’s instructions, with minor modifications: a 1:50 dilution (0.5 μ M) of the unlabeled LNA -modified detection probe, 1 m C i/ m l α [35] S-dATP and no UTP were used in the reaction mixture. [score:1]
From these possible candidate miRNAs (miR-705 and miR-709) were selected by ranking the interactions according to the prediction scores provided by the distinct prediction tools. [score:1]
Radioactive locked nucleic acid (LNA) -based ISH using unlabeled, LNA -modified mmu-miR-709 (Exiqon, Denmark, Cat No 39324-00) and mmu-miR-705 (Exiqon, Cat No 39320-00) detection probes were performed using an ISH protocol as described in [33] with minor modifications: the proteinase K treatment was omitted, pre-hybridization and hybridization of the labeled probes was done in an in situ Hybridization Buffer (Ambion, USA, Cat No B8807G) at 53°C, and post-hybridization washes were done sequentially in 1xSSC, 0.2xSSC and 0.1xSSC at 53° C. Sections were counterstained with Cresyl Violet (0.5%, Sigma) according to standard procedures after exposure for 1–3 weeks. [score:1]
Indeed, co-transduction of HEK-293T cells with the Wnt1 3’UTR sensor vector and miR-709 resulted in an approx. [score:1]
HEK293T (1×10 [5] cells/well) were plated in a 24-well plate and co -transfected 24 hours later with 300 ng of Wnt1 3’UTR-WT or Wnt1 3’UTR-MUT sensor vector, 30 ng of renilla luciferase vector, and mmu-miR-709 (Ambion, Cat No PM11496) or mmu-miR-705 (Ambion, Cat No PM11392) precursor miRNA as indicated in the figures, using Lipofectamine 2000 (Invitrogen) according to the manufacturer’s instructions. [score:1]
We defined a 300 pixel long and 15 pixel wide region from the approximate anterior end the midbrain to the approximate posterior end of the rostral hindbrain (both marked by dashed red lines in Figure  4A) on a darkfield picture taken from a sagittal sections of an E12.5 wild-type embryo hybridized with the radioactive mmu-miR-709 detection probe). [score:1]
Transcription of miR-709 at E12.5 was highest in the midbrain, declined towards the MHB and was lowest in the rostral hindbrain, the region of the hindbrain that is under the influence of the IsO (see Figure  4A). [score:1]
Two candidate miRNAs, miR-705 and miR-709, were identified and analyzed experimentally. [score:1]
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4
[+] score: 76
A previous study has shown that miR-709 is nuclear-enriched and targets other pri-miRNAs in the nucleus, thereby downregulating the expression of their mature forms [31]. [score:8]
Upregulation of miR-709 from promyelocytes to granulocytes correlated with the downregulation of mature miR-20b and miR-92a (Figure 6A); putative binding sites of both pri-miRNA-20b and 92a demonstrated near perfect complementarity to mature miR-709 (Figure 6B). [score:7]
In order to study whether miR-706 can target pri-miRNAs (like miR-709) [31], we transfected cell lines with a miRNA inhibitor and examined mature target miRNA levels. [score:7]
Apart from the validated role of miR-709 in regulating the expression of Myc, knockdown of miR-690 has recently been shown to increase the expression of a key myeloid transcription factor Cebpα[67]. [score:7]
Relevant to our study, miR-709 has previously been shown to target Myc, which is downregulated during myeloid cell differentiation [43]. [score:6]
More recently, mouse-specific miR-709 was found to be enriched in the nucleus to target pri-miR-15a and pri-miR-16, thus regulating the expression of mature miR-15a and miR-16 [31]. [score:6]
We discovered two other predicted pri-miRNA targets of miR-709 based on our in silico analysis using RNAhybrid and anti-correlation of miRNA expression. [score:5]
We observed higher expression of cytoplasmic miR-709 in granulocytes (CT: 20.432) compared to promyelocytes (CT: 21.599) (Additional file 5) suggesting that a greater amount of miR-709 may be present in mature granulocytes to sequester Myc expression. [score:4]
