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12 publications mentioning mmu-mir-706

Open access articles that are associated with the species Mus musculus and mention the gene name mir-706. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 222
Moreover, dual-luciferase reporter analysis indicated that co -expression of miR-706 significantly inhibited firefly luciferase expression with wild-type but not using the mutant 3′UTR of PKCα or TAOK1 (Fig. 4D). [score:7]
From these experiments, we conclude that miR-706 can directly downregulate the expression of PKCα and TAOK1. [score:7]
Interestingly, the overexpression of miR-706 reduced the H [2]O [2] -induced expression of PKCα and TAOK1, consequently blocking α-SMA expression. [score:7]
All together, these results suggest that miR-706 may directly suppress PKCα and TAOK1 translation by binding to the 3′UTR and thus attenuate the oxidative stress -induced hepatocyte EMT. [score:6]
All together, these results indicated that miR-706 may attenuate hepatic fibrogenesis in vivo via downregulation of PKCα and TAOK1 expression. [score:6]
Additionally, we confirmed our results using the human hepatocyte cell line L02, the murine hepatocyte cell line AML12, and the human hepatic stellate cell line LX-2. We found decreased miR-706 expression in H [2]O [2] -treated L02 and AML12 cells, further confirming that miR-706 is hepatocyte specific and suggesting that its downregulation can lead to increased oxidative stress. [score:6]
The reintroduction of miR-706 significantly inhibited the ROS -induced EMT (Fig. 4A), further indicating that miR-706 downregulation may facilitate oxidative stress -induced hepatocyte mesenchymal transition. [score:6]
miR-706 is expressed mainly in hepatocytes, but not in HSCs, and its expression decreases in fibrotic liver. [score:5]
Expression of miR-706 inhibits the activity of the luciferase reporter containing the wild-type 3′UTR of PKCα and TAOK1. [score:5]
Furthermore, the transcript levels of miR-706 confirmed its expression in isolated hepatocytes from normal control livers, whereas miR-706 expression was significantly decreased in isolated hepatocytes from fibrotic livers. [score:5]
Consistently, miR-706 inhibition significantly increased the expression of PKCα and TAOK1 levels (Supporting Fig. 4B). [score:5]
The potential miR-706 binding targets were predicted using TargetScan (www. [score:5]
Concomitantly, miR-706 inhibition promoted H [2]O [2] -induced expression of PKCα and TAOK1. [score:5]
These findings implied that miR-706 reduces hepatic fibrosis by targeting PKCα and TAOK1 -dependent regulation of the MAPK cascade. [score:4]
Consistent with our results in the human L02 cell line, H [2]O [2] stimulation induced EMT in the AML12 murine hepatocyte cell line and primary hepatocytes, a mechanism associated with the downregulation of miR-706 (Supporting Fig. 3). [score:4]
Moreover, indicated that treatment with miR-706 agomir markedly inhibited α-SMA, Col1a1, PKCα, and TAOK1 expression in livers of CCl [4] -treated mice compared with those injected with control agomir (Fig. 5F). [score:4]
miR-706 is abundant in normal hepatocytes and downregulated in fibrotic hepatocytes. [score:4]
Interestingly, our bioinformatic analysis predicted that PKCα and TAOK1 were potentially regulated by miR-706 (Fig. 4C), and the putative miR-706 binding sites in the 3′-untranslated region (UTR) of PKCα and TAOK1 were predicted, as shown in Fig. 4D. [score:4]
miR-706 is downregulated in fibrotic livers. [score:4]
Supplementary Dataset 1. Supplementary Dataset 2. miR-706 is downregulated during liver fibrosis. [score:4]
Interestingly, we observed that miR-706, a miRNA not yet reported in any liver disorder, was dramatically downregulated in CCl [4] -induced fibrotic livers. [score:4]
Therefore, the regulation of miR-706 expression may be a potentially useful therapeutic approach for attenuating the progression of liver fibrosis. [score:4]
These results indicate that miR-706 may inhibit some pro-apoptotic genes during liver fibrosis, but have no direct effect on overall hepatocyte apoptosis. [score:4]
Since no data were available on the function of human miR-706, we next sought to locate the expression of miR-706 in human hepatocytes. [score:3]
Edges describe inhibitive effects of miR-706 on mRNAs. [score:3]
