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73 publications mentioning hsa-mir-136

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-136. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 240
Computational genome-wide predictions for miR-136 targets in 3′UTR regions were performed, using the miRanda target prediction algorithm in combination with the online TargetScan, PITA, and RNA22 programs 15. [score:7]
However, on the other hand, cellular IL-6 mRNA and protein levels were dramatically up-regulated by miR-136 mimic or expression plasmids treatment. [score:6]
In A549 cells, overexpression of RIG-I and miR-136 significantly increased the abundances of IL-6 and IFN-β mRNAs, compared to the expression levels observed when cells overexpressed RIG-I or miR-136 alone (Fig. 6A,C). [score:6]
A549 cells were transfected with miR-136 or the NC, and cells were subsequently infected with a recombinant virus expressing enhanced green fluorescent protein (VSV-eGFP), using MOIs of 1 or 10. eGFP expression levels were detected by fluorescence microscopy and flow cytometry. [score:5]
Overexpression of miR-136 inhibits H5N1 IAV in A549 cells. [score:5]
miR-136 mimic, negative control mimic (NC), miR-136 inhibitor, inhibitor control and other dsRNAs used in this study were obtained commercially from GenePharma (Shanghai, China). [score:5]
miR-136 targets the IL-6 3′UTR, but enhances IL-6 expression. [score:5]
As shown in Fig. 4C, we observed the 17%–25% inhibitory effect of 2′-O-Me -modified miR-136 on IL-6, but not on IFN-β, mRNA expression induced by H5N1/HM virus infection. [score:5]
Together these results indicated that cellular IL-6 expression was greatly enhanced following transfection with either plasmid-expressed miR-136 or miR-136 mimics. [score:5]
However, some types of immune-response genes are not expressed in glioma cells 37, based on which cytokine expression was hardly affected by miR-136 overloading in Y. Yang’s studies. [score:5]
miR-136 targets were computationally predicted using the online miRanda software in combination with the online TargetScan, PITA, and RNA22 programs. [score:5]
It showed that blocking the function of miR-136 resulted in down-regulated RIG-I and its downstream genes IFN-β and IL-6 (Fig. 8A). [score:4]
As shown in Fig. 1B, oscillations in miR-136 expression levels were observed, suggesting the complexity of miRNA regulation disrupted by viral infection. [score:4]
Moreover, similar to previous finding 14, we also detected up-regulation of RIG-I mRNA following miR-136 transfection (Fig. 6D). [score:4]
Antiviral assays were performed, and RT-PCR results showed both the NP mRNA and vRNA levels of H5N1/HM virus in miR-136 inhibitor treated cells were considerably higher than those of the nonsense inhibitor control (Fig. 8B,C). [score:4]
We then found that serial cytokines including IL-6 and IFN-β were strikingly up-regulated under miR-136 transfection. [score:4]
To determine the number of copies of the H5N1/HM NP vRNA in miR-136 inhibitor treated cells, the cell total RNA was prepared using TRIzol reagent. [score:3]
Initially, we sought potential miR-136 targets among host factors that may affect H5N1 IAV replication. [score:3]
In this study, miRNA136 was established as a novel endogenous RIG-I activator and may contribute to the control of virus diseases. [score:3]
However, neutralization of miR-136 with miR-136 inhibitor indeed reduced both cellular RIG-I and IFN-β mRNA level. [score:3]
Following traditional manner, several host factors were predicted and tested, and ultimately the IL-6 3′UTR was validated as a target of miR-136. [score:3]
The A549 cells were transfected with specific miR-136 inhibitors, and the mRNA levels of IL-6, IFN-β and RIG-I were determined 24 hours after transfection. [score:3]
With ~80% confluence, cells were co -transfected with FLAG-RIG-I expression plasmids (15 μg) and miR-136 mimics (60 nM). [score:3]
Altogether, these findings suggest that while miR-136 targets IL-6 mRNA, it may simultaneously mediate the activation of innate immunity. [score:3]
In a recent study, Sining Shen and his colleagues defined miR-136 as a new modulator in promoting Erk1/2 pathway activation by targeting PPP2R2A 38. [score:3]
We further asked whether 2′-O-Me -modified miR136 could competitively inhibit cytokine production resulted by the known RIG-I ligand miR-145. [score:3]
miR-136 expression analysis in H5N1/HM infected cells. [score:3]
Similarly, the inhibition of cellular miR-136 facilitates the propagation of VSV in A549 cells (Fig. 8D). [score:3]
Dose -dependent inductions of IL6 mRNA (G) and protein (H) expression by the miR-136 were detected using RT-qPCR and ELISAs, respectively. [score:3]
IL-6, IFN-α, IFN-β, TNF-α, and OAS1 mRNA levels were all markedly up-regulated in group of naked miR-136 transfection as compared with 2′-O-Me -modified miR136 (Fig. 4A). [score:3]
It demonstrated that 2′-O-Me -modified miR136 reduced IL-6 mRNA level by 25%-45% however had no significant effects on IFN-β expression (Fig. 4B). [score:3]
We speculate that the modified miR-136 competitively bound to RIG-I, but failed to induce cytokine production, thus causing immunosuppression. [score:3]
Here, we selected miR-136 for RT-qPCR assays, the results of which were consistent with our microarray findings in terms of miR-136 up-regulation and statistical significance (Fig. 1A). [score:3]
To determine whether endosomal TLRs were responsible for miR-136 recognition, we pretreated A549 cells with 10 μM chloroquine (an inhibitor of endosomal acidification), which was maintained in culture after miR-136 transfection. [score:3]
miR-136 expression was monitored following H5N1/HM infection in a time -dependent manner. [score:3]
To our great surprise, IL-6 mRNA expression level was elevated by 10 times with miR136 plasmid transfection (Supplementary Figure S4A). [score:3]
Effect of miR-136 on IL-6 expression in A549 cells. [score:3]
When miR-136 was transfected into 293T cells (a cell line that is insensitive to innate immune activation 19), IL-6 and IFN-β expression was minimally induced (Fig. 5B). [score:3]
Suppression of H5N1 and VSV replication in A549 cells by miR-136. [score:3]
This inconsistency drew our attention to the fact that miR-136 is linked to cellular immune responses, which are not limited to sequence-specific targeting. [score:3]
To determine whether miR-136 were associated with RIG-I, 12-well planted A549 cells were co -transfected with a FAM-labeled miR-136 (30 M) (GenePharma) and FLAG-RIG-I expression plasmids (1 μg) for 24 hours. [score:3]
Thereafter, we also asked whether the miR-136 would contribute to IL-6 mRNA suppression during virus infection. [score:3]
After miR-136 delivery, IL-6 and IFN-β mRNA levels were down-regulated by approximately 60%, compared with scrambled siRNA transfectants (Fig. 6F). [score:3]
The miR-136 inhibited the luciferase activity of a reporter encoding an intact 3′UTR by 40%, compared to that observed following treatment with the NC. [score:2]
These results suggested a miR-136 response element was present in the 3′UTR of IL-6. Based on these findings, we subsequently evaluated the regulation of miR-136 on endogenous IL-6 expression. [score:2]
Based on these results, we proposed that miR-136 mediated dual functions: post-transcriptional regulation and immune activation. [score:2]
In fact, our unpublished data have demonstrated that miR136 with poly (UUUU) mutation exhibited lower immunostimulation. [score:2]
How to cite this article: Zhao, L. et al. Identification of cellular microRNA-136 as a dual regulator of RIG-I -mediated innate immunity that antagonizes H5N1 IAV replication in A549 cells. [score:2]
We also validated the miR-136 binding site in the IL-6 3′UTR by site-directed mutagenesis and deletion experiments (Fig. 3A). [score:2]
In a previous report, miR-136 was identified as a negative regulator of Bcl-2 in glioma cells 36. [score:2]
Neutralization of endogenous miR-136 negatively regulates RIG-I -dependent signalling. [score:2]
Our data, together with these findings, imply that miR-136 acts as a multifunctional regulator of crosstalk in signalling pathways and in different cell types. [score:2]
To verify this possibility, the expression levels of additional cytokines were measured by RT-qPCR following miR-136 mimic or pCDNA3.1-miR136 transfection (Supplementary Figure S4B). [score:1]
Full-length blots/gels are presented in Supplementary Figures 6, 7 and 8. (A) A549 cells on coverslips were transfected with FAM-labeled miR-136 (30 nM) and Flag-RIG-I plasmids (1 μg). [score:1]
12-well planted A549 cells were transfected with miR-136 or NC at final concentrations of 60 nM in culture supernatants. [score:1]
Cell lysates were prepared and incubated with biotin-labeled miR-136 (GenePharma) or biotin-labeled negative control (8 μg) in 4 °C for 1 hour. [score:1]