Nuclear expression of miR-709, miR-706, miR-690 and miR-467a* in hemopoietic cell lines. [score:3]
We predicted pri-miRNA targets of the four nuclear-enriched miRNAs: miR-709, miR-706, miR-467a* and miR-690 during mouse granulopoiesis using RNAhybrid [41]. [score:3]
In order to characterize the extent of the nuclear expression of these miRNAs, we analyzed the expression of miR-709, miR-706, miR-690 and miR-467a* in four mouse hemopoietic cell lines: MPRO, EL4, MEL and A20. [score:3]
Predicted pri-miRNA targets of nuclear-enriched miR-709, miR-706, miR-467a* and miR-690. [score:3]
Three of these (miR-706, miR-709 and miR-690) were found to be enriched in the nucleus of all four cell types studied (ratio nuclear:cytoplasmic expression was significantly greater that of the mean nuclear-cytoplasm of controls, p < 0.05). [score:3]
In contrast to the previous finding in mouse liver, we did not observe an anti-correlation between the expression of nuclear miR-709 and cytoplasmic miR-15a/16 in myeloid cells. [score:3]
The retention of miR-709, miR-690 and miR-706 in the nucleus may be important to control the expression of transcription factors or other proteins during granulopoiesis. [score:3]
The nuclear:cytoplasmic expression of miR-709, miR-706 and miR-690 was significantly greater in the nucleus of all four cell lines compared to cytoplasmic-enriched control miRNAs (p < 0.05) (Figure 5C). [score:2]
Both RT-qPCR and western blotting confirm the range of detection and enrichment of nuclear and cytoplasmic fractions (B) Nuclear-enriched miR-709, miR-706, miR-467a* and miR-690 in primary mouse LSK cells, promyelocytes, myelocytes and granulocytes. [score:1]
Both miR-709 and miR-706 are nuclear-enriched throughout granulopoiesis and have putative binding sites of extensive complementarity downstream of pri-miRNAs. [score:1]
All four nuclear-enriched miRNAs, miR-709, miR-706, miR-690 and miR-467a* in hemopoietic cells are mouse specific miRNAs. [score:1]
[1 to 20 of 19 sentences]
5
[+] score: 52
A hypothetical mo del of age -dependent miRNAs regulating LCs development and function is shown in Figure 6. Table 1 miRNAs in aging putative targets function in LC reference miR709↑ RANK LC development and homeostasis↓ 49 IRF8 LC development and homeostasis↓ 29 AhR impair LC maturation 33 miR449↑ TGFβRII LC development and homeostasis↓ 32, 46 RunX3 LC development and homeostasis↓ 30 CSF1R LC development and survival↓ 35 miR9↑ TGFβRII LC development and turnover↓ 32, 46 RunX3 LC development and homeostasis↓ 30 RANK LC development and homeostasis↓ 49 miR10a↓ Gfi1 LC development and homeostasis↓ 28 miR200c↓ C/EBP LC differentiation↓ 31 Langerin LC antigen uptake ↑ 22, 23 Gfi1 LC development and homeostasis↓ 28 miR744↓ TGFβI inhibit LC maturation 32, 46 miR20b↓ RANKL inhibit LC maturation 34 miR205↓ C/EBP LC differentiation↓ 31 The density of LCs in the epidermis is known to decrease with age in mice [21]. [score:19]
A hypothetical mo del of age -dependent miRNAs regulating LCs development and function is shown in Figure 6. Table 1 miRNAs in aging putative targets function in LC reference miR709↑ RANK LC development and homeostasis↓ 49 IRF8 LC development and homeostasis↓ 29 AhR impair LC maturation 33 miR449↑ TGFβRII LC development and homeostasis↓ 32, 46 RunX3 LC development and homeostasis↓ 30 CSF1R LC development and survival↓ 35 miR9↑ TGFβRII LC development and turnover↓ 32, 46 RunX3 LC development and homeostasis↓ 30 RANK LC development and homeostasis↓ 49 miR10a↓ Gfi1 LC development and homeostasis↓ 28 miR200c↓ C/EBP LC differentiation↓ 31 Langerin LC antigen uptake ↑ 22, 23 Gfi1 LC development and homeostasis↓ 28 miR744↓ TGFβI inhibit LC maturation 32, 46 miR20b↓ RANKL inhibit LC maturation 34 miR205↓ C/EBP LC differentiation↓ 31 (A) LCs were isolated using AutoMACS with anti-MHCII-PE and anti-PE microbeadsfollowed by a cell sorter. [score:19]
