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79 publications mentioning mmu-mir-134

Open access articles that are associated with the species Mus musculus and mention the gene name mir-134. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 208
Then we asked whether down-regulation of Dicer1 led to down-regulation of miR-128, miR-134 and miRNA-330, and consequently up-regulation of Mmp3/Mmp10/Mmp13 particularly? [score:10]
We found that knockdown of Dicer1 expression resulted in downregulation of miR-128/miR-134/miRNA-330 and upregulation of Mmp3/Mmp10/Mmp13 (Figure 4C). [score:10]
Murine miR-128, miR-134, and miR-330 directly target and inhibit Mmp3, Mmp10, and Mmp13, respectivelyTo predict whether miRNAs target Mmp3, Mmp10, and/or Mmp13 in murine colon cancer cells, we first utilized the bioinformatics algorithms TargetScan, miRWalk, microRNA. [score:10]
Furthermore, we indicated that knockdown of Dicer1 resulted in downregulation of miR-128/miR-134/miRNA-330 and upregulation of Mmp3/Mmp10/Mmp13 (Figure 4C). [score:8]
MiR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells in vitro and in vivoSince miR-128, miR-134, and miR-330 can target Mmp3, Mmp10, and Mmp13, respectively and are downregulated in the inflammation-cancer link, we next explored the functions of miR-128, miR-134, and miR-330 with respect to their contributions to the tumorigenic potential of the CT26. [score:8]
Because overexpression of miR-128, miR-134, or miR-330 could inhibit tumorigenesis in vitro, we next asked whether these miRNAs could inhibit the metastatic potential of CT26. [score:7]
Gapdh was used as the internal control, and the expression values of “mimics or inhibitor control” were set as 1. (D) Transfection with miR-128, miR-134, or miR-330 mimic decreased Mmp3, Mmp10, and Mmp13 protein levels, respectively, whereas transfection with the miR-128, miR-134, or miR-330 inhibitor increased Mmp3, Mmp10, and Mmp13 levels, respectively, in CT26. [score:7]
Figure 5miR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells and inhibit tube formation of endothelial cells in vitro (A) showing that miR-128, miR-134, and miR-330 suppressed the migration of CT26. [score:7]
Murine miR-128, miR-134, and miR-330 directly target and inhibit Mmp3, Mmp10, and Mmp13, respectively. [score:6]
These results provided evidence that each of miR-128, miR-134, and miR-330 directly recognizes the respective 3′-UTR of the Mmp3, Mmp10, and Mmp13 mRNAs and thereby inhibits their translation. [score:6]
Since miR-128, miR-134, and miR-330 can target Mmp3, Mmp10, and Mmp13, respectively and are downregulated in the inflammation-cancer link, we next explored the functions of miR-128, miR-134, and miR-330 with respect to their contributions to the tumorigenic potential of the CT26. [score:6]
A total of 3761, 1020, and 1686 possible targets for miR-128, miR-134, and miR-330, respectively, were predicted by TargetScan, miRWalk, and miRanda. [score:5]
miR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells and inhibit tube formation of endothelial cells in vitro. [score:5]
WT cells overexpressing miR-128, miR-134, or miR-330 inhibited tube formation. [score:5]
We then used DAVID Resources Analysis Tools to classify the function of these target genes, revealing that most target genes of miR-128, miR-134, and miR-330 are involved in signaling pathways such as MAPK, Wnt, TGF-β, and mTOR and in the function of adherens junctions (Figure 3C), all of which are important for tumorigenesis. [score:5]
Overexpression of the miR-128, miR-134, or miR-330 mimic clearly delayed wound gap closure compared with each mimic control, whereas knockdown of miR-128, miR-134, or miR-330 using the corresponding miRNA inhibitor had the opposite effect (Figure 5A). [score:5]
To verify whether Mmp3, Mmp10, and Mmp13 are direct targets of miR-128, miR-134, and miR-330, respectively, we used a luciferase assay to test the binding of each miRNA to the respective gene's 3′ untranslated region (UTR). [score:5]
These observations suggested that miR-128, miR-134, and miR-330 can suppress the migration, invasion, and proliferation of murine colon cancer cells in vitro and that they also can inhibit endothelial cell tube formation to some extent. [score:5]
The matrigel invasion assay showed that overexpression of the miR-128, miR-134, or miR-330 mimic inhibited the in vitro invasive potential of CT26. [score:4]
Mmp3, Mmp10, and Mmp13 are direct targets of murine miR-128, miR-134, and miR-330, respectively. [score:4]
Figure 3 Mmp3, Mmp10, and Mmp13 are direct targets of murine miR-128, miR-134, and miR-330, respectively (A) Scheme for the potential binding site of miR-128, miR-134, and miR-330 in the 3′-UTR of Mmp3, Mmp10, and Mmp13 and the sequence of each intact miR-128, miR-134, and miR-330 binding site (wild-type, wt) and its mutant (Mut) within the luciferase reporter vector. [score:4]
Inflammation -dependent downregulation of miR-128, miR-134, and miR-330 during murine CAC progression and an inverse correlation with the levels of Mmp3, Mmp10, and Mmp13. [score:4]
The mechanism responsible for the downregulation of miR-128, miR-134, and miR-330 during CAC progression. [score:4]
Transfection of cells with Mmp3, Mmp10, or Mmp13 rescued the angiogenic capabilities of cells overexpressing miR-128, miR-134, or miR-330. [score:3]
The functions of these miRNAs were assessed by transfecting the cells with miR-128, miR-134, and miR-330 mimics (or the corresponding chemically synthesized miRNA inhibitors). [score:3]
Further, immunohistochemical staining revealed that transfection with the miR-128, miR-134, or miR-330 mimic resulted in decreased expression of Mmp3, Mmp10, or Mmp13, respectively, within tumors (Figure 6E). [score:3]
We next searched for possible target genes of miR-128, miR-134, and miR-330 using web -based bioinformatics algorithms. [score:3]
miR-128, miR-134, and miR-330 suppress the metastasis of murine colon cancer cells in a nude mouse xenograft mo del. [score:3]
As shown in Figure 5C, overexpression of the miR-128, miR-134, or miR-330 mimic attenuated CT26. [score:3]
MiR-128, miR-134, and miR-330 suppress the tumorigenicity of murine colon cancer cells in vitro and in vivo. [score:3]
miR-128, miR-134, and miR-330 suppressed the luciferase activity of Mmp3, Mmp10, and Mmp13, respectively, in luciferase wild-type reporter constructs. [score:3]
These results suggested that murine miR-128, miR-134, and miR-330 target Mmp3, Mmp10, and Mmp13, respectively. [score:3]
MiR-128, miR-134, and miR-330 overexpression in murine colon cancer cells attenuated the ability of the cells to proliferate, migrate, and invade other tissues. [score:3]
These results indicated that miR-128, miR-134, and miR-330 can suppress the metastasis of murine colon cancer cells to lung. [score:3]
WT cells with miR-128, miR-134, or miR-330 mimics resulted in decreased expression of Mmp3, Mmp10, or Mmp13, respectively, within the resulting tumors. [score:3]
WT and found that the miR-128, miR-134, and miR-330 mimics reduced the levels of Mmp3, Mmp10, and Mmp13 mRNAs, respectively, whereas each of the inhibitors increased Mmp3, Mmp10, and Mmp13 levels, respectively (Figure 2C). [score:3]
Figure 3B shows that addition of in vitro transcribed miR-128, miR-134, and miR-330 mimics significantly suppressed the luciferase activity of the Mmp3, Mmp10, and Mmp13 3′-UTR upon cotransfection with the luciferase vector (wild-type, mutant, or blank control) with the in vitro transcribed miRNA (miR-128, miR-134, miR-330, or control) mimics into human embryonic kidney (HEK293) cells. [score:3]
Furthermore, the expression levels of miR-128, miR-134, and miR-330 correlated negatively with those of Mmp3, Mmp10, and Mmp13, respectively, in a macrophage mo del of inflammation (r = –0.578, r = –0.65, r = –0.668, respectively; Figure 2E). [score:3]
In the present study, we identified miR-128, miR-134, and miR-330 as negative regulators of Mmp3, Mmp10, and Mmp13, respectively. [score:2]
Moreover, nude mice injected with cells overexpressing miR-128, miR-134, or miR-330 mimic had significantly fewer macroscopic lung metastases compared with the mimic controls (Figure 6D). [score:2]
We thus assessed the intracellular levels of Dicer1 and Drosha in RAW264.7 macrophages to verify whether their dysregulation played a role in the observed decrease in miR-128, miR-134, and miR-330 levels during CAC progression. [score:2]
WT cells overexpressing miR-128, miR-134, or miR-330 when compared with that of the control group cells. [score:2]
When compared with normal colonic tissues, there was a significantly decreased expression of miR-128, miR-134, and miR-330 detected in the colorectal cancer specimens (Supplemental Figure 1B, right). [score:2]