All of these dsRNAs possess the immunostimulatory ability, however, the exact structural features of miR-136 that facilitate RIG-I activation and the involved mechanistic discrepancy are still of great interest. [score:1]
To investigate the effects of mature miR-136 on H5N1/HM replication, we preferentially determined that viral mRNAs were sharply decreased using a plasmid -based expression system of miR-136 (pCDNA3.1-miR136) (Supplementary Figure S1A, B). [score:1]
It was worthy to note that 2′-O-Me -modified miR136 maintained slight cytokine induction with the exception of IL-6 mRNA level (though not significantly). [score:1]
Together, these results suggested a close collaboration between RIG-I and miR-136. [score:1]
Representative images are shown in Fig. 7A that miR-136 was shown to colocalizate with RIG-I protein in cytoplasm. [score:1]
These results indicated that endogenous miR-136 is identically closely associated with RIG-I mediated innate immunity. [score:1]
Our further studies support the hypothesis that miR-136 -induced immune activation is at least dependent on RIG-I, but not on TLRs. [score:1]
Interestingly, we noted that miR-136, in A549 cells, had higher immunostimulatory effect in terms of IL-6 and IFN-β levels than that of known immunostimulatory dsRNA or miRNAs, such as miR21, miR29a, let7 32, and RNA27 33 (data not shown). [score:1]
Because miR-136 restricted both IAV and VSV propagation, we therefore mainly focused on exploring host factors that may be involved in these antiviral processes. [score:1]
Cellular cytokines detection based on miR-136 transfection. [score:1]
Total cellular protein was incubated with biotin-labeled miR-136 or negative control (8 μg), and subjected to streptavidin beads binding. [score:1]
Dose -dependent effects of the miR-136 on IL-6 induction were observed (Fig. 3G,H). [score:1]
Cells were transfected with miR-136 or NC at a concentration of 60 nM. [score:1]
Corresponding cDNA of miR-136 was subjected to qPCR analysis and semiquantitative reverse transcription-PCR. [score:1]
Furthermore, we examined whether the antiviral activity of miR-136 was specific to IAV. [score:1]
We observed that chloroquine treatment did not reverse the cytokine-inducing ability of miR-136 (Fig. 5D). [score:1]
As shown in Fig. 2B, the titre of H5N1/DW was lowered by 1.8 logTCID [50] at 24 ours post-infection in cells transfected with miR-136. [score:1]
The data presented in this report uncovered that miR-136 has high immunostimulatory efficiency and can be abrogated by chemical modification. [score:1]
In the present study, we mainly characterize miR-136 as an IAV replication suppressor in vitro, the underlying mechanism of which is the enhancement of innate immunity by acting as a ligand of RIG-I. The collective data provide insight into the promising role of miRNAs for the treatment of IAV or other viral infections. [score:1]
In some experiments, 293T cells were also cotransfected with miR-136 or the NC, using final mimic concentrations of 60 nM. [score:1]
Furthermore, A549 cells were transfected with a chemosynthetic miR-136 mimic or the NC, followed by infection with H5N1/HM, using a multiplicity of infection (MOI) of 0.1. [score:1]
As expected, the oligonucleotide modification of miR-136 sequences disabled its immunostimulatory ability (Fig. 4A). [score:1]
UD, Undetermined; B-miR136, biotin-miR136; B-NC, biotin -negative control. [score:1]
However, modified miR-136 significantly decreased their mRNA levels, in contrast with the 2′-O-Me -modified NC. [score:1]
Identification of RIG-I as potential receptor for miR-136. [score:1]
Accordingly, it is conceivable that miR-136 most likely has triggered innate immunity just as miR21, miR29a or miR145 does. [score:1]
Thereafter, A549 cells were transfected with miR-136 mimic, the NC, or mock transfected. [score:1]
miR-136 triggers innate immunity by acting as a ligand for RIG-I. Endogenous miR-136 is associated with RIG-I -dependent signalling. [score:1]
Our data, together with a previous report 23, prompted us to study the impact of miR-136 on the IAV life cycle. [score:1]
If that is the case, this biological process could be closely associated with the recruitment of miR-136 to RIG-I. To confirm this assumption, confocal microscopy was used to examine for distribution following FAM-labeled miR-136 and FLAG-RIG-I cotransfection. [score:1]
Repetitively, we found that miR-136 reduced firefly luciferase activity in cells transfected with reporter constructs with IL-6 3′UTR inserts (Fig. 3B). [score:1]
These data indicated that miR-136 might be involved in virus -associated responses. [score:1]
We stimulated the 2′-O-Me -modified miR-136- or modified NC -transfected A549 cells using H5N1/HM virus at a MOI of 5 for 6 hours. [score:1]
miR-136 contains a centrally located poly (UUUU) motif. [score:1]
Thus, we next asked whether RIG-I was associated with miR-136 recognition. [score:1]
As shown in 293T cells, miR-136 clearly enhanced this efficacy on the basis of RIG-I transfection (Fig. 6B). [score:1]
Suppositionally, miR-136 might serve as a representative immune contributor among numerous microRNAs and potential immune activators in cells. [score:1]
These results indicated that miR-136 exerts potent antiviral activity against various H5N1 IAV strains. [score:1]
Genomic DNA encoding the hsa-mir-136 precursor was PCR-amplified from A549 cells and inserted into the pcDNA3.1+ vector (Invitrogen) between the XhoI and BamHI restriction sites. [score:1]
Since exogenous overexpression of miR-136 can activate RIG-I -dependent signalling pathway, we then investigated whether endogenous miR-136 are exactly involved in this biological process. [score:1]
miR-136 activates innate immunity independent of TLRs pathway. [score:1]
However, the specific mechanism whereby miR-136 modulates cellular signalling networks still needs to be further studied. [score:1]
The results indicated the physical interaction was true existed between miR-136 and RIG-I protein (Fig. 7B–D). [score:1]
To further consolidate our presumption, cells were transfected with 2′-O-Me -modified miR136 and modified NC, followed by Poly (I:C) stimulation. [score:1]
Both the microphotographs and flow cytometric data showed that the miR-136 exhibited strong anti-VSV activity (Supplementary Figure S2), suggesting that miR-136 exerts a wide-spectrum of antiviral activity that is not limited to H5N1 IAV. [score:1]
These results implied that miR-136 -mediated immune stimulation was most likely associated with a PRR-linked recognition pathway. [score:1]
Cellular localization and association of miR-136 with RIG-I.. [score:1]
Next, we further determined whether miR136 -mediated virus repression was specific to H5N1/HM. [score:1]
To determine the role that miR-136 may play in response to viral infection, we were interested in exploring potential host factors that contribute to this process. [score:1]
Furthermore, we also observed that VSV proliferation drastically decreased in the presence of miR-136, suggesting that miR-136 most likely interferes with IAV and VSV replication through a common mechanism. [score:1]
Although, it is worth debate that physilogical level of miR-136 was too low to activate RIG-I signal pathway. [score:1]
These observations suggested that an alternative pathway was required for miR-136 -mediated immunostimulatory activation. [score:1]
Western blot analysis showed a band of approximately 102 kDa in cells treated with miR-136 and positive control miR-145 (Fig. 6E upper), and this effect was enhanced by increasing miR-136 thansfection (Fig. 6E lower). [score:1]
Taken all these data together, it strongly suggests that RIG-I acted as a receptor for miR-136 recognition. [score:1]
As expected, we observed potent antiviral activity against two subtypes of H5N1 IAV in miR-136 -treated A549 cells. [score:1]
We found that the miR-136 significantly decreased viral titres at 24 and 36 hours post-infection, in comparison to the NC transfection (Fig. 2A). [score:1]
Full-length blots/gels are presented in Supplementary Figure 5. (A) A549 cells were mock -transfected or transfected with NC, miR-136, or 2′-O-methyl modified miR-136 for 24 hours, using final mimic concentrations of 60 nM in the culture supernatants. [score:1]
In this regard, the contribution to immune activation and inflammatory repression by miR-136 should not be ignored, especially respond to viral invasion. [score:1]
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[+] score: 165
Other miRNAs from this paper: hsa-mir-217, hsa-mir-145, hsa-mir-186, hsa-mir-384
The present study suggests an essential role for the CRNDE-miR-136-5p-Bcl-2/Wnt2 regulatory pathway in the malignant progression of glioma, by showing that CRNDE competitively binds miR-136-5p and thus indirectly inhibits the post-transcriptional expression of Bcl-2 and Wnt2, whose upregulation is known to be associated with glioma malignancy. [score:10]