Thus, upregualated miR-709 and miR-449 in aging LCs may downregulate the expression of IFR and CSFR, causing a deficiency in LCs development in aging mice. [score:7]
Based on the miRNAs potentially linked to LCs development and function, we have further confirmed that miR-709, miR-449 and miR-9 were upregualated in aging, while miR-200c and miR-10a were downregulated in aging by using single TaqMan RT-PCR assays (Figure 5 D). [score:4]
Interestingly, miR-709 and miR-449 also target IFR8 and CSF1R. [score:3]
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6
[+] score: 46
We then focused our study on those miRNAs showing reduced expression in maternal HF fed offspring but excluded those poorly expressed miRNAs (Table 5) plus miR-709, as microarray data suggested that miR-709 had the greatest level of expression in the liver (Additional file 1: Table S1 and Table 6). [score:7]
As miR-709 was the highest expressed miRNA in the liver, it might be an important miRNA for the regulation of hepatic gene expression. [score:6]
MECP2 is a common predicted target for 5 miRNAs including two abundantly expressed miRNAs (miR-709 and miR-122, Fig. 1). [score:5]
Reduced expression of miR-709 (a highly expressed miRNA), miR-122, miR-192, miR-194, miR-26a, let-7a, let7b and let-7c, miR-494 and miR-483* (reduced by ~4.9 fold) was validated by qPCR. [score:5]
Several key proteins involved in epigenetics are predicted targets for miRNAs, in particular, methyl-CpG binding protein 2 are predicted targets for 5 miRNAs (miR-709, let-7s, miR-122, miR-194 and miR-26a) showing reduced levels in maternal HF fed offspring. [score:5]
According to the TargetScan algorithm [12], miR-709 targets include methyl-CpG binding domain protein 6 and methyl CpG binding protein2 (MECP2, Fig. 1). [score:5]
Data from qPCR confirmed the highly expressed miR-709, but also showed marked reduction in expression in maternal HF fed offspring (p < 0.01, Table 6), which was not consistent with microarray results. [score:5]
For example, miR-709 is the most abundantly expressed miRNA in the liver detected with microarray (greater than miR-122). [score:3]
We found that methyl-CpG binding protein 2 was the common predicted target for miR-709, miR-let7s, miR-122, miR-194 and miR-26a using our own purpose-built computer program. [score:3]
At the time of writing, miR-709 was not in the data base of PicTar [55]. [score:1]
We found that ZSWIM3 (zinc finger, SWIM domain containing 3), a protein whose function was yet to be characterised [56], was targeted by 5 miRNAs namely miR-122, miR-192, miR-194, miR-709 and miR-483*. [score:1]
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7
[+] score: 37
The function of miR-709 in pancreas is not clear, whereas it is reported that miR-375-3p is expressed in pancreatic beta cells and regulates the secretion of insulin 27, 28. [score:4]
Expression values of miR-375-3p and miR-709 were determined by the comparative Ct method and normalized using the values of heart and testis set at 1.0, respectively. [score:3]
Expression levels of miR-375-3p and miR-709 were determined by using the comparative Ct methods. [score:3]
MiR-375-3p and miR-709 are highly expressed in pancreas of control mice. [score:3]
In order to identify the possible origin of the radiation -induced miR-375-3p and miR-709 in sera of mice, we analyzed the expressions of miR-375-3p and miR-709 by in various cells and organs of the control animals. [score:3]
MiR-375-3p and miR-709 was highly expressed in pancreas (Fig.   4a and b). [score:3]
Figure 4High expression of miR-375-3p and miR-709 in pancreas. [score:3]
Figure 3MiR-375-3p and miR-709 expression in serum of mice exposed to 7 Gy of X-ray. [score:3]
At 72 h after 7 Gy irradiation the expression of miR-709 in serum was significantly increased as compared with 0 Gy: 3.94-fold (P ≤ 0.05) (Fig.   3b). [score:2]
However, there were no significant differences of the expression of miR-709 in pancreas at 24 h, 48 h and 72 h after 7 Gy irradiation compared with 0 Gy (Fig.   5c). [score:2]