MiR-128, miR-134, and miR-330 have been reported to play substantive roles in regulating cell proliferation, survival, motility, apoptosis, and invasion [31– 35]. [score:2]
In addition, we assayed the expression levels of miR-128, miR-134, and miR-330 in human colorectal cancer and normal colonic tissues. [score:2]
revealed that miR-128, miR-134, and miR-330 decreased the levels of Mmp3, Mmp10, and Mmp13, respectively (Figure 2D). [score:1]
Thus we tested the effect of miR-128, miR-134, and miR-330 on the metastasis-related aspects in murine colon cancer cells. [score:1]
There was perfect base pairing between the seed sequence of mature miR-128/miR-134/miR-330 and the 3′-UTR of Mmp3/Mmp10/Mmp13 mRNAs, respectively. [score:1]
To assess the effect of each miRNA (miR-128, miR-134, miR-330) on tumor metastasis, CT26. [score:1]
Cells that had been transfected with an miR-128, miR-134, or miR-330 mimic or control mimic were injected into the tail vein of nude mice, and the efficiency of transfection was verified (Figure 6A). [score:1]
WT cells transfected with the miR-128, miR-134, and miR-330 mimics or mimics control. [score:1]
WT) transfected with miR-128, miR-134, or miR-330 mimics or mimics control. [score:1]
WT cells that had been transfected with miR-128, miR-134, and miR-330 mimics (or mimics control) were injected into the tail vein of nude mice. [score:1]
As shown in Figure 3A, two miR-128 -binding sites were identified in the 3′-UTR of Mmp3 mRNA, and likewise one miR-134 -binding site was identified for Mmp10 mRNA and one miR-330 -binding site was identified for Mmp13 mRNA. [score:1]
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2
[+] score: 195
Combining FIR treatment with miR-134 overexpressed ECFCs reversed this decrease in NRIP1 expression and results in a similar level of expression to that found in the vector control (Fig 5F). [score:7]
In contrast, DM or HG treatment leads to miR-134 upregulation in ECFCs and a decrease in NRIP1 expression. [score:6]
Previous studies have suggested that miR-134 overexpression promotes neuronal cell death and apoptosis by regulating response element -binding protein (CREB) signaling and targeting heat shock protein A12B (HSPA12B) [59, 60]. [score:6]
At day 0 after injection, miR-134 and NRIP1 were detected using RT-qPCR to confirm that miR-134 expression was reduced and NRIP1 expression was increased by FIR (S10A Fig). [score:5]
The 135 genes were subject to miRTar to narrow down the putative targets of miR-134 and 35 putative targets were identified (Fig 5A). [score:5]
These results suggest that FIR treatment is able to reduce miR-134 expression, which in turn enhances the downstream expression level of NRIP1. [score:5]
Overexpression of miR-134 in dfECFCs (S8B Fig) results in a reduction of 90% in NRIP1 expression (Fig 5E). [score:5]
We next explored whether FIR improved the activities of HG-dfECFCs and dmECFCs via an inhibition of miR-134 expression. [score:5]
NRIP1 is a direct target of miR-134. [score:4]
The increase in cell migration and tube formation activities caused by miR-134 inhibition was reduced by NRIP1 knockdown in dfECFCs (Fig 6D). [score:4]
These results suggest that NRIP1 is a direct target of miR-134 and is involved in ECFCs functioning. [score:4]
These findings suggested that miR-134 directly targets the 3’ UTR of NRIP1 to attenuate angiogenic activity of ECFCs in vitro. [score:4]
We explored how NRIP1 regulates ECFC activities and is the target of miR-134 in this study. [score:4]
The findings were similar to that of ECFCs with only miR-134 overexpression leading to a decrease in cell migration and tube formation (S4E Fig). [score:3]
We next used a 3’UTR luciferase reporter assay to clarify the direct targeting of NRIP1 by miR-134. [score:3]
miR-134 overexpression repressed the luciferase activity of the wild type NRIP1 3’UTR, but this reduction was reversed using a mutated NRIP1’s 3’UTR (Fig 5J). [score:3]
Validation of the putative downstream targets of miR-134. [score:3]
However, only miR-370 and miR-134 show enhanced expression levels in dmECFCs. [score:3]
In addition, ECFCs from DM patients also expressed higher level of miR-134 than DF subjects. [score:3]
Overexpression of miR-134, but not of miR-370, in dfECFCs results in decreased cell migration and poorer tube formation ability (Fig 3A). [score:3]
At 48 hours prior to transplantation, we overexpressed a vector control and miR-134 in the HG-dfECFCs. [score:3]
Cell motility and microvasculature formation were then determined and it was found that miR-134 reduced cell migration by 34% and tube formation ability by 51%, while overexpression of miR-370 in dfECFCs resulted in no significant change (Fig 3A). [score:3]
Inhibition of miR-134 Protects Against Hydrogen Peroxide-Induced Apoptosis in Retinal Ganglion Cells. [score:3]
S8 Fig (A) Validation of the putative miR-134 target genes by RT-qPCR in dfECFCs with or without FIR treatment. [score:3]
Scale bar: 50 μm (B) The expression levels of miR-134 under osmotic culture condition (NG) or under high glucose condition (HG) treated with scramble control and miR-134 antagomir (Anti-134) in dfECFCs as quantified by RT-qPCR. [score:3]
S7 Fig (A) The expression of miR-134 at indicated days after FIR treatment in HG-dfECFCs. [score:3]
In renal cell carcinoma cells, miR-134 also modulates the MAPK/ERK pathway and acts as a tumor suppressor [71]. [score:3]
The effect of miR-370 and miR-134 overexpression on dfECFCs or HUVECs. [score:3]
Among the top 10 enhanced genes that are putative miR-134 targets, 6 genes were reported to be involved in diabetes or angiogenesis. [score:3]
Inhibition of miR-134 did not increase cell migration and tube formation in NG-dfECFCs. [score:3]
The expression of miR-134 was reduced by FIR and was persistent from day1 to day 10 after FIR treatment (S7A Fig). [score:3]
Furthermore, NRIP1 expression not only significantly increased in both antagomir treated NG-dfECFCs and HG-dfECFCs (Fig 5G and S8C Fig), but also in dmECFCs with miR-134 antagomir treatment (Fig 5H). [score:3]
Overexpression of miR-134 in the FIR -treated HG-dfECFCs (the “miR-134 + FIR”) reduced the flow ratio to 0.67 on day 7 and 0.77 on day 14 (Fig 7B). [score:3]
Inhibition of miR-134 in dmECFCs at 2.7 fold (Fig 3D) improved the migration and microvasculature formation activity of these cells by 3 fold and 2 fold, respectively (Fig 3E). [score:3]
The decreased angiogenic activity caused by miR-134 overexpression was found to be rescued by FIR treatment (Fig 4E). [score:3]
Mice were arbitrarily arranged into four groups for different treatments: EGM2 medium, HG-dfECFCs, FIR treated HG-dfECFCs and FIR treated HG-dfECFCs with miR-134 overexpression. [score:3]
S10 Fig (A) Validation of the expression levels of miR-134 and NRIP1 in each group of ECFCs by RT-qPCR on day 0. * p < 0.05 by one-way ANOVA followed by Tukey’s post-hoc test. [score:3]
After overexpression of these two miRNAs in dfECFCs, miR-370 and miR-134 were 11-fold and 3.6-fold increased respectively (S4A Fig). [score:3]
Small RNA sequencing and RT-qPCR reveal high level of expression of miR-134 in HG-dfECFCs and dmECFCs. [score:3]
In this study, we are the first to provide the evidence that FIR treatment suppresses miR-134, which is induced under HG condition. [score:3]
Microarray analyses reveal that NRIP1 was the miR-134 target. [score:3]
We focused on genes that were enhanced by FIR (Fig 5A) and predicted targets of miR-134 using SVMicrO. [score:3]
0147067.g005 Fig 5 (A) A Venn diagram shows the principle used to filter the target genes of miR-134. [score:3]
We detected miR-134 expression using RT-qPCR in dfECFCs from four subjects treated with or without FIR and found that the level of miR-134 was decreased after FIR treatment in four independent experiments (Fig 4C). [score:3]
miR-134 regulates ECFC motility and microvasculature formation ability. [score:2]
We validated these miRNA expression levels using four DF subjects’ ECFCs incubated under NG and HG condition and found that miR-370, miR-183-5p and miR-134 were increased under the HG condition compared to the NG treatment condition (Fig 2C), whereas the other seven miRNAs showed no statistically significant change (S3 Fig). [score:2]
However, miR-134 overexpression in ECFCs did not alter their cell proliferation rate based on the results from the MTT assays or result in cell cycle arrest based on the flow cytometry analysis. [score:2]
To knock down miR-134 in ECFCs, commercial synthetic antagomir with chemical modification (2'-OMe -RNA backbone, first two and last four bases phosphorothioated, 3’-cholesterol tail) (RiboBio Co. [score:2]
However, knock-down of miR-134 partially restored the reduced functionality of HG-dfECFCs (Fig 3C and S5 Fig). [score:2]