Results of qRT-PCR showed that miR-136-5p expression was upregulated in U87 cells transfected with sh-CRNDE and downregulated in U251 cells transfected with pEX-2-CRNDE (Figure 5G and 5H). [score:9]
As shown in Figures 7D-7G, protein expression results paralleled the findings obtained by qRT-PCR, namely, upregulation of Bcl-2 and Wnt2 in pEX-2-CRNDE -transfected cells and downregulation of these proteins in U87 cells transfected with either sh-CRNDE or miR-136-5p mimics. [score:9]
Reports have shown that downregulation of miR-136-5p in human gliomas is significantly associated with a more aggressive and poor prognostic phenotype; conversely, its overexpression promotes apoptosis and modulates sensitivity to cisplatin by targeting AEG-1, Bcl-2, and E2F1 [33– 35]. [score:8]
in vitro data showed that miR-136-5p overexpression inhibited tumor cell proliferation, migration, and invasion, and enhanced apoptosis, implying that miR-136-5p exerts a tumor suppressive function in glioma cells. [score:7]
To determine whether CRNDE acted as a ceRNA by sequestering miR-136-5p and hindering it from binding to its target mRNAs, the expression of candidate miR-136-5p targets was examined by qRT-PCR in U251 cells transfected with pEX-2-CRNDE and in U87 cells transfected with miR-136-5p mimics or sh-CRNDE. [score:7]
These results suggest that CRNDE promotes glioma aggressiveness via suppression of miR-136-5p -mediated downregulation of Bcl-2 and Wnt2 (Figure 8). [score:6]
Our in vitro experiments in glioma cells confirmed that changes in the expression of CRNDE and miR-136-5p result in changes in Wnt2 and Bcl-2 expression at the mRNA and protein levels, although our study did not provide direct evidence for the corresponding miRNA/mRNA interactions. [score:6]
To further explore the function of miR-136-5p in glioma, U87 cells were transfected with miR-136-5p mimics to upregulate miR-136-5p expression (Figure 6A). [score:6]
The lncRNA CRNDE increases Bcl-2 and Wnt2 expression by inhibiting miR-136-5p. [score:5]
Meanwhile, experiments in human glioma cells showed that CRNDE not only binds miR-136-5p but also reduces its expression, which is consistent with the inverse correlation between CRNDE and miR-136-5p expression observed in clinical glioma specimens. [score:5]
Consequently, we run bioinformatics prediction analyses on TargetScan, miRanda, and DAVID, which identified Bcl-2 and Wnt2 as downstream target genes of miR-136-5p. [score:5]
Further bioinformatics analyses using TargetScan, miRanda, and DAVID identified Bcl-2 and Wnt2 as downstream targets of miR-136-5p in gliomas [22, 23]. [score:5]
Overexpression of miR-136-5p inhibits proliferation, migration, and invasion, and promotes apoptosis in glioma cells. [score:5]
Furthermore, compared to normal brain tissues, the expression of miR-136-5p was significantly downregulated in the 47 clinical glioma specimens and in our four glioma cell lines, and was also significantly and negatively correlated with pathological grade of glioma (Figures 5C-5E). [score:5]
Then, we conducted a series of systematic in vitro experiments in human glioma cells to infer molecular interactions from expression data derived from overexpression and silencing of CRNDE and miR-136-5p. [score:5]
We performed a bioinformatics analysis on TargetScan, miRanda, and DAVID and identified several genes, among them Bcl-2 and Wnt2, as candidate targets of miR-136-5p (Figure 7A and 7B). [score:5]
Results showed that among the several genes targeted by miR-136-5p, the expression of Bcl-2 and Wnt2 was significantly decreased in U87 cells transfected with miR-136-5p mimics. [score:5]
These genes attracted our attention because Bcl-2 has been reported to be a direct target of miR-136-5p [33], while both Wnt2 and Bcl-2 have been linked to the pathogenesis of glioma [36, 37]. [score:4]
Our results suggest that CRNDE functions as a ceRNA to promote glioma malignancy by indirectly inducing Bcl-2 and Wnt2 expression through binding and repression of miR-136-5p. [score:4]
CRNDE promotes glioma malignancy by preventing miR-136-5p -mediated downregulation of Bcl-2 and Wnt2. [score:4]
CRNDE binds to miR-136-5p and negatively regulates its expression. [score:4]
Plasmids encoding specific short-hairpin RNAs against CRNDE(sh-CRNDE), full-length CRNDE (pEX-2-CRNDE), or miR-136-5p (miRNA mimics), or their respective scrambled, non -targeting sequences, i. e. short-hairpin negative control (sh-NC), pEX-2 negative control (pEX-2-NC), and miR negative control (miR-NC) were designed and synthesized by GenePharma (Shanghai, China). [score:3]
Based on our present study and previous reports, we conclude that CRNDE promotes glioma progression by competitively binding miR-136-5p and inhibiting the post-transcriptional repression of Bcl-2 and Wnt2 mediated by this miRNA. [score:3]
These results indicated that miR-136-5p could suppress the activity of a luciferase reporter harboring CRNDE-Wt, and does not affect CRNDE-Mut activity. [score:3]
This evidence indicates that miR-136-5p exerts a tumor suppressor role in glioma. [score:3]
Correlation between CRNDE and miR-136-5p expression was analyzed by Spearman's correlation analysis. [score:3]
Figure 8 Based on our present study and previous reports, we conclude that CRNDE promotes glioma progression by competitively binding miR-136-5p and inhibiting the post-transcriptional repression of Bcl-2 and Wnt2 mediated by this miRNA. [score:3]
The involvement of miR-136-5p in tumor development has been studied by many groups, and diverse mechanisms have been proposed. [score:2]
Figure 5 (A) Schematic diagram of the predicted binding sites between CRNDE and miR-136-5p, and mutation of the putative miR-136-5p binding sequence in CRNDE. [score:2]
On the other hand, the migration and invasion assays revealed that miR-136-5p overexpression weakened both the migratory and invasive potential of glioma cells (Figures 6C-6F). [score:2]
We searched for potential binding sites of CRNDE to miRNAs on bioinformatics databases and found a putative, specific binding site for miR-136-5p. [score:1]
To verify this prediction, we generated wild type (Wt) CRNDE luciferase plasmids containing potential miR-136-5p binding sites, as well as mutant variants of each site. [score:1]
Figure 7 (A) Schematic diagram of the predicted binding sites between miR-136-5p and Bcl-2. (B) Schematic diagram of the predicted binding sites between miR-136-5p and Wnt2. [score:1]
The results predicted that miR-136-5p can bind the lncRNA product of the CRNDE gene (Figure 5A and Table 1). [score:1]
In addition, transfection with miR-136-5p mimics increased apoptosis (9.57% ± 0.88% vs 3.61% ± 0.44% in the miR-NC group; P< 0.01) (Figure 6G and 6H). [score:1]
HEK-293T cells were seeded in 12-well plates, and the cells were co -transfected with luciferase reporter plasmids and miR-136-5p mimics or miR-NC plasmids usingLipofectamine2000transfection reagent when they reached 80% confluence. [score:1]
miR-NC, negative control miR plasmid; miR-136-5p, miR-136-5p mimics. [score:1]
The predicted miR-136-5p binding sites in the 3′-UTR of CRNDE (CRNDE-Wt) and the designed mutant sequence (CRNDE-Mut) are indicated. [score:1]
A bioinformatics database (starBase v2.0) was examined to predict miRNA binding sites in the CRNDE sequence, and miR-136-5p was identified as a putative CRNDE -binding miRNA [21]. [score:1]
Figure 6 (A) miR-136-5p levels in U87 cells transfected with miR-136-5p mimics. [score:1]
As shown in Figure 5B, luciferase activity in the pEX-2-CRNDE Wt+miR-136-5p group was lower than in the pEX-2-CRNDE Wt group, the pEX-2-CRNDE-Mut+miR-136-5p group, and the pEX-2-CRNDE-Wt+miR-NC group(P<0.01). [score:1]
Moreover, Spearman's correlation analysis showed that CRNDE and miR-136-5p levels were inversely correlated in glioma samples(r =−0.74, P<0.01) (Figure 5F). [score:1]
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[+] score: 147
In this study, we clarified miR-136 suppressed PPP2R2A expression by directly targeting two conserved regions at positions 149–155 and 712–719 in its 3′-UTR. [score:8]
Overexpression of miR-136 Overcomes TGF- β1-Induced Proliferation ArrestPrevious studies showed that TGF- β1 inhibited cell proliferation in keratinocytes [21]; to investigate whether forced expression of miR-136 is able to modulate TGF- β1 -induced proliferation arrest of keratinocytes, HaCaT cells were transfected with miR-136 mimics or miR-NC and subsequently stimulated with 2 ng/mL TGF- β1 for 72 h. Successful increased expression of miR-136 was confirmed by qRT-PCR (Figure 2(a)). [score:7]
Recently, results of others indicated that miR-136 enhanced phosphorylation of Erk1/2 through inhibition of PPP2R2A expression to promoted cell proliferation in human non-small cell lung cancer, and the sequence at position 149–155 of the PPP2R2A 3′-UTR was determined to be the target site of miR-136 [25]. [score:7]