In addition, we investigated the expressions of miR-375-3p and miR-709 in pancreas exposed to 7 Gy of X-rays. [score:1]
This suggests that the high, radiation -induced levels of miR-375-3p and miR-709 in serum may be released from this organ. [score:1]
We found that serum miR-375-3p and miR-709 increased in mice exposed to an X-ray dose of 7 Gy which induced a strong ARS. [score:1]
MiR-375-3p and miR-709 levels increase in serum of mice exposed to 7 Gy of X-ray. [score:1]
The expression of (a) miR-375-3p and (b) miR-709 in serum of mice at 0 h, 24 h, 48 h and 72 h after 7 Gy X-irradiation (each n = 4−7), measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR). [score:1]
These values suggest that miR-375-3p and miR-709 in serum are sensitive and specific biomarkers of exposure to 7 Gy. [score:1]
The origin of miR-709 remains unclear. [score:1]
We chose miR-375-3p and miR-709 as candidate serum biomarkers of a strong ARS because these miRNAs were most frequently reported among increasing 12 miRNAs. [score:1]
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8
[+] score: 31
Description miR-451[39] Upregulated in heart due to ischemia miR-22[40] Elevated serum levels in patients with stablechronic systolic heart failure miR-133[41] Downregulated in transverse aortic constrictionand isoproterenol -induced hypertrophy miR-709[42] Upregulated in rat heart four weeks after chronicdoxorubicin treatment miR-126[43] Association with outcome of ischemic andnonischemic cardiomyopathy in patients withchronic heart failure miR-30[44] Inversely related to CTGF in two rodent mo delsof heart disease, and human pathological leftventricular hypertrophy miR-29[45] Downregulated in the heart region adjacent toan infarct miR-143[46] Molecular key to switching of the vascular smoothmuscle cell phenotype that plays a critical role incardiovascular disease pathogenesis miR-24[47] Regulates cardiac fibrosis after myocardial infarction miR-23[48] Upregulated during cardiac hypertrophy miR-378[49] Cardiac hypertrophy control miR-125[50] Important regulator of hESC differentiation to cardiacmuscle(potential therapeutic application) miR-675[51] Elevated in plasma of heart failure patients let-7[52] Aberrant expression of let-7 members incardiovascular disease miR-16[53] Circulating prognostic biomarker in critical limbischemia miR-26[54] Downregulated in a rat cardiac hypertrophy mo del miR-669[55] Prevents skeletal muscle differentiation in postnatalcardiac progenitors To further confirm biological suitability of the identified miRNAs, we examined KEGG pathway enrichment using miRNA target genes (see ). [score:31]
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9
[+] score: 25
In the present investigation, the majority of differentially regulated miRNAs were primarily up-regulated with only one miRNA down-regulated at 0.13 Gy (miR-365) and five down-regulated at 13 Gy (miR-709, miR-6239, miR-690, let-7k, and miR-1902); no down-regulated miRNAs were found at the intermediate dose levels (0.34–4.3 Gy). [score:12]
No down-regulated miRNAs were found at 0.34, 1.3, or 4.3 Gy, while only one miRNA (miR-365) was down-regulated at 0.13 Gy, and five miRNAs (let-7k, miR-690, miR-709, miR-1902, and miR-6239) were down-regulated at 13 Gy. [score:10]
The remaining eighteen differentially regulated miRNAs identified in the present study (miR-484, miR-677-3p, miR-690, miR-709, miR-1839-3p, miR-1902, miR-2137, miR-3077-5p, miR-3084-3p, miR-3090-5p, miR-3096b-3p, miR-3102-5p, miR-5627-5p, miR-6239, miR-6240, miR-6244, miR-6402, and miR-6538) have not previously been associated with ionizing radiation. [score:2]
Eighteen miRNAs found in the present study have not previously been associated with ionizing radiation, i. e. miR-484, miR-677-3p, miR-690, miR-709, miR-1839-3p, miR-1902, miR-2137, miR-3077-5p, miR-3084-3p, miR-3090-5p, miR-3096b-3p, miR-3102-5p, miR-5627-5p, miR-6239, miR-6240, miR-6244, miR-6402, and miR-6538. [score:1]