Our results and previous studies both show that decreased ECFC proliferation in DM and in high glucose condition, but it seems that this occurs in a miR-134-independent manner. [score:1]
Vec, plasmid control; Scr, scramble; Anti-134, miR-134 antagomir. [score:1]
These findings suggested that FIR is able to reduce miR-134 to promote the functions of ECFCs and this effect could be persisted at least 10 days. [score:1]
We have also identified that HG increases three miRNAs in ECFCs, namely miR-370, miR-183-5p and miR-134. [score:1]
Next we used an oligonucleotide antagomir to reduce the level of miR-134 in dfECFCs under NG and HG treatment conditions (Fig 3B). [score:1]
a 2.4 fold decreased in NG-dfECFCs) because the original level of miR-134 was higher in HG-dfECFCs. [score:1]
The expression level of miR-134 was measured by qPCR after 48 hours. [score:1]
The reduction of miR-134 results in increasing NRIP1 level and thus improves the angiogenic activities of ECFCs in vitro. [score:1]
We next used a double manipulation approach to confirm the relationship between FIR and miR-134 (Fig 4D). [score:1]
Mice in the FIR treated HG-dfECFCs group (the “Vec + FIR” group) presented with more CD31 [+]/PKH-26 [+] double -positive cells (white arrowheads) in the capillaries of the limb muscle than the Vec and miR-134/FIR groups (Fig 7C; quantitative data in Fig 7D). [score:1]
NRIP1 is involved in ECFC activity and is crucial for miR-134 functionality. [score:1]
In addition, the capillary densities of the limb muscle were also higher in mice treated with FIR than the Vec and miR-134/FIR groups (Fig 7D). [score:1]
Ctrl: plasmid control, shNRIP1: NRIP1 shRNA, Anti-miR-134: miR-134 antagomir. [score:1]
The putative miR-134 binding region within the 3’UTR of NRIP1 is shown in Fig 5I. [score:1]
0147067.g003 Fig 3. (A) Representative images (left) and quantitative data (right) from the Transwell migration assays (upper) and tube formation assays (lower) of dfECFCs with miR-370 and miR-134 overexpression. [score:1]
Lower: representative images of mouse ventral side during the measurement of hindlimb blood flow by laser Doppler before operation (Pre-Op), immediately after hindlimb ischemia surgery (Post-Op), and 2 weeks after intramuscular injection of culture medium (EGM2), HG-dfECFCs (Vec), HG-dfECFCs with FIR treatment (Vec + FIR), and miR-134 overexpressed HG-dfECFCs with FIR treatment (miR-134 + FIR). [score:1]
These results suggested that miR-134, which is abundant in HG-dfECFCs and dmECFCs, hampers the angiogenic activity of ECFCs. [score:1]
In retinal ganglion cells (RGCs), miR-134 is increased by H [2]O [2] treatment and lead to RGC apoptosis [61]. [score:1]
NRIP1 is involved in various ECFC activities and is crucial for miR-134 functionality. [score:1]
In contrast, miR-134 was first identified as an angiogenic modulator that decreases ECFC migration and microvascular formation. [score:1]
S4 Fig (A) dfECFCs were infected with lenti-miR-370 and lenti-miR-134. [score:1]
The results suggest the FIR modulates the functions of ECFCs through miR-134-NRIP1 axis. [score:1]
We further used an anti-miR-134 antagomir combined with shNRIP1 to clarify the interaction between miR-134 and NRIP1 (Fig 6C). [score:1]
Nevertheless, miR-134 seems to be a marker for determining the effectiveness of FIR treatment. [score:1]
Both miR-370 and miR-134 had no effect on cell proliferation or on cell cycle arrest (S4B and S4C Fig). [score:1]
We also measured the effect of miR-370 and miR-134 overexpression on cell motility and microvasculature formation of HUVECs (S4D Fig). [score:1]
We further investigated whether NIRP1 is a downstream target of miR-134. [score:1]
The decreased level of miR-134 in HG-dfECFCs was more than that in NG-dfECFCs (a 6.8 fold decrease in HG-dfECFCs vs. [score:1]
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3
[+] score: 127
The results showed that miR-134, miR-155 and miR-222 were down-regulated while miR-34 was up-regulated in the HIFU group (Figure 3). [score:7]
Taken together, these results imply that HIFU suppresses the expression of miR-134 in melanoma cells to enhance CD86 expression, which enhances anti-tumor immunity by triggering IFN-γ and TNF-α secretion from lymphocytes. [score:7]
Collectively, these results suggest that miR-134 directly binds to the 3′UTR of CD86 to suppress CD86 expression in B16F10 cells, and miR-222 is unlikely involved in ICAM-1 regulation. [score:7]
miR-134 directly bound to CD86 mRNA 3′UTR to suppress CD86 expression. [score:6]
We further determined that HIFU promoted CD86 expression through down-regulation of miR-134. [score:6]
The results suggest that HIFU down-regulates miR-134 to release the inhibition of miR-134 on CD86 in melanoma cells, thereby enhancing anti-tumor immune response. [score:6]
miR-134 directly bound to CD86 mRNA 3′UTR to suppress CD86 expression in B16F10 cells and the cytotoxic activity of lymphocytes. [score:6]
In summary, our results demonstrate that HIFU down-regulates miR-134 to increase CD86 expression, which promotes T cell activation that, in turn, potentiates HIFU's anti-tumor effects. [score:6]
All these results support the idea that HIFU enhances anti-tumor immunity through suppressing miR-134 to increase CD86 expression in B16F10 cells that promotes T cell activation. [score:5]
These results suggest that miR-134 mediates inhibition of CD86 in melanoma cells, which leads to suppression of IFN-γ and TNF-α secretion from lymphocytes. [score:5]
Furthermore, when B16F10 cells were transfected with miR-134 mimics, the expression of CD86 was significantly suppressed mainly at the protein level. [score:5]
After confirming that HIFU can enhance anti-tumor immunity, we focused on differential expression of miRNAs in tumors after HIFU treatment and searched the target genes of these miRNAs with a bioinformatics approach and a signal cascade consists of HIFU, miR-134 and CD86 was identified. [score:5]
By a luciferase reporter assay, we clearly demonstrated that miR-134 directly binds to the 3′UTR of CD86 mRNA to suppress CD86 expression in B16F10 cells. [score:5]
Consistently, transfection of miR-134 mimic inhibited the expression of CD86 mRNA and protein (Figure 5D). [score:5]
HIFU treatment promoted anti-tumor immunity of splenic lymphocytes by down -regulating miR-134 level and increasing CD86 expression in B16F10 cells. [score:4]
HIFU promoted anti-tumor immunity of splenic lymphocytes by down -regulating miR-134 level and increasing CD86 expression in B16F10 cells. [score:4]
The luciferase activity of the luciferase reporters containing WT but not the mutated 3′UTR of CD86 was significantly inhibited by miR-134 mimics (p < 0.01, Figure 5B). [score:3]
miR-134 increased the survival rate of B16F10 cells and inhibited the secretion of IFN-γ and TNF-α. [score:3]
Functionally, overexpression of miR-134 in B16F10 cells weakened the cytotoxicity of splenic lymphocytes against B16F10 cells, which was associated with reduced secretion of IFN-γ and TNF-α from co-cultured splenic lymphocytes. [score:3]
The expression of miR-134 and CD86 was reversely correlated and was in an HIFU exposure time -dependent manner (Figure 6D). [score:3]
By bioinformatics analysis, we found that the positive co-stimulatory molecule CD86 is a potential target gene of miR-134. [score:3]
Our results showed that the expression of miR-134, which is closely associated with immune response, was decreased in HIFU -treated tumor tissues. [score:3]
To determine whether miR-134 directly binds to the 3′UTR of CD86 mRNA and miR-222 binds to ICAM-1 mRNA, luciferase reporters that carry either the wild-type (WT) 3′UTR sequences or the mutant (MUT) 3′UTR sequences of the CD86 (for miR-134) or ICAM-1 (for miR-222) were constructed (Figure 5A), and co -transfected into B16F10 cells with or without miRNAs mimics. [score:2]
Next, we investigated if HIFU enhanced anti-tumor immunity by inhibiting the negatively regulatory role of miR-134 on CD86 in B16F10 cells. [score:2]
C. B16F10 cells were transfected with miR-134 mimics or miR-222 mimics for 48 h and the miRNA levels of miR-134 and miR-222 were determined by qPCR. [score:1]
B16F10 cells were evenly seeded in a 24-well plate and transfected with pMIR-REPORT constructs (200 ng per well) and Renilla luciferase (pRL-TK Vector, 200 ng per well; Promega, Madison, Wis), plus miR-134, or miR-222 mimics, or miRNA negative control (25 nmol/L, GenePharma, Shanghai, China). [score:1]
To construct p [MIR-LUC-3′UTR-CD86] and p [MIR-LUC-3′UTR-ICAM-1], CD86 3′UTRs containing miR-134 binding sites and ICAM-1 3′UTR containing miR-222 binding site were generated by Chemical synthesis, and then cloned into downstream of luciferase of pMIR-REPORT™ System (Applied Biosystems/Ambion, Austin TX), respectively. [score:1]