3.2. miR-136 Suppression by TGF- β1 Was Smad3-DependentIt was reported that Smad2/3 signaling as well as downstream gene targets such as PAI-1 expression is required for TGF- β mediated cytostasis in HaCaT cells [19, 20]. [score:7]
In conclusion, our results indicated that the miR-136 treatment bypassed TGF- β1 -induced proliferation arrest, at least partially through downregulation of PPP2R2A expression (Figure 5). [score:6]
However, miR-136 was found to target tumor suppressor PTEN in breast cancer cells [24]. [score:5]
To elucidate the underlying mechanisms by which miR-136 exerts its function, we explored miR-136 targets using the TargetScan bioinformatics algorithm. [score:5]
PPP2R2A Was Involved in TGF- β1-Induced Proliferation ArrestTo further establish whether the counteraction of miR-136 overexpression against TGF- β1 -induced proliferation arrest is mediated by repression of PPP2R2A, the expression of PPP2R2A in HaCaT cells treated with 2 ng/mL TGF- β1 for 48 h was analyzed by Western blot and the proliferation of PPP2R2A knockdown HaCaT cells stimulated with TGF- β1 was assessed by proliferation assay and flow cytometry. [score:5]
Previous studies showed that TGF- β1 inhibited cell proliferation in keratinocytes [21]; to investigate whether forced expression of miR-136 is able to modulate TGF- β1 -induced proliferation arrest of keratinocytes, HaCaT cells were transfected with miR-136 mimics or miR-NC and subsequently stimulated with 2 ng/mL TGF- β1 for 72 h. Successful increased expression of miR-136 was confirmed by qRT-PCR (Figure 2(a)). [score:5]
miR-136 is proposed to be a tumor suppressor in glioma and is capable of targeting the antiapoptosis genes AEG-1 and BCL-2 [23]. [score:5]
Our analysis revealed that PPP2R2A was a potential target of miR-136 based on putative conserved target sequences at positions 149–155, 712–719, and 1471–1478 of the PPP2R2A 3′-UTR (Figure 3(a)). [score:5]
To further establish whether the counteraction of miR-136 overexpression against TGF- β1 -induced proliferation arrest is mediated by repression of PPP2R2A, the expression of PPP2R2A in HaCaT cells treated with 2 ng/mL TGF- β1 for 48 h was analyzed by Western blot and the proliferation of PPP2R2A knockdown HaCaT cells stimulated with TGF- β1 was assessed by proliferation assay and flow cytometry. [score:5]
Our data suggested that modulation of keratinocytes proliferation by miR-136 depends on the cellular environment, especially in the presence of TGF- β1, which likely has major effects on the expression of miR-136 target gene PPP2R2A. [score:5]
To further examine whether miR-136 directly targets PPP2R2A, the luciferase reporters containing wild-type or mutant predicted miR-136 binding sites were cotransfected with miR-136 mimics or NC into Cos-7 cells. [score:4]
The effects of PPP2R2A knockdown were similar to those induced by miR-136 overexpression. [score:4]
3.1. miR-136 Was Downregulated by TGF- β1 in HaCaT and NHEK Cells. [score:4]
PPP2R2A Was a Direct Target of miR-136. [score:4]
The results showed that miR-136 was also significantly downregulated by TGF- β1 treatment in NHEK (Figure 1(b)). [score:4]
Moreover, transfection of miR-136 mimics could negatively regulate the proliferation inhibition of TGF- β1 and caused 29% proliferation enhancement. [score:4]
Taken together, these findings indicated that PPP2R2A was a functionally important target of miR-136 and was involved in the TGF- β1 regulated proliferation of HaCaT cells. [score:4]
Therefore, we proposed that, in the presence of TGF- β1, miR-136 was a positive modulator of keratinocytes proliferation and PPP2R2A was a functional target of miR-136 via binding to its 3′-UTR region. [score:3]
Overexpression of miR-136 Overcomes TGF- β1-Induced Proliferation Arrest. [score:3]
Cos-7 cells plated on 24-well plates were cotransfected with 50 nmol of either miR-136 mimics or NC oligos and with 200 ng reporter plasmid containing either wild-type or mutant target site using Lipofectamine 2000 Transfection Reagent according to the manufacturer's instructions. [score:3]
These results indicated that miR-136 was suppressed by TGF- β1 in a Smad3 -dependent manner in HaCaT cells. [score:3]
3.2. miR-136 Suppression by TGF- β1 Was Smad3-Dependent. [score:3]
Notably, the expression of PPP2R2A in HaCaT cells substantially decreased at 48 h after miR-136 transfection (Figure 3(e)). [score:3]
Reintroduction of miR-136 by transient transfection, as well as silencing by siRNA of target PPP2R2A, blocked TGF- β1 -induced proliferation arrest and increased the percentage of keratinocytes in the S phase of the cell cycle, while reducing the percentage of those in the G0/G1 phase. [score:3]
The result showed that the expression level of miR-136 in HaCaT decreased to 0.19-fold at 48 h after TGF- β1 treatment at 2 ng/mL and 0.13-fold for 5 ng/mL TGF- β1 (Figure 1(a)). [score:3]
To analyze miR-136 expression, reverse transcription PCR was performed using specific stem-loop RT primers from a Hairpin-it miRNAs qPCR Quantitation Kit (GenePharma, Shanghai, China), and quantitative real-time PCR was performed using the same kit on Applied Biosystems 7500 system. [score:2]
Here, we aimed to clarify the biological role of miR-136 in keratinocytes proliferation regulation by TGF- β1. [score:2]
3.1. miR-136 Was Downregulated by TGF- β1 in HaCaT and NHEK CellsTo investigate miR-136 expression changes during proliferation regulation of TGF- β1, we performed quantitative real-time PCR assay to measure miR-136 in keratinocytes treated with different concentration of TGF- β1. [score:2]
Taken together, these results indicated that miR-136 negatively regulated PPP2R2A in a posttranscriptional manner in HaCaT cells. [score:2]
Our results supported the notion that TGF- β1 -induced proliferation arrest was partially mediated by miR-136 reduction in HaCaT cells. [score:1]
Smad3 siRNA, miR-136 mimics, and NC were chemical synthesized by GenePharma (Shanghai, China) and the sequences were as follows: 5′-GAGCCTGGTCAAGAAACTCAATT-3′ for Smad3 siRNA, 5′-ACUCCAUUUGUUUUGAUGAUGGA-3′ for miR-136 mimics, and 5′-UUCUCCGAACGUGUCACGUTT-3′ for NC. [score:1]
Taken together, these findings indicated that miR-136 might act as a modulator of TGF- β1 -induced proliferation arrest in keratinocytes. [score:1]
Nonetheless, the crucial role of miR-136 in the TGF- β1 -induced proliferation arrest is largely unknown. [score:1]
Further studies are needed to determine whether miR-136 based therapeutic strategies could be exploited to protect keratinocytes proliferation and function in the condition of enhanced TGF- β1 during wound healing. [score:1]
These results suggested that miR-136 repressed PPP2R2A through 2 specific 3′-UTR binding sites at positions 149–155 and 712–719. [score:1]
There are several reports that miR-136 was implicated in cell proliferation and played different roles in different types of cells. [score:1]
The experiments showed significant reduction of miR-136 in keratinocytes treated with TGF- β1 and canonical Smad2/3 signaling pathway was involved. [score:1]
To investigate whether canonical Smad2/3 signaling is required for miR-136 repression during TGF- β1 -induced proliferation arrest in keratinocytes, HaCaT cells were transfected with Smad3 siRNA for 24 h and then treated with 2 ng/mL TGF- β1 for 48 h. By quantitative real-time PCR, the mRNA level of Smad3 was decreased to 0.2-fold at 48 h after transfection (Figure 1(c)), and in Smad3-silenced HaCaT cells, TGF- β1 treatment showed little effect on miR-136 expression (Figure 1(d)). [score:1]
Furthermore, the protein level of PPP2R2A was significantly reduced by miR-136 mimics transfection in HaCaT cells. [score:1]
In the present study, we identified and characterized PPP2R2A as a functional downstream target of miR-136 and examined the roles of miR-136 and PPP2R2A in TGF- β1 -induced proliferation arrest in keratinocytes. [score:1]
Briefly, 25 pmol of miR-136 mimics, PPP2R2A siRNA (Santa Cruz, CA, USA), Smad3 siRNA, or negative control (NC) was used with 7.5  μL of the transfection reagent and the medium was replaced with fresh medium 24 h after transfection. [score:1]
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[+] score: 43
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-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-127, mmu-mir-132, mmu-mir-133a-1, mmu-mir-136, mmu-mir-144, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-10b, mmu-mir-185, mmu-mir-190a, mmu-mir-193a, mmu-mir-203, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-215, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-144, hsa-mir-152, hsa-mir-127, hsa-mir-146a, hsa-mir-185, hsa-mir-190a, hsa-mir-193a, hsa-mir-206, mmu-mir-148a, 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-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-337, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-29b-2, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, hsa-mir-337, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-215, mmu-mir-411, mmu-mir-434, hsa-mir-486-1, hsa-mir-146b, hsa-mir-193b, mmu-mir-486a, mmu-mir-540, hsa-mir-92b, hsa-mir-411, hsa-mir-378d-2, mmu-mir-146b, mmu-mir-193b, mmu-mir-92b, mmu-mir-872, mmu-mir-1b, mmu-mir-3071, mmu-mir-486b, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, hsa-mir-203b, mmu-mir-3544, hsa-mir-378j, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-let-7k, hsa-mir-486-2