Similarly, miR-706 was substantially expressed in immortalized mouse and human hepatocyte AML12 and L02 cell lines, but barely detectable in the human stellate cell line LX2 (Fig. 2C). [score:3]
Interestingly, miR-706 expression was scarce in human fibrotic liver and bile duct ligation (BDL) -induced fibrotic liver (Supporting Fig. 2A,C). [score:3]
However, miR-706 agomir did not prevent the increase in expression of Bak1 and Bbc3 induced by CCl [4] treatment (Fig. 6D). [score:3]
Interestingly, the expression of miR-706 was barely detectable in fibrotic liver and non-parenchymal cells. [score:3]
miR-706 inhibits oxidative stress -induced PKCα and TAOK1 signaling cascade. [score:3]
How to cite this article: Yin, R. et al. miR-706 inhibits the oxidative stress -induced activation of PKCα/TAOK1 in liver fibrogenesis. [score:3]
In network, blue box node represented miR-706, and purple nodes represented target mRNAs. [score:3]
Among them, Bax and Bad can be inhibited by adding miR-706 agomir. [score:3]
Furthermore, the inhibition of miR-706 using antagomir aggravated hepatic fibrosis. [score:3]
Interestingly, bioinformatics analysis predicted PKCα and TAOK1 as targets of miR-706. [score:3]
miR-706 inhibits oxidative stress -induced fibrotic related genes in L02 cells. [score:3]
miR-706 expression was examined by RT-PCR (D), * P < 0.05. [score:3]
Restoration of miR-706 expression alleviates hepatic fibrogenesis in vivo. [score:3]
Furthermore, CCl [4] treatment induced increased cleaved Caspase-3 expression, which was not alleviated by miR-706 agomir injection (Fig. 6E). [score:3]
Furthermore, the injection of miR-706 antagomir promoted liver fibrosis characterized by increased α-SMA and Col1 expression, associated with high PKCα and TAOK1 expression (Supporting Fig. 5). [score:3]
We found that miR-706 expression levels in hepatocytes of fibrotic livers was dramatically lower than that of control livers. [score:3]
By ISH, we determined that the expression of miR-706 was located in the nuclei of normal hepatocytes. [score:3]
However, little expression of miR-706 was detected in nonparenchymal cells in both fibrotic and in control livers. [score:3]
The restoration of miR-706 attenuated H [2]O [2] -induced PKCα and TAOK1 protein levels, consequently inhibiting the increase in α-SMA (Fig. 4A). [score:3]
The addition of H [2]O [2] markedly decreased the levels of miR-706 in L02 cells in a time -dependent manner (Fig. 3D) and induced a fibroblast-like phenotype characterized by increased α-SMA expression and decreased albumin expression as assessed by immunofluorescence (Fig. 3E). [score:3]
MiR-706 expression was detected by ISH in human liver adjacent to carcinoma tissue. [score:2]
To further confirm that dysregulation of miR-706 promotes fibroblast-like transformation of hepatocytes, we treated hepatocytes with miR-706 mimics. [score:2]
Mutations were generated in the complementary site that binds to the seed region of miR-706. [score:2]
Restoration of miR-706 expression alleviates hepatic fibrogenesis in vivoWe next investigated whether reintroduction of miR-706 could attenuate CCl [4] -induced hepatic fibrosis in vivo. [score:1]
After 4 weeks of CCl [4] treatment, mice were injected intravenously either with control agomir or miR-706 agomir once per week for a period of 2 weeks. [score:1]
Our results were further validated by the levels of mRNA transcripts for miR-706 using qPCR (Fig. 1B). [score:1]
Furthermore, treatment with miR-706 agomir significantly reduced the mRNA levels of α-SMA, Col1a1, Prkca, and Taok1 in the livers of CCl [4] -treated mice (Fig. 5E). [score:1]
These results indicated that miR-706 was abundant in normal hepatocytes but not in HSCs. [score:1]
These data indicated that miR-706 may attenuate liver fibrosis progression to some extent. [score:1]
293 T cells were co -transfected with NC or miR-706 duplexes and psiCHECKTM-2 Vectors carrying either the wild-type (WT) or the mutant (MUT) 3′UTR of PKCα and TAOK1. [score:1]
L02 cells were transfected with negative control (NC) or miR-706 duplex for 8 h, and then stimulated with 300 μM H [2]O [2] or remained untreated for 48 h before immunoblotting analysis for α-SMA, PKCα, and TAOK1. [score:1]
Since our results showed that H [2]O [2] induced EMT and that this phenomenon was associated with decreased levels of miR-706, we used miR-706 mimics. [score:1]
miR-706 mimic and scrambled oligonucleotides were purchased from Oligobio (China) and transfected into L-02 and AML12 cell lines (ATCC, Manassas, VA) using Lipofectamine 2000 reagent (Invitrogen, USA) according to the manufacturer’s instructions. [score:1]