These included miR-34, miR-106a, miR-126a, miR-134, miR-155, miR-181a, miR-221, and miR-222. [score:1]
When the co-stimulatory signal such as CD86 is blocked by miRNA-134, T cells cannot be effectively activated [28]. [score:1]
Thus, we proceeded to focus on miR-134 in the subsequent experiments. [score:1]
The levels of IFN-γ and TNF-α in co-cultured supernatant were significantly decreased in cells transfected with miR-134 mimics (p < 0.05, Figure 5G). [score:1]
Total protein and RNA were collected after 48 h. One part of the cells transfected with miR-134 were co-cultured with activated splenic lymphocyte for 24 h and 48 h. B16F10 cells cultured in vitro were collected and evenly put into three polyvinyl chloride pipe, and then exposed to HIFU for 0 s, 5 s, 10 s at 4.5 W, respectively. [score:1]
Construction of p [MIR-REPORT] luciferaseTo construct p [MIR-LUC-3′UTR-CD86] and p [MIR-LUC-3′UTR-ICAM-1], CD86 3′UTRs containing miR-134 binding sites and ICAM-1 3′UTR containing miR-222 binding site were generated by Chemical synthesis, and then cloned into downstream of luciferase of pMIR-REPORT™ System (Applied Biosystems/Ambion, Austin TX), respectively. [score:1]
In addition, a part of splenic lymphocytes from normal mice (2 × 10 [7]) were pre-stimulated with B16F10 cells (1 × 10 [6]) for 5 days in order to activate them in vitro, and then were separated and used as effector cells when co-cultured with B16F10 cells which were transfected with miR-134 mimics or treated with HIFU. [score:1]
B16F10 cells transfected with miR-134 mimics or negative control (miR-NC) were co-cultured with normal splenic lymphocytes that were pre-stimulated by B16F10. [score:1]
Our study determined a role of miR-134 in HIFU-enhanced anti-tumor immunity, which may be exploited for clinical application of HIFU in cancer therapy. [score:1]
Transfection efficiency of miR-134 and miR-222 was confirmed by qPCR (Figure 5C). [score:1]
Total protein and RNA were collected after 48 h. One part of the cells transfected with miR-134 were co-cultured with activated splenic lymphocyte for 24 h and 48 h. HIFU ablation of B16F10 cells in vitroB16F10 cells cultured in vitro were collected and evenly put into three polyvinyl chloride pipe, and then exposed to HIFU for 0 s, 5 s, 10 s at 4.5 W, respectively. [score:1]
D. B16F10 cells were transfected with miR-134 mimics for 48 h and the mRNA (upper panel) and protein (lower panel) levels of CD86 were determined. [score:1]
As shown in Figure 4A, there were three miR-134 binding sites in CD86 3′UTR and one miR-222 binding site in ICAM-1 3′UTR. [score:1]
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4
[+] score: 88
After that, we overexpressed miR-134 in J1 ES cells and found that miR-134 overexpression can down-regulate the expression of four of the aforementioned pluripotency markers (Figure 3E). [score:10]
Our data suggested that AICAR can down-regulated the expression of miR-134 in ES cells. [score:6]
Down-regulation of miR-134 is partly responsible for increased expression of pluripotency markers. [score:6]
Nanog and Sox2 are direct targets of miR-134; thus, we constructed luciferase reporters that contain Nanog and Sox2 target sequence. [score:6]
Further research indicated that miR-134 can modulate mouse ES cell differentiation by targeting Nanog and LRH1 and repressing their expression [34]. [score:5]
0103724.g003 Figure 3. (A) MiR-134 expression vector pCDH-mir134 and its negative control were transfected into J1 ES cells, and the expression of miR-134 was detected by real-time PCR. [score:5]
Those down-regulated miRNAs included miR-134-5p, miR-296-3p, miR-381-3p, miR-449a-5p, miR-449c-5p, and miR-302 clusters. [score:4]
To investigate miR-134 function in AICAR -induced up-regulation of pluripotency markers, we constructed vector pCDH-mir134 that can express the miR-134 precursor to perform the succeeding experiment. [score:4]
MiR-134 was first considered as a brain-specific miRNA that can regulate synapse development by targeting Limk1 [40]. [score:4]
Thereafter, miR-134 was found to be up-regulated after RA treatment, which caused Tay YM et. [score:4]
indicated that pCDH-mir134 can decrease the luciferase activity of reporters that contain the target sequence of miR-134 (Figure 3B). [score:3]
The results indicated that AICAR can compromise miR-134 reduction on Nanog and Sox2 expression. [score:3]
J1 ES cells were seeded on gelatin-coated 12-well plates in the presence of 1,000 U/ml LIF and transfected with miR-134 expression vector pCDH-mir134 or its negative control. [score:3]
The results showed the expression of miR-134 can significantly decrease AP activity of ES cells and the addition of AICAR reversed this phenomena (Figure 3G). [score:3]
Furthermore, we added AICAR into the medium of J1 ES cells transfected with pCDH-mir134 to detect Nanog and Sox2 expression. [score:3]
MiR-134, which was identified as a differentiation -associated miRNA, was decreasingly expressed after. [score:3]
Therefore, AICAR modulation on miR-134 expression may suggest the function of AICAR in ES cell pluripotency maintenance and cancer therapy. [score:3]
The expression level of miR-134 increased after RA- or N2B27 -induced differentiation of mouse ES cells [34]. [score:3]
Among these miRNAs, miR-134 expression was elevated after retinoic acid (RA) -induced differentiation. [score:3]
A recent study also found that miR-134 expression was correlated with tumor cell proliferation, survival, migration, and invasion [41]. [score:3]
Real-time PCR result showed J1 ES cells, which transfected with pCDH-mir134, exhibited high miR-134 expression level compared with those transfected with the control vector, pCDH-CMV-MCS-EF1-copGFP (pCDH-GFP) (Figure 3A). [score:2]
In summary, these results indicated that AICAR can partly antagonize miR-134 function on ES cell differentiation. [score:1]
This functional experiment indicated the role of miR-134 in ES cells differentiation and the function of AICAR in their stemness maintenance. [score:1]
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5
[+] score: 42
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]
Further, seven miRNAs were predicted to be related to the regulation of RNA expression, with the putative functions of mRNA process regulation (mmu-let-7a-2-3p, mmu-let-7b-3p, and mmu-let-7c-1-3p) and regulation of gene expression (mmu-miR-92a-2-5p, mmu-miR-125b-1-3p, mmu-let-7a-2-3p, mmu-miR-134-5p, and mmu-miR-27a-5p). [score:8]
Among them, seven miRNAs including three that were down-regulated (mmu-miR-708-5p, mmu-miR-92a-2-5p, and mmu-miR-711) and four that were up-regulated (mmu-miR-714, mmu-miR-134-5p, mmu-let-7a-2-3p, and mmu-miR-27a-5p) were predicted to be involved in cellular response to stimulus. [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]
Different types of cancer cells express either high or low levels of miR-92 [44- 46] and the high levels of circulating miR-134 was proposed as a diagnostic and prognostic biomarker for certain diseases [47, 48]. [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]
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]
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]
Cancer progression is associated with miR-92a and miR-134 that acts as oncomirs to promote cell proliferation, migration, and invasion [42, 43]. [score:1]
Combining the use of miR-134 and other miRNA biomarkers may enhance the diagnostic sensitivity of detection of mild cognitive impairment [48]. [score:1]
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[+] score: 21
For example, miR-134 regulates LimK1 at the spine by stimulation of BDNF [19], miR-138 regulates palmitoylation in neurons by inhibiting the translation of LYPLA [16], [18], miR-132 targets p250GAP to enhance spine growth [20] and the FMRP associated miRNA, miR-125b blocks the translation of NR2B resulting in neuronal structural changes [21]. [score:11]
On the other hand, miR-134, miR-138 and miR-34b showed bigger changes in the expression of their primary transcripts than their mature forms (Figure 5F to H). [score:3]
In mouse, the deacetylase SIRT1 modulates learning and synaptic plasticity via miR-134, which represses translation of BDNF and CREB [14], [19]. [score:3]
Recently, it was also shown that miR-134 regulates learning and memory in a mouse mo del [14]. [score:2]
Especially, in the case of miR-134, about 20% of the mature form decreased in 24 hours after contextual conditioning, but 80% of primary transcript was decreased at the same time point. [score:1]
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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7
[+] score: 21