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
It remains unknown whether the down-regulated miRNA* strands, miR-136-3p, -337-3p, -434-5p, -3071-3p, and -3544-5p, have regulatory roles contributing to muscle aging. [score:5]
These results suggested that Rybp and its putative regulatory miRNA, miR-136, could contribute to muscle aging process. [score:2]
miRNA Fold Change P-value mmu-miR-337-5p −5.2 0.0149 mmu-miR-3544-3p −5.1 0.0147 mmu-miR-540-5p −4.9 0.0200mmu-miR-337-3p [a] −3.0 0.0324mmu-miR-3544-5p [a] −3.0 0.0308 mmu-miR-434-3p −2.1 0.0001 mmu-miR-3071-5p −2.0 0.0004mmu-miR-136-3p [a] −2.0 0.0004mmu-miR-3071-3p [a] −1.6 0.0000 mmu-miR-136-5p −1.6 0.0000 mmu-miR-143-5p −1.2 0.0004 mmu-miR-190a-5p −1.0 0.0139 mmu-miR-872-3p −0.9 0.0152 mmu-miR-193a-3p −0.9 0.0164 mmu-miR-144-3p −0.8 0.0298 mmu-miR-127-3p −0.7 0. 0002mmu-miR-434-5p [a] −0.6 0.0082 mmu-miR-148a-3p −0.6 0.0130 mmu-miR-411-5p −0.6 0.0091 a miRNA* (passenger) strand processed from opposite arm of the mature miRNA. [score:1]
Of note, in our dataset, five miRNAs, miR-136, -337, -434, -3071, -3544, exhibited a high dominance in both the guide and passenger strands. [score:1]
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[+] score: 37
We confirmed that MMP13 repression via circRNA-CER knockdown was reversed by the miR-136 inhibitor, and the effect regarding the high expression of COL2 and aggrecan was also eliminated (Fig. 7A). [score:6]
Additionally, MMP-13 protein expression was significantly increased by si-CER treatment, and this effect was reduced by co-transfection with the miR-136 inhibitor and si-CER in chondrocytes (Fig. 7B). [score:5]
Type II collagen protein expression was significantly elevated by si-CER treatment, and this increase was reversed through co-transfection with the miR-136 inhibitor and si-CER in chondrocytes. [score:5]
We co -transfected the miR-136 inhibitor and si-CER into chondrocytes. [score:3]
The luciferase signal of the wild-type MMP13 reporter was suppressed by miR-136, whereas the luciferase signal of the mutant reporter was not affected (Fig. 6D). [score:3]
In our study, we only focused on miR-136, as the only miRNA could target both circRNA-CER and MMP13. [score:3]
How to cite this article: Liu, Q. et al. Circular RNA Related to the Chondrocyte ECM Regulates MMP13 Expression by Functioning as a MiR-136 ‘Sponge’ in Human Cartilage Degradation. [score:3]
Several studies reported that miR-136 might play important roles in regulating chondrogenic differentiation of human Adipose-Derived Stem Cell and affect the process of chondrogenesis 23. [score:2]
MMP13 3′-UTR containing the putative binding site of miR-136, as well as its identical sequence with a mutation of the miR-136 seed sequence, was inserted between the restrictive sites Xho I and Not I of pmiR-RB-ReportTM and validated by sequencing. [score:2]
According to the network above, there were 5 miRNA binding sites for circRNA-CER, and they were miR-636, miR-665, miR-217, miR-646 and miR-136, respectively. [score:1]
We found that circRNA-CER harbors miRNA -binding sites, including miR-636, miR-665, miR-217, miR-646 and miR-136. [score:1]
In addition, miR-136 could also bind to the 3′-UTR of MMP13. [score:1]
The result showed that miR-136 also matched the 3′UTR of MMP13 (Fig. 6C). [score:1]
We confirmed that circRNA-CER is the decoy for MMP13 and that circRNA-CER functions like a “sponge” by competitively binding miR-136. [score:1]
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[+] score: 26
The gene expression in HIV/MDD of genes which are targets of miRNAs that show significant target bias is illustrated in Figure 4. MiR-367 (Accession Number 442912), miR-125a-3p (Accession Number 406910), miR-502-5p (574504), and miR-136 (Accession Number 406927) showed significant target bias across all four windows (asterisks in Figure 3). [score:9]
The gene expression in HIV/MDD of genes which are targets of miRNAs that show significant target bias is illustrated in Figure 4. MiR-367 (Accession Number 442912), miR-125a-3p (Accession Number 406910), miR-502-5p (574504), and miR-136 (Accession Number 406927) showed significant target bias across all four windows (asterisks in Figure 3). [score:9]
The direction of the dysregulation of the miRNA is indication by the arrow; for miR-367, miR-136, and miR-125a, the majority of targets are dysregulated in accordance with the miRNAs; while for miR-502, the majority of targets are anticorrelated. [score:8]
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[+] score: 23
Each scatter spot representing average normalized expression level of miRNA in three repeats of each treatment; (b) 13 miRNAs exhibiting aberrant expression in Jurkat cells cultured with TNF-α (20 ng/mL) for 7 days; (c) decreased expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 in RA T cells miRNA, compared with normal T cells. [score:6]
Initially, our studies showed that among the expression of T cell miRNAs affected by TNF-α in Jurkat cells, the expression levels of miR-139-3p, miR-204, miR-760, miR-383, miR-524-5p, miR-136, miR-548d-3p, and miR-214 were significantly decreased in RA T cells. [score:5]
The expression levels of 12 miRNAs, including miR-139-3p, miR-204, miR-760, miR-432, miR-524-5p, miR-136, miR-548d-3p, miR-206, miR-214, miR-383, miR-224, and miR-887 were significantly lower, whereas the expression level of miR-146a was significantly higher, in Jurkat cells after being cultured with TNF-α for 7 days (fold change > 4, p < 0.05, Fig.   1b). [score:5]
Decreased expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 were noted in RA T cells. [score:3]
The expression of miR-139-3p, miR-204, miR-760, miR-524-5p, miR-136, miR-548d-3p, miR-214, miR-383, and miR-887 was found to be significantly lower in RA T cells (p < 0.05), compared with controls (Fig.   1c). [score:2]
The fold changes of expression levels for these miRNAs were 0.42-fold for miR-139-3p, 0.43-fold for miR-204, 0.13-fold for miR-760, 0.32-fold for miR-524-5p, 0.45-fold for miR-136, 0.19-fold for miR-548d-3p, 0.37-fold for miR-214;0.36-fold for miR-383, and 0.14-fold for miR-887, compared with controls. [score:2]
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[+] score: 22
Overall, 18 miRNAs were differentially expressed; 5 miRNAs were found up-regulated in the group of patients that are in complete remission when compared to the relapsed or the control groups; miR-3681 (A), miR-601 (B), miR-642a (C), miR-136 (D) and miR-26b (E). [score:5]
Specifically, 2 miRNAs; miR-720a and miR-891a were down-regulated and 6 miRNAs; miR320e, miR-3681, miR-601, miR-642a, miR-136 and miR-26b were overexpressed in the patient cohort when compared to the control group. [score:5]
Based on our findings, following both initial and meta-analyses, we report the up-regulation of miR-3681, miR-34a, miR-136, miR-26b and miR-192 in the patient group, subsequently leading to the conclusion that they might possess oncogenic activities. [score:4]
Based on the current findings, 8 miRNAs; miR-3681, miR-601, miR-320e, miR-34a, miR-642a, miR-136, miR-26b and miR-192 were found overexpressed in the patient group. [score:3]
In particular, miR-3681 (A), miR-642a (B), miR-26b (C), miR-136 (D) and miR-320e (E) were increased in alive samples as well as manifested linear regression with respect to expression moving from alive samples to controls. [score:3]
In total, 8 miRNAs were associated with patients’ clinical outcome; miR-3681, miR-601, miR-320e, miR-642a, miR-720, miR-891a, miR-136 and miR-26. [score:1]
However, the oncogenic role of miR-3681, miR-26b and miR-136 were validated with meta-analyses (Table  1). [score:1]
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[+] score: 17
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-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
Ssc-miR-136 was highly expressed in mpiPSCs but it had low expression in hpiPSCs. [score:5]
Ssc-miR-182, ssc-miR-187, ssc-miR-136, ssc-miR-210, ssc-miR-217 and ssc-miR-10b participate in regulation Neurotrophin signaling pathway by targeting corresponding genes, including BNDF, SHC4, KRAS and FOXO3. [score:4]
We also assessed another three selected miRNAs, ssc-miR-136, ssc-miR-217 and ssc-miR-182, which were found to be more highly expressed in mpiPSCs (Fig 3C). [score:3]