We then assessed their respective dual luciferase reporter activities after co-transfection with miR-706 mimics or negative control in 293-T cells. [score:1]
In vitro treatment with H [2]O [2] induced human hepatocyte cell line L02 EMT, associated with decreased miR-706. [score:1]
Tissue sections were hybridized to biotin-labeled oligos (Scrambled oligo probe and anti-miR-706), captured with alkaline phosphatase-conjugated streptavidin, and the signal (blue dot) was developed with nitro blue tetrazolium/5-bromo-4-chloro-3-indolyl phosphate (NBT/BCIP), n = 4 in each group. [score:1]
Our miRNA microarray analysis indicated that miR-706 was significantly decreased in fibrotic liver. [score:1]
Altogether, these results revealed that the remission of liver fibrosis can be attributed to the anti-fibrotic role of miR-706 via reversing EMT in hepatocytes. [score:1]
miR-706 sequence and the wild-type and mutant 3′UTR segment of PKCα and TAOK1 are shown. [score:1]
The restoration of miR-706 dramatically reduced the amount of α-SMA associated with lower levels of PKCα and TAOK1. [score:1]
miR-706 has little effect on oxidative stress -induced apoptosis in hepatocytes. [score:1]
Noticeably, the transcript levels of miR-706 were significantly lower in isolated HSCs from both control and fibrotic livers (Fig. 2B, Supporting Fig. 2B). [score:1]
Reintroduction of miR-706 in the liver. [score:1]
Altogether, these results indicated that miR-706 is a hepatocyte-specific and nucleus-rich miRNA. [score:1]
Moreover, miR-706 progressively decreased throughout the 8-week period of CCl [4] treatment (Fig. 1C). [score:1]
CCl [4] -treated mice were randomly divided into four groups after 4 weeks; miR-706 agomir negative control, miR-706 agomir, miR-706 antagomir negative control and miR-706 antagomir. [score:1]
Concomitant with our data, miR-706 was reported as a nuclear-enriched miRNA 48. [score:1]
Briefly, tissue sections were treated with 3% H [2]O [2] at room temperature for 10 min, pre-hybridised in the Exiqon hybridization buffer at 38 °C for 4 h, then hybridised with 20 μL miR-706 probe at 38 °C overnight, washed with 2 × SSC, 0.5 × SSC, and 0.2 × SSC buffers for 10 min at 38 °C, respectively. [score:1]
miR-706 has a minor effect on oxidative stress -induced apoptosis in hepatocytes. [score:1]
These results indicated that miR-706 may attenuate the progression of liver fibrogenesis, particularly at early time-points. [score:1]
Injection of miR-706 agomir increased miR-706 levels in liver tissue (Fig. 5A). [score:1]
Here, we aimed to detect the levels and the location of miR-706 in both CCl [4] -induced fibrotic livers and olive-oil control livers. [score:1]
We found that miR-706 had little effect on H [2]O [2] -induced decreased hepatocyte cell viability and pro-apoptotic genes Bax, Bak1, Bbc3, and Bad (Fig. 6B,C). [score:1]
Oxidative stress -induced hepatocyte EMT is associated with decreased levels of miR-706. [score:1]
Gene transfer of miR-706 prevents CCl [4] -induced liver fibrosis in mice. [score:1]
The 293-T cells (1 × 10 [4] cells/well) transiently transfected with miR-706 (50 nM) or miR-control (50 nM) were seeded in 96-well plates. [score:1]
In contrast to previous studies, we provided new evidence for the functional role of miR-706 in both murine and human liver fibrosis. [score:1]
Quantitative real-time PCR of miR-706, α-SMA, col1a1, taok1, prkca, bax, bad, bak, and bbc3 was performed using SYBR Green Master mix on a 7500 system (Applied Biosystems, Foster City, CA). [score:1]
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[+] score: 123
Inhibition of miR-706 in MEL and MPRO cells, however, did not result in significant accumulation of predicted miRNA targets, indicating either these miRNAs are not the actual targets or nuclear miR-706 may not function by targeting pri-miRNA transcripts. [score:9]
Alternatively, since the miRNA inhibitor was expressed in the cytoplasm, it is possible that there was little to no reduction in nuclear miR-706 expression levels in these cells. [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]
Figure 7 The effect of miR-706 inhibition on the expression of putative target miRNAs and mRNAs in MEL and MPRO cells. [score:7]
It is therefore possible that retention of miR-706 in the nucleus, which would result in decreased cytoplasmic miR-706 expression, may act to fine-tune expression of target genes such as Stat1. [score:7]