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-330, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-181d, hsa-mir-505, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-505, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The functional relevance of miRNAs in brain disease is illustrated by miR-134, activity of which is upregulated in the brain of animals with status epilepticus and, when silenced, reduces hippocampal dendritic spine density and makes mice refractory to seizures and resulting hippocampal damage (Jimenez-Mateos et al., 2012). [score:6]
Silencing microRNA-134 produces neuroprotective and prolonged seizure-suppressive effects. [score:3]
Silencing of miR-134 expression reduces dendritic spine density and renders mice refractory to seizures and hippocampal injury caused by status epilepticus (Jimenez-Mateos et al., 2012). [score:3]
The expression of miR-134 is reduced in gastrointestinal stromal tumors (Haller et al., 2010). [score:3]
miRNA Gene targets miR-134Brain-derived neurotrophic factor (BDNF) and cAMP response element -binding factor (CREB) miR-204 BDNF and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) miR-211 BDNF and AMPA miR-505 BDNF and AMPA miR-590-3p BDNF and CREB MiR-134 has an important role in the brain, where it is essential for activity -dependent dendritic outgrowth, nerve growth cone guidance, and size of dendritic spines of hippocampal neurons (Schratt et al., 2006; Khudayberdiev et al., 2009; Han et al., 2011). [score:3]
MiR-134 is also a powerful inducer of pluripotent stem cell differentiation and functions as a regulator of cell proliferation, apoptosis, and migration during lung development (Zhang et al., 2012c). [score:2]
MiR-134 functions as a regulator of cell proliferation, apoptosis, and migration involving lung septation. [score:1]
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8
[+] score: 18
Other miRNAs from this paper: mmu-mir-132, mmu-mir-212
Associated microRNAs are miR-132 regulating Rac1 activity via modulation of a GTP hydrolysis protein (p250GAP) and miR-134 directly suppressing LIMK1 levels. [score:5]
As LIMK1 protein levels were down-regulated without related changes in gene expression (Figure  3G) in cortex and hippocampus, we measured the level of miR-134, a negative regulator of LIMK1. [score:5]
As LIMK1 is directly targeted by miR-134 [30], the increased levels of miR-134 are in good agreement with the decrease in LIMK1 without corresponding changes in Limk1 transcripts in both hippocampus and cortex as also shown by others in primary neurons [30]. [score:4]
The miR-132 and miR-134 regulate the Rac1-Cofilin pathway [30, 31]. [score:2]
These changes were coupled to epigenetic modulation via increased levels of microRNAs (miR-132/miR-212, miR-134). [score:1]
The decrease of LIMK1 protein was coinciding with a significant increase in miR-134 levels both in cortex and hippocampus (Figure  3F). [score:1]
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9
[+] score: 17
In the present study we have found that in whole brain and brain regions concerned with neurogenesis (SVZ and hippocampus) and affected by motor neuron degeneration (primary motor cortex and brainstem motor nuclei), altered expression of neural fate miR-124a and miR-9 (but not miR-134), cell cycle-related miR-19a and -19b, astrocyte-related miR-125b and oligodendrocyte -related miR-219 occur in late stage disease (18 weeks). [score:5]
We found that the expression of miR-134 did not differ significantly between ALS and control brain, while the expression of the other miRNAs did. [score:5]
Interestingly, at week 18, expression levels of miR-9 and miR-124a, but not miR-134, were significant lower in G93A-SOD1 whole spinal cord than in Wt-SOD1 spinal cord (p < 0.05 and p < 0.01, respectively), whereas miR-19a and -19b expression levels were significantly higher in ALS than Wt-SOD1 mice (p < 0.01 and p < 0.05, respectively) (Additional file 1: Figure S1). [score:5]
In the present study, we first investigated the expression of miR-9, miR-124a, miR-19a, miR-19b and miR-134 in the whole brain of G93A-SOD1 mice in comparison with that of B6. [score:1]
Here we investigated neural miR-9, miR-124a, miR-125b, miR-219, miR-134, and cell cycle-related miR-19a and -19b, in G93A-SOD1 mouse brain in pre-symptomatic and late stage disease. [score:1]
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10
[+] score: 15
To correct (to the extent possible) for this difference, we excluded a further 20 target sites with GU pairs and mismatches in the seed region for miR-134, and 8 target sites for miR-296 (all target sites for miR-375 have WC matches in the seed region), and report the results of 65 target genes examined for miR-134, 6 for miR-296 (for miR-296, all six sites examined were validated), and 22 for miR-375. [score:9]
miRNA Condition Number of targets miR-134 WC bp at nt 2–7 True positives 43 Sensitivity = 0.551 False negatives 35 Specificity = 0.666 False positives 3 True negatives 6 Total 87 WC bp at nt 2–7, and 40% FE threshold (−18.64) True positives 36 Sensitivity = 0.462 False negatives 42 Specificity = 0.666 False positives 3 True negatives 6 Total 87 miR-296 WC bp at nt 2–7 True positives 8 Sensitivity = 0.80 False negatives 2 Specificity = 0.50 False positives 1 True negatives 1 Total 12 WC bp at nt 2–7, and 40% FE threshold (−19.44) True positives 7 Sensitivity = 0.70 False negatives 3 Specificity = 0.50 False positives 1 True negatives 1 Total 12 miR-375 WC bp at nt 2–7 True positives 9 Sensitivity = 0.375 False negatives 15 Specificity = 0.929 False positives 1 True negatives 13 Total 38 WC bp at nt 2–7, and 40% FE threshold (−16.68) True positives 8 Sensitivity = 0.333 False negatives 16 Specificity = 0.929 False positives 1 True negatives 13 Total 38Of 158 genes experimentally tested for regulation by miR-134, 85 occur in our database, as do 14 of 24 tested for regulation by miR-296, and 22 of 44 tested for regulation by miR-375. [score:6]
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[+] score: 14
In addition, miR-134, which is also expressed in the DRG, is pro-nociceptive in chronic pain mo dels [22] and miR-183 cluster controls neuropathic pain-regulated genes in DRG [23]. [score:4]
Expression of miR-21-5p was comparable to miR-let7b, miR-124, and miR-134, which were selected as positive-control miRs (Fig.   2a). [score:3]
i Expression of miRs 21-5p, Let7b-5p, 124-3p and 134-5p in the exosomal fraction of DRG neurons media treated with buffer control or CAPS for 3 h. Data are means ± S. E. M., n = 4 cultures; * P < 0.05, ** P < 0.01 and *** P < 0.001 compared to control, Student’s t test Expression analysis of miRs in the exosome fraction of cultured DRG media indicated that capsaicin significantly increased levels of miR-21-5p, let7b, miR-124, and miR-134 compared to control conditions (Fig.   2i). [score:3]
i Expression of miRs 21-5p, Let7b-5p, 124-3p and 134-5p in the exosomal fraction of DRG neurons media treated with buffer control or CAPS for 3 h. Data are means ± S. E. M., n = 4 cultures; * P < 0.05, ** P < 0.01 and *** P < 0.001 compared to control, Student’s t test Expression analysis of miRs in the exosome fraction of cultured DRG media indicated that capsaicin significantly increased levels of miR-21-5p, let7b, miR-124, and miR-134 compared to control conditions (Fig.   2i). [score:3]
Ni J Regulation of mu-opioid type 1 receptors by microRNA134 in dorsal root ganglion neurons following peripheral inflammationEur. [score:1]
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12
[+] score: 11
To identify putative targets of miR-1, miR-133a, miR-124a-3, miR-134, and miR-206, we searched the literature to identify targets of these miRNAs that had been detected by expression arrays in tumors and had been further validated by other methods. [score:7]
Following analysis, six miRNAs (miR-1, miR-133a, miR-124a-3, miR-134, miR-206, and miR-9-1) showed a significant difference in average expression and had a 2.0 fold or greater difference across one or more probe sets. [score:3]
Probes were specific to either mature (miR-1, miR-133a, miR-124a-3, miR-206) or precursor (miR-134, miR-206, miR-9-1) miRNAs concordant with the array results. [score:1]
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[+] score: 11
To validate our target gene prediction approach, we tested the recovery rate of predicted target genes in a set of 129 murine mir-134 targets, which were independently predicted and verified with luciferase-reporter assays by Miranda et al. [31]. [score:6]
Since possible target genes have been identified for only a few imprinted microRNAs, e. g. miR-134, miR-376a, miR-370, and the microRNAs embedded in the antisense transcript of the Retrotransposon-like 1 (Rtl1) gene [19, 22, 29- 32], we established a pipeline that combines different algorithms to predict microRNA target genes computationally. [score:5]