In the porcine Dlk1-Dio3 locus, most miRNAs were silenced except miR-136, which was highly expressed in the mpiPSCs. [score:3]
The sequencing studies only detected reads for ssc-miR-493-3p, ssc-miR-493-5p and ssc-miR-136. [score:1]
Of the miRNAs in the porcine Dik1-Dio3 region, there were four annotated miRNAs: ssc-miR-127, ssc-miR-495, ssc-miR-493 and ssc-miR-136. [score:1]
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[+] score: 16
Evidence of the concerted interplay of miRNAs regulated by CpG-ODN and their potential target mRNAs was observed (Fig. 4) for 2 miRNAs upregulated (hsa-miR-302b and hsa-miR-374b) and for 13 miRNAs downregulated in CpG-ODN -treated mice (hsa-miR-135a, hsa-miR-136, hsa-miR-340, hsa-miR-445-5p, hsa-miR-424, hsa-miR-96, hsa-miR-142-3p, hsa-miR-140-5p, hsa-miR-542-3p, hsa-miR-18a, hsa-miR-18b, hsa-miR-101, and hsa-miR-99a). [score:10]
Comparison of hsa-miR-18a, hsa-miR-18b, hsa-miR-140-5p, hsa-miR-101, hsa-miR-556-3p, hsa-miR-424, hsa-miR-136, hsa-miR-340, hsa-miR-302b expression obtained by miRNA expression profile and qRT-PCR on tumors collected from human IGROV-1 ovarian tumor-bearing mice treated daily i. p. with CpG-ODN or saline (control group). [score:5]
RT-qPCR using the RNA profiled in microarray analysis validated all 9 miRNAs (Fig. S1), whereas RT-qPCR using the RNA of the replica confirmed 6 of 9 miRNAs (p<0.05), with a trend observed for hsa-miR-18b and hsa-miR-101 but not for hsa-miR-136 (Fig. 2). [score:1]
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11
[+] score: 16
Ssc-miR-124a was found to target the NP genes isolated in all 38 different times, while ssc-miR-145 targeted the NP genes isolated at 35 different times and ssc-miR-136 targeted the NA and NP genes isolated in 31 of the 38 times. [score:7]
Interestingly, some miRNAs were found to target more than one gene of SIV-H1N1/2009, for example, the binding sites for ssc-miR-361-3p located in both viral PB2 and HA, and the binding sites for ssc-miR-136 located in both viral NA and NP. [score:3]
Only miR-145 was predicted to have putative target sites in the HA gene [39], and an unpublished data mentioned that miR-136 also had potential binding sites in the HA gene [29]. [score:3]
Zhao L. Zhu J. Zhou H. Zhao Z. Zou Z. Liu X. Lin X. Zhang X. Deng X. Wang R. Identification of cellular microRNA-136 as a dual regulator of RIG-I -mediated innate immunity that antagonizes H5N1 IAV replication in A549 cellsSci. [score:2]
Interestingly, our genomic RNA screen also predicted the interaction pairs of ssc-miR-136 and NA, and ssc-miR-136 and NP. [score:1]
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12
[+] score: 15
This lack of miR-136 expression could be due to lack of necessary cis-regulatory elements or trans-regulatory factors required for miR-136 biogenesis; we did not investigate the possibility that an alternative approach to successfully express miR-136 in NALM6 would validate a growth inhibitory role for this miR. [score:7]
Since NALM6 cells transduced with miR-432∼136 did not result in miR-136 overexpression, we did not include miR-136 targets in Set 2 (Figure 4A). [score:5]
However, no expression of miR-136 was detected in miR-432∼136 cluster-transduced NALM6 cells. [score:3]
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[+] score: 13
Shen S Upregulation of miR-136 in human non-small cell lung cancer cells promotes Erk1/2 activation by targeting PPP2R2ATumour Biol. [score:6]
By considering the fold-change threshold and percentage of incidence, among the 95 screened miRNAs which have functional significance with regard to potential roles in cancer, cell development and apoptosis, ten miRNAs (miR-205, miR-196a, miR-149, miR-183, miR-224, miR-210, miR-150, miR-136, miR-200c and miR-141) were identified which may play a putative role in cancer development, metastasis and have potential as biomarkers for the detection of NPC. [score:3]
The incidence of up and down regulation of these ten miRNAs, including miR-205 (94.1%), miR-196a (88.2%), miR-149 (82.4%), miR-183 (64.7%), miR-224 (58.8%), miR-210 (58.8%), miR-136 (47.1%), miR-200c (64.7%), miR-141 (52.9%) and miR-150 (82.4%) between non-NPC controls and NPC patients ranges from about 47% to 94% incidence rate. [score:2]
They were miR-205, miR-196a, miR-149, miR-183, miR-224, miR-210, miR-136, miR-200c, miR-141 and miR-150. [score:1]
Among these 10 miRNAs candidates, 6 (miR-196a, miR-183, miR-224, miR-136, miR-200c and miR-150) and 3 (miR-136, mi141 and 150) miRNAs have no data reported in HNSCC and ESCC, respectively. [score:1]
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[+] score: 12
MiR-485 has been implicated in synaptic formation and maintenance and has been reported to be dysregulated in Alzheimer’s disease and Huntington’s disease [32], miR-124 is known as a neurodevelopmental regulator [33], miR-219 required for neural precursor differentiation in zebrafish [34] and promotes myelination in rats [35], miR-127 regulates cell proliferation and senescence by targeting BCL6 [36] while miR-136, miR-873 and miR-410 have all been studied in the context of glioma growth, invasiveness and apoptosis 37– 39. [score:11]
miRNAlog [2]FoldChange P-value Corrected P-value hsa-mir-577 −3,28 1,46E-10 3,87E-08 hsa-mir-182-5p −2,70 6,50E-15 3,44E-12 hsa-mir-485-5p −2,12 8,79E-05 8,45E-03 hsa-mir-124-3p −1,83 1,05E-05 1,85E-03 hsa-mir-218-5p −1,68 1,54E-04 1,16E-02 hsa-mir-183-5p −1,62 3,14E-04 2,08E-02 hsa-mir-873-5p −1,58 9,80E-04 3,25E-02 hsa-mir-133a −1,53 6,05E-04 2,29E-02 hsa-mir-487b −1,45 1,56E-03 4,59E-02 hsa-mir-219-5p −1,44 9,55E-04 3,25E-02 hsa-mir-409-3p −1,34 1,12E-03 3,48E-02 hsa-mir-889 −1,23 5,71E-04 2,29E-02 hsa-mir-136-3p −1,15 1,75E-03 4,87E-02 hsa-mir-410 −1,12 4,02E-04 2,29E-02 hsa-mir-127-3p −0,95 5,61E-04 2,29E-02 hsa-mir-148a-3p 1,23 4,99E-04 2,29E-02 hsa-mir-155-5p 1,82 9,56E-05 8,45E-03 hsa-mir-221-3p 2,10 4,82E-04 2,29E-02For each differently expressed miRNA we report the standard name according to MirBase database, the log [2] fold-change, the P-value and the corresponding corrected P-value as calculated by DESeq. [score:1]
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15
[+] score: 11
severe (p<0.05) cfa-let-7d, cfa-miR-101, cfa-miR-10a, cfa-miR-1296, cfa-miR-1306, cfa-miR-1307, cfa-miR-130a, cfa-miR-136, cfa-miR-17, cfa-miR-181b, cfa-miR-196b, cfa-miR-197, cfa-miR-215, cfa-miR-22, cfa-miR-30d, cfa-miR-33b, cfa-miR-497, cfa-miR-503, cfa-miR-574, cfa-miR-628, cfa-miR-676Comparing the miRNA differential expression analyses between disease states obtained by RT-qPCR and RNAseq, we observed discordances between the two methods. [score:5]
severe (p<0.05) cfa-let-7d, cfa-miR-101, cfa-miR-10a, cfa-miR-1296, cfa-miR-1306, cfa-miR-1307, cfa-miR-130a, cfa-miR-136, cfa-miR-17, cfa-miR-181b, cfa-miR-196b, cfa-miR-197, cfa-miR-215, cfa-miR-22, cfa-miR-30d, cfa-miR-33b, cfa-miR-497, cfa-miR-503, cfa-miR-574, cfa-miR-628, cfa-miR-676 Comparing the miRNA differential expression analyses between disease states obtained by RT-qPCR and RNAseq, we observed discordances between the two methods. [score:5]
severe (p<0.05) cfa-let-7c, cfa-miR-10a, cfa-miR-1307, cfa-miR-132, cfa-miR-136, cfa-miR-181a, cfa-miR-181b, cfa-miR-196b, cfa-miR-20a, cfa-miR-30d, cfa-miR-33b, cfa-miR-34c, cfa-miR-497, cfa-miR-499, cfa-miR-676 Mild vs. [score:1]
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[+] score: 11
With respect to a number of studies, miR-515 and miR-136 were up-regulated in cancer tissues (Table 5). [score:4]
Except for miR-515 and miR-136, which were only cited once (oral squamous cell [44] and lung cancer [51] respectively), which showed an increasing number of miRNAs in tumor tissues), no other literature is available regarding the number of other miRNAs predicted for targeting CD3G in tumor tissues or blood sera of cancer patients (Table 5). [score:3]
In In this study, the TargetScanHuman database identified13 miRNAs (miR-1200, miR-378d,e,i,c,h,b,f, miR-422a, miR-3690, miR-619, miR-4446-3p, miR-2909, miR-4777-5p, miR-136, miR-515-5p, miR-4659a,b-3p, miR-494 and miR-593) which were conserved and similar to the CD3G gene. [score:3]
From the first group only 6 miRNAs (miR-378, miR-422a, miR-593 and miR-494, miR-515 and miR-136), from the second group one miRNA (miR-138) and from the third group only one miRNA (miR-214) were identified and studied, based on their levels in tissues or blood sera of different cancer patients. [score:1]
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[+] score: 11
The literature shows that miR-136 promotes downregulation in osteoblast differentiation [26], suggesting that in the present work this microRNA benefited the deposition of extracellular matrix in MR group as seen in our biochemical results. [score:4]
Real-time quantitative PCR allowed analysis of six miRNAs that were differentially expressed in the experimental groups: miR-31-3p, miR-134, miR-136-3p, miR-376C-3p, miR-494, and miR-424-5p (Table 6). [score:3]