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10
[+] score: 25
Other miRNAs from this paper: mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-130a, mmu-mir-186, mmu-mir-200b, mmu-mir-202, mmu-mir-30e, mmu-let-7d, mmu-mir-130b, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-192, mmu-mir-200a, mmu-mir-15a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-19a, mmu-mir-200c, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-466a, mmu-mir-467a-1, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-467b, mmu-mir-669c, 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-574, mmu-mir-466d, mmu-mir-467e, mmu-mir-466l, mmu-mir-669k, mmu-mir-669g, mmu-mir-669d, mmu-mir-466i, mmu-mir-669j, mmu-mir-669f, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-669e, mmu-mir-467g, mmu-mir-467h, mmu-mir-669l, mmu-mir-669m-1, mmu-mir-669m-2, mmu-mir-669o, mmu-mir-669n, mmu-mir-466m, mmu-mir-669d-2, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-669p-2, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-21b, mmu-mir-130c, mmu-mir-21c, mmu-mir-30f, mmu-mir-466c-3
Compared to the control, miR-21 expression level increased 1.33-fold, miR-186 expression level increased 1.36-fold, while miR-709 decreased to 0.58-fold. [score:4]
The expression level change of miR-21, miR-186 and miR-709 was shown in Fig 4A. [score:3]
0175242.g004 Fig 4 A) Expression of miR-21, miR-186 and miR-709 in response to CsA treatment at 1 μg/ml for 24 hours. [score:3]
A) Expression of miR-21, miR-186 and miR-709 in response to CsA treatment at 1 μg/ml for 24 hours. [score:3]
While miR-709 represented the decreased expressed of microRNAs (decreased to 0.168 fold in kidney tissue). [score:3]
MiR-21, miR-186 and miR-709 were selected as the candidate microRNAs to test whether parallel changes in expression level can also be induced in the in vitro cell mo del. [score:3]
There is no report on the effect of miR-709 being related to nephrotoxicity, but miR-709 has been identified as the nuclear-enriched microRNA with the ability to regulate other microRNA biogenesis [33]. [score:2]
Three microRNAs (miR-21, miR-186, and miR-709) and three mRNAs (SMAD7, SMURF1 and BMPR1a) were selected to validate whether the same trend of change will be induced by CsA treatment in HEK 293 cells. [score:1]
The results observed in the HEK 293 cells (miR-21 and miR-186 increased while miR-709 decrease), were similar to the results observed in the animal mo del. [score:1]
One example is miR-709 which is decreased to fold 0.17 in the CsA -treated mice. [score:1]
More interestingly, our results discovered some novel miRNAs that have not been reported to be involved in kidney or CsA, such as miR-186, miR-709, and so on. [score:1]
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11
[+] score: 24
The combinatorial effect of six up-regulated miRNAs (miR-691, miR-709, miR-31-5p, miR-5617-5p, miR-31-3p, and miR-185-3p) leads to the following important signaling pathways such as MAPK signaling, pathways in cancer, Ca [+2] signaling, ubiquitin proteolysis, lysine degradation, endocytosis, glycosaminoglycan biosynthesis (chondroitin sulfate and keratin sulfate), Fc gamma -mediated phagocytosis, amphetamine addiction, bladder cancer, ECM-receptor interaction, steroid biosynthesis, dopaminergic synapse, and steroid hormone biosynthesis using pathways union mode. [score:4]
The expression patterns of miR-31-5p, miR-127-3p, miR-411-5p, miR-322-5p, miR-709, and miR-379-5p were similar to the microarray results in our profiling study among four mice groups namely WT, WT + UVR, TNFα KO, and TNFα KO+UVR following acute UVR treatment (Figure 2A). [score:3]
Some of the miRNAs were significantly down-regulated [miR-196a-5p (p=0.05), miR-709-5p (p=0.003), miR-206-3p (0.001), miR-411-5p (p=0.03)] along with others miR-127-3p, miR-322-5p in UVR -induced SCC samples (n=3) compared to the uninvolved skin (n=3) (Figure 2B). [score:3]