However, inhibition of miR-706 function did not lead to a significant increase in the expression of predicted miRNA targets in MEL cells (Figure 7C). [score:7]
Downregulation of nuclear-enriched miR-706 from promyelocytes to granulocytes occurred in conjunction with the upregulation of 7 mature miRNAs (Figure 6A). [score:7]
Knockdown of miR-706 resulted in a significant upregulation of Stat1 by 6 to 8-fold in both cell lines, indicating its role in the regulation of this transcription factor (P < 0.05) (Figure 7D). [score:6]
MEL and MPRO cells were transfected with the 2′-O-methylated miRIDIAN mmu-miR-706 hairpin inhibitor (Thermo Scientific) or the miRIDIAN miRNA hairpin inhibitor transfection control with Dy547. [score:5]
T-tests were also used to compare the expression of Stat1 in cell lines transfected with miR-706 inhibitors and control. [score:5]
Analysis of miR-706 levels showed no significant decrease in expression, suggesting that this inhibitor may form a heteroduplex (Figure 7C). [score:5]
We therefore determined its expression in myeloid cell lines MEL and MPRO following inhibition of miR-706. [score:5]
miR-706 has previously been shown to regulate the expression of myeloid transcription factor Stat1[44]. [score:4]
Consistent with others [44], we have shown that miR-706 regulates the expression of Stat1; a transcription factor involved in myeloid differentiation. [score:4]
Predicted pri-miRNA targets of nuclear-enriched miR-709, miR-706, miR-467a* and miR-690. [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]
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]
Inhibition of miR-706 function. [score:3]
Notably, the primary transcript of miR-142-3p, a miRNA recently found to be important in promoting granulopoieisis, was amongst the putative targets of miR-706 (Figure 6B). [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]
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]
Nuclear expression of miR-709, miR-706, miR-690 and miR-467a* in hemopoietic cell lines. [score:3]
Whether miR-706 and other nuclear-enriched miRNAs target pri-miRNAs during hemopoiesis remains to be determined. [score:3]
Analysis of miR-706 knockdown in MPRO cells showed a ~1.5-fold increase in miR-192 levels, however this increase was not statistically significant (Figure 7C). [score:2]
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]
It is interesting to note the enrichment of miR-706 and miR-467a* in the nucleus of primary mouse hemopoietic cells and cell lines because these miRNAs have not been reported as being nuclear-enriched in other cell types [23- 31]. [score:1]
Amongst these 6 miRNAs, miR-706 and miR-467a* (now renamed miR-467a-3p) had nuclear:cytoplasmic ratios > 1 in promyelocytes (Additional file 5). [score:1]
Of these 7 miRNAs, miR-142 and miR-192 possessed putative binding sites in their primary transcripts that demonstrated near perfect binding to mature miR-706 (Figure 6B). [score:1]
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]
There were four nuclear-enriched miRNAs that are ubiquitously present in mouse hemopoietic cells, including two miRNAs, miR-467a* and miR-706 that have never been reported to be nuclear-enriched. [score:1]
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[+] score: 66
Other miRNAs from this paper: mmu-let-7g, mmu-let-7c-1, mmu-mir-3472
Predicted 3′-untranslated region (UTR) target binding sites for miR-706 were compared across 4 target prediction databases: miRanda, miRDB, miRWalk, and TargetScan. [score:8]
Putative miR-706 targets were then crosschecked with the transcript list generated from the microarray to determine whether putative miR-706 targets were dys-regulated in maternal obese (Mat-Ob) offspring adipose tissue. [score:6]
Of these 2 validated targets, we focused our studies on miR-706, because detailed information on miR-3472 and its targets was not available at the time of analysis. [score:5]
E, Target sequence and mutated target sequence of miR-706 on IL-33 3′-UTR subcloned in a pGL3-enhancer vector (pGL3-IL33 3′-UTR-wt and pGL3-IL-33 3′-UTR-mut, respectively). [score:5]
Luciferase reporter constructs were generated by subcloning either the IL-33-3′-UTR target sequence of miR-706 or a mutated IL-33-3′-UTR target sequence downstream of the luciferase gene in a pGL3-control vector (Promega). [score:5]