We showed that miR-136-3p exhibits a lower expression in cells seeded on rough microtexture surfaces when compared to N and MR surfaces in microarray and qRT-PCR data. [score:2]
mRNA and microRNA oligoarray data were confirmed by qRT-PCR for five mRNAs (SMURF2, NOTCH1, PHOSPHO1, COL24A1, and FGF1) and six microRNAs (miR-31-3p, miR-134, miR-136-3p, miR-376c-3p, miR-424-5p, and miR-494). [score:1]
These miRNAs are associated with several functions like apoptosis (miR-134 and miR-494), bone mineralization (miR-31-3p, miR-136-3p, miR-376C-3p, and miR-424-5p), and cell growth and proliferation (miR-134) (http://geneontology. [score:1]
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[+] score: 10
miRNA Expressionp-value Expression fold change (log2) Survivalp-value hsa-miR-136 7.52E-14 −1.69 NS hsa-miR-145 5.88E-04 −1.04 0.005 hsa-miR-155 1.18E-21 1.94 NS hsa-miR-181b 5.44E-02 −0.22 NS hsa-miR-342 4.35E-10 −1.25 NS hsa-miR-129 1.29E-16 −3.39 NS hsa-miR-376a 4.35E-07 −0.63 NS hsa-miR-376b 7.37E-02 0.07 NS Survival p-value was calculated from miRNA expression data with Kaplan-Meier analysis. [score:5]
Five miRNAs, hsa-miR-136, -145, -376a, -342, and -129, showed significantly lower expression values in the GBM patient tissue samples compared to normal brain tissue. [score:2]
Six miRNAs (hsa-miR-136, -145, -155, -376a, -342, and -129) had significantly different expression values when compared to normal brain tissue (Table 1). [score:2]
Eight of the nine previously identified miRNAs (hsa-miR-136, -145, -155, -181b, -342-5p, -342-3p, -376a/b) were also validated in the Dharmacon precursor miRNA screenings in the A172 and LN405 cell lines. [score:1]
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[+] score: 9
Four of these five miRNAs (mir-127-3p, mir-136, mir-376a and mir-376c) were found to be down-regulated but not entirely silenced in nevi and melanoma (Additional file 2). [score:4]
Four of these miRNAs (namely mir-127-3p, mir-136, mir-376a and mir-376c) were shown to be down-regulated but not completely silenced in nevi and melanomas. [score:4]
obtained with the more sensitive method of qRT-PCR verified that mir-376a, mir-376c and mir-136 can be significantly induced following treatment with epigenetic modifiers in most of the melanoma cell lines (Figure  2E and results not shown). [score:1]
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20
[+] score: 9
Liu et al. [29] found that expression of 4 miRNAs was significantly upregulated (miR-136, miR-703, miR-30b, and miR-107), while miR-653 and miR-598 were significantly downregulated. [score:9]
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[+] score: 9
Other miRNAs from this paper: hsa-mir-146a, hsa-mir-326
Meanwhile, in non-solid neoplasms such as chronic myeloid leukemia (CML), the overexpression of SMO has been associated with a loss of expression of miR-136 in marrow-derived CD34+ cells, while overexpression of miR-326 decreases the expression of SMO, diminishing cell proliferation and increasing the apoptotic activity of CD34+ CML cells. [score:9]
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22
[+] score: 9
As determined in a previous study, circRNA_100876 could regulate MMP-13 expression through inhibiting miR-136 activity and thus participated in chondrocyte extracellular matrix degradation [134]. [score:6]
Foxo3P and circ-Foxo3 were highly expressed in noncancerous cells and could function as miRNA sponges for several cancer -associated miRNAs, including miR-22, miR-136, miR-138, miR-149, miR-433, miR-762, miR-3614-5p, and miR-3622b-5p. [score:3]
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23
[+] score: 9
To validate the accuracy of our heatmap results, we performed qPCR to confirm the expression levels of the top up-regulated miRNAs (such as miR365a-3p, miR-2277-3p, and miR-184-3p) and down-regulated miRNAs (such as miR-21-5p, miR-136-3p, and miR-127-3p) (Fig.   1g). [score:9]
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24
[+] score: 8
RT-qPCR was performed to evaluate the expression levels of hsa_circ_0043497 (A) and its top 5 predicted miRNA targets (miR-335-3p, miR-186-5p, miR-380-5p, miR-296-3p and miR-522-3p) (B), hsa_circ_0001204 (C) and its top 5 predicted miRNA targets (miR-612, miR-657, miR-362-3p, miR-377-3p and miR-136-5p) (D) in ten human MDMs after 24 h of infection with H37Rv. [score:5]
For hsa_circ_0001204, the potential miRNAs targets include miR-612, miR-657, miR-362-3p, miR-377-3p and miR-136-5p. [score:3]
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[+] score: 8
However, other reports showed that miR-136 inhibited IL-6 expression by binding with 3′-UTR of IL-6 [71], and the mechanism underlying action of miR-136 remains to be clarified. [score:5]
Zhao L. Zhu J. Zhou H. Zhao Z. Zou Z. Liu X. Lin X. Zhang X. Deng X. Wang R. Identification of cellular microRNA-136 as a dual regulator of RIG-I -mediated innate immunity that antagonizes H5N1 IAV replication in A549 cells Sci. [score:2]
Another miRNA, H5N1 -induced host miR-136, was indicated as an immune agonist of RIG-I, causing IL-6 and IFN-β accumulation in A549 cells. [score:1]
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26
[+] score: 8
Further, they did not find any significant difference in miR-9, miR-10b, miR-15a, miR-16, miR-125b, miR-136 and let-7f expression levels among the examined groups [18]. [score:3]
Our findings revealed a gradual decrease in miR-10b, miR-125b, miR-136 and let-7f expression levels from normal mammary tissue, through benign tumours and non-metastatic malignant tumours, to metastatic tumours. [score:3]
Von Deetzen et al. compared the expression profiles of 16 microRNAs (miR-136, miR-143, let-7f, miR-29b, miR-145, miR-9, miR-10b, miR-203, miR-125b, miR-15a, miR-16, miR-21, miR-101, miR-210, miR-194 and miR-125a) in three types of canine mammary tumours (adenoma, non-metastasising carcinoma, metastasising carcinoma), lymph node metastases and in a normal mammary gland. [score:2]
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[+] score: 8
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
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[+] score: 7
This study led to detect seven differentially expressed miRNAs: miR-136, miR-743a and miR-463* that were over-expressed, while miR-290-5p, miR-291a-5p, miR-293 and miR-294* were down-expressed [79]. [score:7]
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[+] score: 7
They identified 13 miRNAs that were differentially expressed in OSCC when compared to healthy controls and, among them, 11 miRNAs were down-regulated (miRNA-136, miRNA-147, miRNA-1250, miRNA-148a, miRNA-632, miRNA-646, miRNA-668, miRNA-877, miRNA-503, miRNA-220a, miRNA-323-5p), and two miRNAs were over-expressed (miRNA-24, miRNA-27b). [score:7]
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f Lentiviral expression of miR-770, miR-136, miR-379, and miR-410 (n = 4) and g RNAi (shRNA) -mediated knockdown of DLK1, MEG3, MEG8, and MEG9 (n = 5) in CD34 [+] HSPCs in vitro. [score:4]
We ectopically expressed four miRNAs representing different clusters and/or miRNA-families: miR-770 located in the intron of MEG3, miR-136 from the miR-127~136 cluster, and miR-379 and miR-410 as the first and last miRNAs from the megacluster (Supplementary Fig.   7a). [score:3]
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Seven over-expressed microRNAs that were altered at least four fold, including hsa-miR-671-5p, hsa-miR-542-5p, hsa-miR-542-3p, hsa-miR-1185, hsa-miR-539, hsa-miR-148a and hsa-miR-301a, (Figure 4A) and six over-expressed microRNAs that were highly expressed (normalized data ≥6), including hsa-miR-1290, hsa-miR-136, hsa-miR-424, hsa-miR-30a, hsa-miR-148a and hsa-miR-1246 (Figure 4B), were selected for further qRT-PCR analyses. [score:7]
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[+] score: 6
The expression patterns of miRNAs that were previously reported in adipocytes or their precursors are in agreement with published data, as summarized in Additional file 3. However, the adipogenesis -dependent regulation of many of the differentially expressed miRNAs we identified has never been described before; these include miR-642a-3p, miR-345, miR-193b, miR-29c, miR-664, miR-10b, miR-136, miR-22*, miR-181a, miR-154*, let-7a, let-7b and let-7c. [score:6]
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[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-198, hsa-mir-148a, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-205, hsa-mir-210, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-186, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-299, hsa-mir-26a-2, hsa-mir-373, hsa-mir-376a-1, hsa-mir-342, hsa-mir-133b, hsa-mir-424, hsa-mir-429, hsa-mir-433, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-455, hsa-mir-376a-2, hsa-mir-33b, hsa-mir-644a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-301b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-3613, hsa-mir-4668, hsa-mir-4674, hsa-mir-6722