The B. is showing the expression pattern of miRNAs miR-31-5p, miR-196-5p, miR-127-3p, miR-206-3p, miR-411-5p, miR-709-5p, and miR-322-5p in UVR -induced SCC samples from wild type FVB mice. [score:3]
A comparison between WT and WT+UVR group revealed the up regulation of six miRNAs (miR-31-5p, miR-31-3p, miR-709, miR-5617, miR-691, and miR-185-3p) and down regulation of sixteen miRNAs (see Table 1). [score:3]
A. is showing the real time expression pattern of miR-31-5p, miR-127-3p, miR-411-5p, miR-322-5p, miR-709, and miR-379 in WT, WT + UVR, TNFα KO and TNFα KO + UVR mice. [score:3]
Figure 2 A. is showing the real time expression pattern of miR-31-5p, miR-127-3p, miR-411-5p, miR-322-5p, miR-709, and miR-379 in WT, WT + UVR, TNFα KO and TNFα KO + UVR mice. [score:3]
We also observed the suppression of miRNAs in SCC samples compared to uninvolved mice skin for miR-195-5p, miR-127-3p, miR-206-3p, miR-411-5p, miR-709-5p, and miR-322-5p. [score:2]
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12
[+] score: 24
Among the ten miRNAs validated by qRT-PCR, we found that mmu-miR-487b-5p, mmu-miR-709, mmu-miR-182-5p, mmu-miR-214-3p and mmu-miR-467a-3p were up-regulated in HCC-activated Tregs, mmu-miR-142-5p, mmu-miR-30b-5p, mmu-miR-409-3p and mmu-miR-129-5p were down-regulated (P < 0.01), while miR-344e-5p did not change significantly, as shown in Figure 1C. [score:7]
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]
Because miR-487b-5p, miR-709 and miR-467a-3p did not express in human tissue (miRBase 19), we validated the expression levels of the rest six miRNAs. [score:5]
Because miR-487b-5p, miR-709 and miR-467a-3p did not express in human tissue (miRBase 19), we checked the expression levels of the rest six miRNAs in Tregs from peripheral blood samples. [score:5]
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13
[+] score: 15
However, using SAM analysis, we identified a new HF diet -associated miRNA upregulation (miR-466e); additionally, the modulation of miR-709 expression was under the fold-change cut-off value of 1.5 but was potentially associated with HF diet as suggested by SAM analysis. [score:6]
miR-709 was recently described as a tumor-suppressor miRNA targeting Myc, Akt and Ras, which participates in the regulation of apoptosis through the miR-15a/miR-16-1 pathway [80], [81]. [score:6]
A functional analysis of the putative target genes of miR-709 and miR-466e suggested that these miRNAs might be involved in lipid metabolism. [score:3]
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14
[+] score: 13
analysis of the plasma showed upregulation of miR-223-3p and miR-709 in the plasma of SKG mice treated with ß-glucan relative to untreated SKG mice. [score:4]
Upregulation of miR-223-3p, but not of miR-709, was statistically significant. [score:4]
The top five upregulated miRNAs (miR-1195, miR-223-3p, miR-129-2-3p, miR-709, and miR-224-5p) were selected for subsequent analysis, which was performed via quantitative real-time PCR analysis of the plasma from individual mice in each group. [score:4]
Five miRNAs (miR-1195, miR-223-3p, miR-129-2-3p, miR-709, and miR-224-5p), whose levels were found to be significantly elevated in the pooled plasma of ß-glucan -injected SKG mice by panel real-time PCR, were analyzed. [score:1]
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15
[+] score: 13
Figure 5 shows that the miRNAs let-7a-5p, let-7c-5p, miR-122-5p, miR-142-3p, miR-29b-3p, and miR-30c-5p are up-regulated and the miRNA species miR-669n and miR-709 are down-regulated in livers of vaccination -induced self-healing infections on day 11 p. i. in comparison to lethal infections in non-vaccinated mice, thus confirming our microarray analyses. [score:7]