We then used a luciferase reporter system to show that there was a direct interaction between miR-706 and its putative target sequence within the 3′-UTR of IL-33. [score:4]
The complete spectrum of targets of miR-706 in adipose tissue and the phenotype consequences of its dysregulation are unknown. [score:4]
The expression of Wnk1 did not differ between the 2 experimental groups (Figure 6D), suggesting miR-706 is regulated independently of its host in this mo del. [score:4]
A significant down-regulation of miR-706 and miR-3472 was confirmed in Mat-Ob offspring; there was no significant difference let-7c-1-3p between the 2 groups (Figure 6A). [score:4]
We searched for potential miR-706 targets using the miRWalk miRNA database, as described in. [score:3]
Upon exposure to miR-706 mimetic, cells bearing the IL-33 constructs showed an inhibition in luciferase activity. [score:3]
Putative targets of miR-706 and miR-3472 were scanned using the microRNA database miRWalk (21). [score:3]
HeLa cells were transfected with luciferase constructs containing the target sequence for miR-706 in the 3′-UTR (Figure 6E). [score:3]
This was indeed the case for 2 putative targets of miR-706: CAMK1D and IL-33, both of which are involved in inflammatory signaling and were found to be significantly elevated at the protein level in adipose tissue from programmed offspring. [score:3]
F, Normalized luciferase activity of the wild-type (pGL3-IL-33 3′-UTR-wt) and mutant (pGL3-IL33 3′-UTR-mut) IL-33 3′-UTR/miR-706 binding site in HeLa cells after negative control (NC) or miR-706 mimic transfection (n = 6 per group); *, P <. [score:1]
Of the programmed miRNAs identified in this study, we demonstrated that miR-706 had biological actions that were consistent with a programmed inflammatory phenotype. [score:1]
miR-706 lies within intron 1 of its host gene WNK lysine -deficient protein kinase 1 (Wnk1). [score:1]
Luciferase activity in lysates of cells transfected with the mmu-miR-706 mimic was normalized by the signal acquired in the respective negative control transfection. [score:1]
Cells were cotransfected with 10nM mmu-miR-706 mimic or a negative control RNA (Life Technologies). [score:1]
The data from the current study suggest a mechanistic role for miR-706 in contributing to the inflammation in adipose tissue programmed by maternal obesity. [score:1]
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[+] score: 49
In the present study, our results show that down-regulation of caspase-3, a putative target of miR-706, combined with the high level of miR-706 and down-regulation of miR-542-3p expression, suggests cellular apoptosis may to some extent be inhibited in S. japonicum infected mice. [score:13]
Further analysis using qRT-PCR indicated that the levels of three selected target genes were inversely related to the levels of the corresponding miRNAs in plasma or liver of mice infected with S. japonicum (Figure  6), suggesting miR-706, miR-210-5p, and miR-134-5p regulate the expression of genes encoding their respective targets (Caspase-3, Bnip3, and Creb1, respectively) during S. japonicum infection of the final host. [score:8]
Moreover, we found that S. japonicum infection up-regulated miR-706 levels in the plasma of infected mice, and miR-706 and miR-542-3p co-regulate target genes according to DAVID analysis. [score:7]
To investigate the link between altered levels of miRNAs and the expression of putative targets, qRT-PCR was performed to determine the expression of the genes encoding Caspase-3 for miR-706 [20], cAMP responsive element binding protein 1 (Creb1) for miR-134 [21], and Bcl2/adenovirus E1B interacting protein 3 (Bnip3) for miR-210 [22] in S. japonicum infected mice. [score:5]
Interestingly, miR-706 regulates cell differentiation, and up-regulation of miR-706 decreases vesicular stomatitis virus -induced apoptosis in BHK cells [20]. [score:5]
In particular, the altered levels of miR-706 and miR-134-5p were associated with altered levels of expression of the Caspase-3 and Creb1 genes, respectively, which may serve as important mediators of the pathology of hepatic schistosomiasis. [score:3]
Among them, it is noteworthy that the level of mmu-miR-706 was inversely related to that of its target gene Caspase-3 in the plasma and livers of mice infected with S. japonicum at 25 dpi. [score:3]