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[+] score: 10
In recent study of Jimenez-Mateos et al. (2015), the authors have demonstrated the vital function of miR-134 in alleviating pilocarpine -induced status epilepticus: the research provides compelling evidence that application of antagonist against miRs significantly suppresses seizures in an animal mo del. [score:3]
Antagomirs targeting microRNA-134 increase hippocampal pyramidal neuron spine volume in vivo and protect against pilocarpine -induced status epilepticus. [score:3]
However, unlike studies on miR-134, the potential of miR-155 as a novel therapeutic target for epileptic disorders is only partially revealed. [score:3]
Previous study of Jimenez-Mateos et al. (2015) reported that in vivo silencing of miR-134 resulted in a potent anticonvulsant effect through increasing volume of neuron spines in hippocampal CA3 pyramid, inferring the involvement of miRs in the pathophysiology of epilepsy. [score:1]
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[+] score: 10
Other miRNAs from this paper: mmu-mir-124-3, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-124b
SIRT1 deficiency increases brain-specific miR-134 expression, leading to decreased expression of cAMP response element -binding protein (CREB) and brain-derived neurotrophic factor (BDNF), and this results in impaired synaptic plasticity [20]. [score:5]
SIRT1 agonist resveratrol suppresses miR-134 and miR-124, which increase CREB and BDNF expression [21]. [score:5]
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[+] score: 10
The results suggested that SIRT1 cooperated with Yin Yang 1 (YY1) in binding to the upstream regulatory elements of miR-134 and then limited the expression of miR-134 resulting in overexpression of CREB and BDNF, thereby regulating synaptic plasticity and long-term memory formation in SIRT1- KO mice [91]. [score:7]
Recent studies have shown that SIRT1 promotes plasticity and memory in a direct manner via a miR-134 -mediated posttranscriptional mechanism. [score:2]
Although miR-134 was not detected in the above three studies, we still suggested that SIRT1 protects learning and memory via the SIRT1-miR-134 pathway. [score:1]
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[+] score: 10
b Box-plots of miRNA expression levels of mmu-miR-134-5p, mmu-miR-136-5p, mmu-miR-214-3p, mmu-miR-296-5p in mouse quadriceps muscle at 2 days, 2 weeks, 4 weeks and 12 weeks after birth. [score:3]
Of interest, all 4 top-ranked miRNAs in cluster B were predicted to target one of the Pax gene family members with a high degree of certainty, potentially indicating a similar role for mmu-miR-134-5p, mmu-miR-136-5p and mmu-miR-296-5p. [score:3]
Finally, mmu-miR-134-5p (down regulated by close to 100-fold between 2 days and 12 weeks of age) has not been described in skeletal muscle. [score:2]
Whether mmu-miR-134–5p has a similar role in the muscle remains to be elucidated. [score:1]
The top-ranked miRNAs for cluster B were mmu-miR-134–5p, mmu-miR-136–5p, mmu-miR-214–3p and mmu-miR-295–5p. [score:1]
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18
[+] score: 9
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-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-25, 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-134 regulates the proliferation and invasion of glioblastoma cells by reducing Nanog expression. [score:3]
Stage-specific modulation of cortical neuronal development by Mmu-miR-134. [score:2]
miR-134. [score:1]
Thus, in this review we focus on the role of two subsets of miRNAs (miR-134,, and) and (,, and) that are highly conserved during evolution and play an important role in the early steps of neurogenesis. [score:1]
miR-134 belongs to the miR-379-410 cluster (Rago et al., 2014) and itself is a powerful inducer of pluripotent ESCs differentiation (Gaughwin et al., 2011). [score:1]
MiR-134 functions as a regulator of cell proliferation, apoptosis, and migration involving lung septation. [score:1]
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19
[+] score: 8
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 A. Scatterplot showing relative expression of miRNAs by macroarray. [score:4]
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 Because miRNAs typically regulate translation in animal cells, we compared CXCL10 and STAT1 protein levels in both control and Dicer [d/d] animals and cells. [score:4]
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20
[+] score: 8
Other miRNAs from this paper: hsa-mir-134
The downregulation of WWOX expression in advanced-stage tumor samples of HNSCC is associated with methylation of the WWOX promoter region but not with miR-134 expression. [score:8]
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21
[+] score: 8
Other miRNAs from this paper: mmu-mir-132, mmu-mir-491
qPCR established that reduced expression of Dgcr8 mRNA in Dgcr8+/-mice at P25 resulted in the reduced expression of a subset of miRNAs (miR-134, 57 ± 6%, P = 0.001; miR-491, 61 ± 6%, P = 0.004; Figure 1C). [score:5]
In vitro targeting studies in neuronal culture systems have implicated miR-132 in neurite sprouting [25] and the miR-379-410 cluster (which includes miR-134) in activity -dependent dendritic outgrowth [26]. [score:3]
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22
[+] score: 8
RT-qPCR using TaqMan probes was performed in triplicate to determine the expression of miR-145, miR-296, miR-134, and miR-21, normalized to RNU6B expression, and reported as average differences in fold change from RNU6B expression. [score:7]
The levels of miR-134 and miR-296 were measured, because they are reported to target the coding sequence of Sox2 mRNA [37]. [score:1]
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23
[+] score: 8
miR-134 is also highly expressed in the hippocampus, a major site of mengovirus pathology, and may serve as an additional alternative to miR-124 or miR-125 targets, expanding the versatility of this virotherapy. [score:5]
However, we did not see additive effects when miR-125 and miR-134 target sequences were combined for the purpose of enhancing the safety of vesicular stomatitis virus (44). [score:3]
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24
[+] score: 7
miR-134 on the other hand is required for activity -dependent dendritic arborization and the restriction of spine growth by targeting Pumilio-2 and Lim-domain containing protein kinase (Limk1), respectively (Schratt et al., 2006; Fiore et al., 2009). [score:3]
A novel pathway regulates memory and plasticity via SIRT1 and miR-134. [score:2]
Arguably the two most extensively studied examples in the context of synapse development are miR-132 and miR-134. [score:2]
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25
[+] score: 7
Hsa-miR-134 suppresses non-small cell lung cancer (NSCLC) development through down-regulation of CCND1. [score:7]
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26
[+] score: 7
Other miRNAs from this paper: mmu-mir-182, mmu-mir-34b, mmu-mir-18a, mmu-mir-210
Notably, a correlation coefficient >0.9 indicated a strong correlation between the level of serum creatinine and temporal expression of miR-134/-214. [score:3]
However, based on the latest release of miRTarBase (Chou et al., 2016), no miRNA-target interactions were found for miR-134, -182, and -214 in the 10 pathways. [score:3]
Among miRNAs, a selected few, such as miR-134 and -214, may play critical roles in this pathological course. [score:1]
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27
[+] score: 7
We also observed significant inhibition of immunostimulatory ssRNA sensing by select LNA/DNA phosphorothioate AMOs from Classes 3 and 4. Although miRNA -based mechanisms could be at play for LNA/DNA AMOs targeting abundant miRNAs (such as miR-191-5p, miR-16-5p, miR-29a-3p or miR-100-5p), such effects can be ruled out for other AMOs of Class 3 targeting poorly abundant miR-224-5p, miR-331-3p, miR-134-5p or miR-31-5p. [score:7]
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28
[+] score: 7
For example, miR-134, which is down-regulated in the brains of AD mice, is specifically expressed in the brain and has been demonstrated to negatively regulate dendritic spine formation in vitro [26]. [score:7]
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29
[+] score: 6
Silencing microRNA-134 produces neuroprotective and prolonged seizure-suppressive effects. [score:3]
Antagomirs targeting microRNA-134 increase hippocampal pyramidal neuron spine volume in vivo and protect against pilocarpine -induced status epilepticus. [score:3]
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30
[+] score: 6