SCLC 26587830 miR-669n −55 Involved in control of LPS -induced macrophage activation 26807181 miR-709 −35 miR-709 may positively regulate invasion and metastasis of HCC through targeting GPC5 25818666 miR-5126 −43 Unknown miR-6538 −53 Unknown To further substantiate these differences in miRNA expression toward the end of the crisis phase, we have also performed quantitative PCR of arbitrarily selected miRNAs. [score:6]
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16
[+] score: 10
Besides, another miRNA, miR-709, could regulate the chemokine signaling pathway by targeting genes belonging to the CCL and CXCL families. [score:4]
MiR-709 could regulate the chemokine signaling pathway and miR-3473a might regulate leukocyte trans-endothelial migration. [score:3]
miRNA Fold change at 3 dpi Fold change at 5 dpi mmu-miR-466h-3p NS (Not significant) 14.311053 mmu-miR-346-5p NS 3.4766614 mmu-miR-877-3p NS 3.416667 mmu-miR-7a-5p NS 2.1413074 mmu-miR-5107-5p NS −2.047792 mmu-miR-3473a −2.2872427 −2.1317267 mmu-miR-150-5p NS −2.1770155 mmu-miR-3473b −3.2475147 −2.282881 mmu-miR-721 NS −2.6864858 mmu-miR-669b-5p NS −2.9408455 mmu-miR-709 NS −3.0065749 mmu-miR-669n NS −3.0094464 mmu-miR-468-3p NS −3.40051 mmu-miR-466m-5p NS −4.33538 mmu-miR-32-3p NS −4.5324426 mmu-miR-466h-5p NS −4.9673104 mmu-miR-3082-5p NS −6.01648 mmu-miR-466i-5p NS −7.6776285 mmu-miR-1187 NS −8.772696 mmu-miR-574-5p NS −9.259378 To confirm the validity of the differentially expressed miRNAs that had been identified by microarray analysis, we performed real-time PCR on all 20 of these miRNAs using the polyA tailing technique. [score:3]
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17
[+] score: 9
Let-7f-2-3p (GD 17.0), miR-30e (GD 18.0), and miR-709 (GD 18.0) were upregulated by flutamide in our experiment, whereas they were upregulated by hyperoxia during the postnatal period [60, 61]. [score:7]
Among these, insulin-like growth factor 1 gene (IGF1) was under positive regulation by androgens through miR-215 on GD 17.0, and through miR-30e, miR-1251, miR-709, miR-344f-3p, and miR-466l-5p on GD 18.0. [score:2]
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18
[+] score: 8
As shown in table 1, 20 microRNAs were significantly deregulated in the knockout mice compared to wild type littermate controls, with three miRNAs differing more than two fold, miR-7 being up-regulated and miR-709 and miR-449b being down-regulated in the antrum of Gastrin knockout mice compared to wild types. [score:8]
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19
[+] score: 8
The miRNA targets that were significantly dysregulated in the array experiments are shown in Table  1. In the whole blood samples, when compared to those with untreated isograft, there were 5 (miR-720, miR-709, miR-2145, miR-1195, and miR-690) and 4 (let-7d, miR-26a, let-7i, and left-7a) downregulated miRNA targets in the mice receiving allograft without and with FK506 treatment, respectively. [score:8]
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20
[+] score: 7
Interestingly, six genes encoding miRNA were upregulated in the K3/pCI group, but only two of them (miR-669o-5p and miR-709) were also upregulated in the 3NF/pCI group. [score:7]
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21
[+] score: 7
In particular, the up-regulation of microRNA-709, microRNA-320 and microRNA-128a, and down-regulation of microRNA-181a-1-3p, microRNA-30b and microRNA-374 were confirmed by RT-PCR (Fig. 3E). [score:7]
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22
[+] score: 6
MiR-709, [83] for example, is upregulated specifically in the transition from p53 wt MEFs to iPS cells, while it is downregulated when p53 is not functional. [score:6]
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23
[+] score: 5
The top 5 high expression value miRNAs were miR-709, miR-29a, miR-210, miR-810 and miR-143; miR-709 was the most highly expressed with a copy number of 23,676 per cell. [score:5]
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24
[+] score: 5
com/1999-4915/8/3/75/s1, Figure S1: Distribution of the number of predicted miR-770-3p targets in viral genomes and expression of miR-770-3p and miR-709 in mouse tissues. [score:5]