In particular, the altered levels of miR-706 and miR-134-5p were associated with altered levels of expression of the Caspase-3 and Creb1 genes, respectively, suggesting that circulating miRNAs may serve as important mediators of the pathology of hepatic schistosomiasis. [score:3]
Although the level of mmu-miR-706 in the plasma of S. japonicum infected mice was increased, we did not observe obvious increase (Figure  3). [score:1]
Eight altered levels of miRNAs (let-7b-3p, miR-1194, miR-134-5p, miR-1981-3p, miR-210-5p, miR-542-3p, miR-706, and miR-92a-2-5p) were selected for qRT-PCR analysis. [score:1]
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[+] score: 25
Other miRNAs from this paper: mmu-mir-138-2, mmu-mir-138-1, mmu-mir-709
In the middle and posterior bulb, Zcsl3 is expressed in a gradient that extends from dorsal to ventrolateral, while a probe containing the miR-706 sequence is expressed in a subset of cells that span a similar region. [score:5]
The expression pattern we observed may therefore reflect the expression of miR-706 pri-miRNA. [score:5]
We obtained locked nucleic acid (LNA) -modified oligos corresponding to miR-706 and miR-138 (a control miRNA known to be expressed in the bulb; [32]). [score:3]
The pattern is distinct from miR-706, with no punctate expression. [score:3]
E) Expression pattern using a dig-labeled LNA-oligo corresponding to miR-706. [score:3]
H) The remainder of the element corresponds to sequence upstream of the presumed pri-miRNA (shown as dashed lines and filled circles) of miR-706. [score:1]
The pattern of the miR-706 probe suggests, however, that miRNAs may also be present selectively within subsets of cells in a spatially distinct fashion. [score:1]
The remainder of the 134 bp element was ~ 95% identical to sequence immediately upstream of the miR-706 sequence [31], corresponding to what we assume is part of the primary miRNA (pri-miRNA) sequence for miR-706 (Fig. 3H). [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]
For miR-706, a subset of the cDNAs matched the sequence perfectly, with others matching at 21/22 or 20/22 positions. [score:1]
Although the signal for the miR-706 probe was weaker than that of the common element, punctate signal was also observed in the nascent EPL/GL in a similar pattern as well (compare Fig. 3A with 3E). [score:1]
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[+] score: 7
The most significantly downregulated (mmu-miR-31, mmu-miR-455, mmu-miR-744, mmu-miR-695, mmu-miR-181a, mmu-miR-181d, mmu-miR-182, mmu-miR-190, mmu-miR-194) and upregulated miRNAs (mmu-miR-34c, mmu-miR-124, mmu-miR-142–3p, mmu-miR-706, mmu-miR-29c) were analyzed. [score:7]
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[+] score: 6
Yin R Guo D Zhang S Zhang X miR-706 inhibits the oxidative stress -induced activation of PKCalpha/TAOK1 in liver fibrogenesisSci. [score:3]
MicroRNA-706 is downregulated in hepatocytes but unchanged in non-parenchymal cells under oxidative stress [47]. [score:3]
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[+] score: 4
Using a similar approach, we identified that the most upregulated circulating miRNAs in the mouse cMPs fraction following CS (heat map in Fig. 2B) were miR-142, miR-126, and miR-706 (Supplementary Table 3). [score:4]
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[+] score: 3
Additionally, prior studies from various mo dels of retinal degeneration identified over 300 differentially expressed miRNAs 63– 90, a total of 16 common miRNAs were identified (miR-1187, miR-125b-5p, miR-331-3p, miR466d-3p, miR-467f, miR-542-3p, miR-574-5p, miR654-3p, miR669h-3p, miR-882, miR-342-3p, miR-466a-5p, miR-466d-5p, miR-706, miR-345-3p, miR532-5p). [score:3]
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[+] score: 3
Although the impact of miRNAs on Star expression has yet to be examined, one prospective miRNA (mmu-miR-706) site has already been identified within the 3′-UTR of rodent Star mRNA [19], [32]. [score:3]
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[+] score: 3
The results presented in Fig.   1 confirm a drastic overexpression of miR-181, miR-137, miR-199, miR-706 and miR-719 and repression of miR-155 in Cbx7 KO MEFs in comparison with the WT ones. [score:3]
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[+] score: 1
The top 5 fold-increased miRNA were miR-124 (450-fold), miR-706 (345-fold), miR-801 (171-fold), miR-685 (109-fold) and miR- 494 (93-fold). [score:1]
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