Of these, we found only miR-128 to be expressed in adult mouse NPCs (Additional file 2: Fig. S2) in agreement with a previous report [35] showing the presence of miR-128 but not miR-134 in the neurogenic areas of the mouse adult brain. [score:3]
Specifically, miR-134 [33] was shown to regulate Dcx in mouse embryonic brain tissues, while miR-128 [34] was found to modulate Dcx levels in a human neuroblastoma cell line. [score:2]
The IDs of the TaqMan Probe used were: miR-125 (000449); let-7c (000379); miR-134 (001186); miR-128 (002216); snoRNA55 (001228); snoRNA135 (001230). [score:1]
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31
[+] score: 6
MiRNAs significantly dysregulated in the mid-phase of infection (dpi 30), such as mmu-miR-146b and mmu-miR-155, may relate to the regulation of hepatic inflammatory responses, whereas miRNAs exhibiting a peak expression in the late phase of infection (dpi 45), such as mmu-miR-223, mmu-miR-146a/b, mmu-miR-155, mmu-miR-34c, mmu-miR-199, and mmu-miR-134, may represent a molecular signature of the development of schistosomal hepatopathy. [score:6]
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32
[+] score: 6
It would be interesting to determine whether ADAMTS-4 may induce mechanisms previously described to downregulate neurotrophic factor production, for instance, by modulating the nuclear translocation of transcription factors such as the histone deacetylase HDAC6 (negative regulator) [35], CREB (cAMP response element -binding protein) or NF-κB (nuclear factor kappa B) (positive regulators) [36– 38], and/or by modulating micro -RNAs (miR) production such as miR-15a, miR-132, miR-134, miR-221 or Let-7 miR [39– 41]. [score:6]
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33
[+] score: 6
Pseudogene Parental gene Other genes Shared microRNAs Context Reference Oncosuppressive pseudogenes PTENP1 PTEN miR-17, 19, 21, 26, and 214 families Prostate cancer(23) Melanoma(39) Endometrial cancer(44) ccRCC(15) Hepatocellular carcinoma(30) Gastric cancer(45)(40) PTENP1 HRASLS5 miR-135b Breast cancer(13) TUSC2P TUSC2 miR-17, 93, 299-3p, 520a, 608, and 661 Breast cancer(46) INTS6P1 INTS6 miR-17-5p Hepatocellular carcinoma(47) Oncogenic pseudogenes OCT4-pg4 OCT4 miR-145 Hepatocellular carcinoma(34) OCT4-pg5 OCT4 miR-145 Endometrial carcinoma(48) HMGA1P6 HMGA1 miR-15, 16, 214, and 761 Thyroid carcinoma(49) HMGA1P7 Pituitary tumors(50) CYP4Z2P CYP4Z1 miR-125a-3p, 197, 204, 211, and 1226 Breast cancer(51) BRAFP1 BRAF miR-30a, 182, 590, and 876 DLBCL(52) Braf-rs1 Braf miR-134, 543, and 653 Diffuse large B-cell lymphoma(52) Additionally, it has been shown that pseudogenes can act as ceRNAs not only for their parental genes but also for other genes (Figure 1K and Table 1). [score:3]
Finally, the authors identified three microRNAs (miR-134, miR-543, and miR-653) as Braf-rs1 and Braf -targeting and, by mutagenizing their MREs on Braf mRNA, proved that they are the mediators of the protective effects exerted by the pseudogene on the parental gene. [score:3]
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34
[+] score: 6
The dysregulated expression of selected DLK1-Dio3 miRNAs such as miR-134, miR-433, miR-494, and miR-379 has also been noticed in human lupus [21, 29]. [score:4]
The dysregulation of DLK1-Dio3 miRNAs was also evident in B6- lpr and NZB/W [F1] lupus mice (such as miR-127 and miR-379) [28, 44], and in human lupus patients (such as miR-134, miR-379, and miR-433)[21, 29]. [score:2]
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35
[+] score: 6
One of the 66 was miR-134, which can target Nanog and LRH1, two transcription factors that upregulate Oct4[31]. [score:6]
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36
[+] score: 6
Other miRNAs, including miR-134, miR-145, miR-296 and miR-470 become upregulated during differentiation and have been found to inhibit pluripotency factors such as Oct4, Sox2 and Nanog [10]. [score:6]
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37
[+] score: 5
In addition, miR-134 inhibits epithelial to mesenchymal transition by targeting FOXM1 (forkhead box protein M1) in non-small cell lung cancer cells [40]. [score:5]
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38
[+] score: 5
Moreover, miR-134 and miR-337 were strongly upregulated in livers from FLS W mice, and we selected these miRNAs for the first round of predictions (S1 Table). [score:4]
For example, miR-134, -337, -381, and -412 were included in our microarray analysis. [score:1]
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39
[+] score: 5
Indeed, mmu-miR-127 and mmu-miR-337 (encoded within the anti- Rtl1 transcript), both displayed decreased expression conservatively estimated at >1000-fold, while mmu-miR-134 and mmu-miR-494 (encoded within the Mirg cluster) showed >1000-fold and >100-fold decreased expression, respectively. [score:5]
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40
[+] score: 5
It should be cautioned, however, that while several brain miRNAs (e. g., miR-124, miR-29, miR-134, miR-107, miR-9) are, as expected, downregulated in the neuronal Dicer c KO mice [33], not all miRNAs are quantitatively reduced in this mo del, as denoted recently by Babiarz et al. using RNA deep sequencing [34]. [score:4]
For instance, miR-132 and miR-134 have been implicated in neuronal outgrowth and synaptic plasticity, respectively [22], [23]. [score:1]
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41
[+] score: 5
Hsa_circ_0013958 was up-regulated in lung adenocarcinoma and identified as a sponge of miR-134, thus up -regulating oncogenic cyclin D1 [11]. [score:5]
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42
[+] score: 4
Other miRNAs from this paper: hsa-mir-134
Moreover, Limk1 transcripts are translated locally in dendrites of cultured hippocampal neurons and regulated through the 3′-UTR by miR134 [33]. [score:4]
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43
[+] score: 4
Some miRNAs have been identified to regulate the expression of FoxM1, including miR-149, miR-134, miR-370, miR-494, miR-194, and miR-24-1 [37– 43]. [score:4]
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44
[+] score: 4
Thus, p73, by increasing the expression of Ago-1/2, it could increase the processing of miRNAs, such as let-7 (HMGA2; lin-28; EGFR; Kras; c-myc; Bcl-xL), miR-134 (Nanog; LRH1; Oct-4; Collagenase-3; Stromelysin), miR-130b (ERK2; Fosl1; TGFβR1; ERα; Tcf-4; Collagenase-3; Ago4; Dicer; p63), miR-214 (EZH2; CTNNB1), miR-449a (CDK6; SirT1; HDAC1; E2F-1), miR-503 (CCND1; Fosl1), miR-181d (ERK2; TGFβR1; Tcl-1; ERα; AID; Bcl-2) and miR-379 (lin-28) [Figure 2] [31], [32]. [score:3]
The C-terminal NHL domain of TRIM-32 forms complex with Ago1, and thereby promotes the efficiency of processing of a number of miRNAs [Figure 2], including let-7, miR-134, miR-130, miR-214, 449, 379, 181, and miR-503 [31]. [score:1]
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45
[+] score: 4
We confirmed that subset of these 50 miRNAs (miR-382, miR-369-5p, miR-544 and miR-134) could target the 3′ UTR of cMYC transcript. [score:3]
Out of the 50 miRNAs, 2 miRNAs, miR-134 and mir-544, shared 100% conservation with the canine genome and mapped to the predicted synteny in canine osteosarcoma [14]. [score:1]
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46
[+] score: 4
A previous study from our research has demonstrated that HIFU can enhance host anti-tumor immunity by inhibiting the negative regulatory effect of microRNA-134 on CD86 in a murine melanoma mo del. [score:4]
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47
[+] score: 4
FUS also regulates miR-134 and miR-143, both of which display differential neural expression with age (Inukai et al., 2012). [score:4]
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48
[+] score: 4
In the current study Let-7b was increased and two additional putative OPRM1 mRNA targeting miRNAs were decreased [miR-154 and miR-199b, (He and Wang, 2012)] but not miR-134, (Ni et al., 2013). [score:3]
Regulation of mu-opioid type 1 receptors by microRNA134 in dorsal root ganglion neurons following peripheral inflammation. [score:1]
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49
[+] score: 4
Other miRNAs from this paper: mmu-mir-204, mmu-mir-223, mmu-mir-501
For instance, in the miRNA‐mediated synaptic plasticity regulating pathway, miR501 (Hu et al., 2015), miR223 (Harraz et al., 2012) and miR134 (Jimenez‐Mateos et al., 2012) target GluR1, GluR2 and NR2B, and DHX36, respectively. [score:4]
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50
[+] score: 4
[31] Recently, a number of miRNAs such as miR-200a, [32] miR-27a/27b, 33, 34 miR-133a, [35] miR-134, [36] miR-143, [37] miR-145 [38] and miR-146a [39] have been demonstrated to target EGFR directly. [score:4]