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25
[+] score: 5
Tang R. Li L. Zhu D. Hou D. Cao T. Gu H. Zhang J. Chen J. Zhang C. Y. Zen K. Mouse miRNA-709 directly regulates miRNA-15a/16-1 biogenesis at the posttranscriptional level in the nucleus: Evidence for a microRNA hierarchy system Cell Res. [score:3]
mir-709 was already described as a regulator of mir-15a/16 clusters at the post-transcriptional level in the nucleus of a mouse mo del [33]. [score:2]
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26
[+] score: 5
miRNAs were selected based on a combination of p-values and an average expression level of greater than 50% as referenced to miR-709, the highest expressing miRNA in microglia in all three groups. [score:5]
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27
[+] score: 3
Fifteen miRNAs were highly expressed in both liver and brain: miR-709, let-7a, let-7f, let-7c, let-7d, miR-26a, let-7b, let-7g, miR-26b, miR-29a, miR-126-3p, miR-23b, miR-30c, miR-16, and miR-23a. [score:3]
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28
[+] score: 3
A study by Tang et al. had shown that miR-709 is localised in the mouse nucleus and binds to miR-15a/16-1 recognition element and inhibits further processing of miR-15a/16-1 primary transcript (pri- miR-15a/16-1) into miR-15a/16-1 precursor (pre- miR-15a/16-1) [49]. [score:3]
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29
[+] score: 2
Birc5 is predicted to be regulated by miR-27b, miR-125b-3p, miR-150, miR-200a, miR-146a, miR-709, miR-705, and miR-762. [score:2]
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30
[+] score: 2
Other miRNAs from this paper: mmu-mir-138-2, mmu-mir-138-1, mmu-mir-706
Sequence contained within the element matches that of miR-709 at 17/19 positions (mismatches indicated by "+"). [score:1]
Pair-wise alignment identified a 134 basepair common element that contained two microRNA (miRNA) sequences, miR-706 and miR-709 (Fig. 3G). [score:1]
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31
[+] score: 2
For example, miR-709 was the most abundant miRNA in FCx and HP as detected by microarrays. [score:1]
These differences might be partly attributed to the multi-organism probe content on the Affymetrix array, as miR-709 is represented by mouse-specific probe sets, while miR-9 has similar probe sets for 23 different organisms, all of which were called “present” in our dataset. [score:1]
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32
[+] score: 1
MiR-709, miR-1224, and miR-342-3p/5p are increased several-fold in the DP subset, while miR-150 and miR-342-3p are increased in all the thymocyte subsets. [score:1]
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33
[+] score: 1
In aspirin -treated mice exposed to MCS, modulation of 9 miRNAs in both lung and blood serum (miR-30c, miR-181b, miR-183, miR-301a, miR-350, miR-466a/i, miR-500, and miR-709) correlated with protection against pulmonary microadenomas, while no miRNA related to protection against pulmonary adenomas was modulated at the same time in both body compartments. [score:1]
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34
[+] score: 1
However, mmu-miR-709 and mmu-miR-1195 are identical to ribosomal sequences and still valid in the current mirBase release 19. [score:1]
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35
[+] score: 1
Several other studies have studied the role of miR-21, miR-34, miR-9, miR-132, miR-140, miR-148b-3p, miR-210, miR-29a, miR-709 in SC proliferation and migration in vitro 8, 17, 26, 28, 39– 43. [score:1]
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36
[+] score: 1
miRNAs that showed high variance between samples in the microarray show strong consistency between microarray and qPCR (mmu-miR-208b-3p, mmu-miR-3473a, mmu-miR-709). [score:1]
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