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51
[+] score: 4
Recently it was shown that, analogous to Drosophila, loss of Pum2 function in rat hippocampal neurons leads to an increase in dendritic outgrowth [14], and that in primary rat neurons Pum2 translation is regulated by the brain-specific dendritic microRNA (miRNA) miR-134 [15]. [score:4]
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52
[+] score: 4
Down regulation of miRNA-134 protects neural cells against ischemic injury in N2A cells and mouse brain with ischemic stroke by targeting HSPA12B. [score:4]
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53
[+] score: 3
Stage-specific modulation of cortical neuronal development by Mmu-miR-134. [score:2]
Moreover, our findings further support previous work, which have found a causal link between specific miRNAs such as miR-134, miR-34, miR-124, miR-9, and miR-132 with neurite outgrowth and elaboration in vitro (Vo et al., 2005; Yu et al., 2008; Agostini et al., 2011; Gaughwin et al., 2011; Clovis et al., 2012; Franke et al., 2012). [score:1]
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54
[+] score: 3
Other miRNAs from this paper: hsa-mir-134
In U87 cell lines, nanog inhibition by miR-134 was sufficient to decrease proliferation and invasion [16, 19]. [score:3]
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55
[+] score: 3
Moreover, miR-134 was recently shown to regulate negatively Limk1 [61], Nanog, and LRH1 [62]. [score:2]
In comparison to Mirg, the longest Meg9 clone has nine additional upstream exons and contains four more microRNAs: miR-382, miR-134, miR-668, and miR-485. [score:1]
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56
[+] score: 3
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, 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-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
CYP11A1, the gene encoding cholesterol side-chain cleavage enzyme (P450scc), was predicted to be the target gene of miRNA-134. [score:3]
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Kitamura K. Seike M. Okano T. Matsuda K. Miyanaga A. Mizutani H. Noro R. Minegishi Y. Kubota K. Gemma A. MiR-134/487b/655 cluster regulates TGF-β -induced epithelial-mesenchymal transition and drug resistance to gefitinib by targeting MAGI2 in lung adenocarcinoma cells Mol. [score:3]
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58
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But only 13 miRNAs had significantly differential expression, they were let-7e, miR-30b, miR-30c, miR-34a, miR-96, miR-129-3p, miR-132, miR-134, miR-135a, miR-143, miR-146a, mkiR-154 and miR-183, respectively (Fig. 1C). [score:3]
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59
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A novel pathway regulates memory and plasticity via SIRT1 and miR-134. [score:2]
Chronic administration tetrahydroxystilbene glucoside promotes hippocampal memory and synaptic plasticity and activates ERKs, CaMKII and SIRT1/miR-134 in vivo. [score:1]
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60
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Seven miRNAs (miR-31, miR-95, miR-99a, miR-130b, miR-10a, miR-134, and miR-146a) were expressed at 6-fold lower level in SLE patients than that of healthy controls (Tang et al., 2009). [score:3]
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SIRT1 was recently shown to enhance synaptic plasticity in a mouse hippocampus through a mechanism involving repression of miR-134, resulting in increased expression of BDNF and CREB [44]. [score:3]
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62
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The proposed microRNAs that are regulated through the processing machinary include let-7, miR-200c, miR-143, miR-107, miR-16, miR-145, miR-134, miR-449a, miR-503, and miR-21 [16]. [score:2]
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63
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A novel pathway regulates memory and plasticity via SIRT1 and miR-134. [score:2]
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64
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Class 1 (11.6% of profiled miRNA) is composed miRNAs that increase in response to ECS and includes the activity-regulated miRNA, miR-134 [11]. [score:2]
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65
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For instance, miR-134 is localized to the synaptodendritic area in rat hippocampal neurons and is associated with synaptic development, maturation, and plasticity [1]. [score:2]
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66
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A novel pathway regulates memory and plasticity via SIRT1 and miR-134. [score:2]
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67
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In line with this hypothesis, miR-134 was recently proposed to regulate migration and differentiation of cortical neurons (Gaughwin et al., 2011). [score:2]
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MiR-134, for example, is localised to the synapto-dendritic compartment of rat hippocampal neurones and has been linked to synaptic development, maturation and plasticity [23]. [score:1]
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Most candidates had 5′seed sequences distinct from known miRNAs; however the following candidates, conserved with humans, were similar to those in parentheses: 5 (miR-190/190b), 19 (miR-29b-2), 92 (miR-1195), 93 (miR-134), 132 (miR-486), and 183 (miR-345-3p). [score:1]
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70
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In contrast to decreased miRs, miR-758, miR-134 and miR-27b were significantly increased and interestingly miR-758 is predicted to bind conserved seed regions within Col4a1, a basement membrane collagen type that was found to be significantly decreased (0.67-fold, p = 5.29E-03) in Scx [-/-] embryos. [score:1]
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71
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Reduced miR-155, miR-134, miR-373, miR-138, miR-205, miR-181d, miR-181c, and let-7 in CAsE-PE cells correlate with increased KRAS protein [47]. [score:1]
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For example, Hertel reported that mir-134 cluster has more than 50 miRNA genes [37]. [score:1]
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73
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Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
Other families that had a high abundance of reads were miR-134, miR-136, miR-154, miR-370, miR-412, miR-431, miR-432, miR-433, miR-485, miR-493, miR-541; a total of 11 miRNA families. [score:1]
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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-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-25, 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-134/mir-412 case (See additional file 6: Multiple sequence alignments of selected miRNA families), in which the hairpin sequences are similar while the mature sequences differ greatly. [score:1]
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These genes have been shown to be silenced by various miRNAs, such as miR-134, miR-145, miR-296 and miR-470 [18]. [score:1]
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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-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-25, 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
For instance, miR-208, miR-302 (a-d), miR-367 were not detected (at >10 cpm on average) in the heart tissue; miR-134 and miR-208a were not detected in skeletal muscles; miR-483 in liver; or miR-483 and miR-377 in bone [36]. [score:1]
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Examples of helicases that are miRNA-related include DHX36, which is required for dendritic localization of pre-miR134 [7], and DDX6, which binds TRIM32 to increase the activity of RISC [8]. [score:1]
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The DEAH-box helicase DHX36 mediates dendritic localization of the neuronal precursor-microRNA-134. [score:1]
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41 mmu-miR-33 −59.71 mmu-miR-222 1.23 mmu-miR-93 −1.52 mmu-miR-124 −97.01 mmu-miR-429 1.07 mmu-miR-192 −1.52 mmu-miR-129-5p −111.43 mmu-miR-100 −1.74 mmu-miR-210 −157.59 mmu-miR-20a −2 mmu-miR-134 −194.01 mmu-miR-137 −2 mmu-miR-215 −222.86 mmu-miR-194 −2.14 mmu-miR-452 −675.59 mmu-miR-196a −2.64 mmu-miR-223 −955.43 Differentiated sample versus control sample [DIF EBs d8/CONTROL EBs d8]. [score:1]
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