Boese et al. (2016) recently demonstrated that during preclinical stage of prion disease, miRNAs enriched in synaptoneurosomes including miRNA-124a-3p, miRNA-136-5p and miRNA-376a-3p were elevated. [score:3]
It is demonstrated that during preclinical stage of prion disease, miRNAs abundant in synaptoneurosomes including miRNA-124a-3p, miRNA-136-5p and miRNA-376a-3p are increased. [score:3]
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[+] score: 6
We have also reported that miR-136-3p targets LHR mRNA to induce the transient downregulation of LHR mRNA in granulosa cells after ovulation [19]. [score:6]
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[+] score: 6
To test this, we randomly selected five additional mIRs located in these two clusters: miR-127, miR-136, miR-154, miR-337, and miR-379 to examine their expression in our CLL patients. [score:3]
Expression levels of five miRNAs in treated and untreated CLL patients for b miR-127, c miR-136, d miR-154, e miR-337, and f miR-379. [score:3]
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[+] score: 6
miR-136, down-regulated in our study, was up-regulated during chondrogenesis of human adipose-derived stem cells suggesting that it can be considered as a player in the switch from white adipocyte to chondrocyte [27]. [score:6]
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As described recently miR-136-3p expression levels were increased after the administration of human chorionic gonadotropin to ovarian cells (Kitahara et al., 2013). [score:3]
Role of microRNA-136-3p on the expression of luteinizing hormone-human chorionic gonadotropin receptor mRNA in rat ovaries. [score:3]
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[+] score: 6
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-139, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-190a, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-429, hsa-mir-491, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, hsa-mir-517a, hsa-mir-500a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-637, hsa-mir-151b, hsa-mir-298, hsa-mir-190b, hsa-mir-374b, hsa-mir-500b, hsa-mir-374c, hsa-mir-219b, hsa-mir-203b
In a review, Gramantieri et al. (2008) show miRNAs aberrantly expressed in HCC compared to non-tumorous liver tissue (up -expression of miR-33, miR-130, miR-135a, miR-210, miR-213, miR-222, miR-331, miR-373, miR-376a, and down -expression of miR-130a, miR-132, miR-136, miR-139, miR-143, miR-145, miR-150, miR-200a, miR-200b, miR-214). [score:6]
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39
[+] score: 6
In regards to age, we discovered that the expression levels of 14 miRNAs (miR-654-5p, miR-493*, miR-410, miR-376a*, miR-758, miR-381, miR-543, miR-539, miR-487b, miR-337-5p, miR-136*, miR-154*, miR-330-3p, and miR-421) were significantly higher in HCC up to 66 years old than in HCC over 67 years old. [score:3]
o.   fold changep-valuehsa-miR-654-5p3.880.00014hsa-miR-493*3.100.00016hsa-miR-4102.930.00029hsa-miR-376a*2.660.00072hsa-miR-7582.870.00073hsa-miR-3812.390.00094hsa-miR-5432.070.00119hsa-miR-5393.060.00124hsa-miR-487b2.020.00186hsa-miR-337-5p2.540.00195hsa-miR-136*2.790.00246hsa-miR-154*2.270.00337hsa-miR-330-3p2.440.00759 hsa-miR-421 2.45 0.01282We also identified miRNAs with expression levels that varied according to gender and age. [score:3]
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40
[+] score: 5
For the few other pre-miRNAs transfected to Hela cells (e. g., pre-miR-136) no Dicer specific cleavage products were detected using either miRNA or miRNA*-specific probes (Figure S4). [score:1]
The pre-miRNAs used for transfection, pre-miR-132, pre-miR-136, pre-miR-139 and pre-miR-526b, were chemically synthesized (Curevac) and purified by polyacrylamide gel electrophoresis. [score:1]
of the products generated from synthetic pre-miR-136 that was transfected into HeLa cells using Oligofectamine. [score:1]
Figure S4 Analysis of endogenous Dicer activity in Hela cells on pre-miR-136. [score:1]
RNA was isolated 24 h after transfection with the indicated pre-miRNA and northern blotted (lanes labeled “in cell”) with a specific probe for miRNA derived from 5′-arm or 3′-arm of pre-miR-136, as indicated by the label 5′ or 3′. [score:1]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-770
Two miRNAs (miR-770-5p and hsa-miR-136*, red circle) were more highly expressed (p < 0.0001) in the CR group, and one (hsa-miR-9, green circle) was more highly expressed in the IR group. [score:5]
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42
[+] score: 5
While expression of miR-136, miR-376a and miR-377 did not significantly change during treatment, expression of miR-376c and miR-127-3p was significantly increased by Aza treatment and was further elevated by the combined treatment with Aza and PBA. [score:5]
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43
[+] score: 4
Within hsa-mir-136, hsa-mir-423, hsa-mir-376b and hsa-mir-1307, their 5p arm miRNAs have higher expression level in the normal tissue; while their 3p arm miRNAs dominated in the tumor tissue. [score:3]
For the pre-miRNAs originally annotated to encode miRNAs at both arms, the major arms of hsa-mir-374a, hsa-mir-500a, hsa-mir-625 and hsa-mir-136 are their 5p arms; while, the major arms of hsa-mir-664, hsa-mir-144, hsa-mir-493 and hsa-mir-376a-1 are their 3p arms. [score:1]
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44
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-140, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-125b-2, gga-mir-155, gga-mir-222a, gga-mir-221, gga-mir-92-1, gga-mir-19b, gga-mir-20a, gga-mir-19a, gga-mir-18a, gga-mir-17, gga-mir-16-1, gga-mir-15a, gga-mir-1a-2, gga-mir-206, gga-mir-223, gga-mir-106, gga-mir-302a, gga-mir-181a-1, gga-mir-181b-1, gga-mir-16-2, gga-mir-15b, gga-mir-140, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-146a, gga-mir-181b-2, gga-mir-181a-2, gga-mir-1a-1, gga-mir-1b, gga-let-7a-2, gga-mir-34b, gga-mir-34c, gga-let-7j, gga-let-7k, gga-mir-23b, gga-mir-27b, gga-mir-24, gga-mir-122-1, gga-mir-122-2, hsa-mir-429, hsa-mir-449a, hsa-mir-146b, hsa-mir-507, hsa-mir-455, hsa-mir-92b, hsa-mir-449b, gga-mir-146b, gga-mir-302b, gga-mir-302c, gga-mir-302d, gga-mir-455, gga-mir-367, gga-mir-429, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-1458, gga-mir-1576, gga-mir-1612, gga-mir-1636, gga-mir-449c, gga-mir-1711, gga-mir-1729, gga-mir-1798, gga-mir-122b, gga-mir-1811, gga-mir-146c, gga-mir-15c, gga-mir-449b, gga-mir-222b, gga-mir-92-2, gga-mir-125b-1, gga-mir-449d, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-122b-2
Another two human miRNAs (miR-507 and miR-136) have potential target binding sites in polymerase basic 2 (PB2) and hemagglutinin (HA) genes of AIV, respectively [15]. [score:3]
Two human encoded miRNAs (miR-136 and miR-507), have been shown to have potential binding sites for the genes that code for the polymerase basic 2 (PB2) and hemmagglutinin (HA) proteins and are reported to be involved in the pathogenesis of H5N1 AIV [15]. [score:1]
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45
[+] score: 4
Specifically, from among the miRNAs that are differentially expressed in estrogen -depleted mice, miR-127 and miR-136 negatively regulate bone mass [112], whereas miR-30b-5p may be a suitable serum biomarker for osteoporosis and osteopenia in postmenopausal women [93]. [score:4]
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46
[+] score: 4
Five potential candidate miRNAs (miR-103; miR-107; miR-129-5p; miR-136; miR-339-5p) were predicted to have target sites in 3′UTR of VCP mRNA. [score:3]
Five predicted miRNAs (miR-103, miR-107, miR-129-5p, miR-136, miR-339-5p) were transfected in HepG2 cells, respectively, with VCP 3′UTR report. [score:1]
[1 to 20 of 2 sentences]
47
[+] score: 4
In addition, 17 miRNAs (miR-136, miR-143, miR-148a, miR-15b, miR-18a, miR-181a, miR-181a*, miR-20b, miR-27b, miR-29b, miR-30d, miR-30e*, miR-301a, miR-376a, miR-376b, miR-410 and miR-7), which are differentially expressed in our retinal induction treatment, are involved in the regulation of developing mouse retina 25. [score:4]
[1 to 20 of 1 sentences]
48
[+] score: 3
Especially for the placenta, except miR-136, miR-184 and miR-381, 40 out of 43 (93.02%) placenta-specific miRNAs were clustered miRNAs, suggesting that these clustered miRNAs have similar expression patterns and play related or particular functions in this tissue. [score:3]
[1 to 20 of 1 sentences]
49
[+] score: 3
Brain miRNAs analyzed at 5 days post-stroke revealed a small cohort of miRNAs (miR-15a, miR-19b, miR-32, miR-136, and miR-199a-3p) highly expressed exclusively in adult females. [score:3]
[1 to 20 of 1 sentences]
50
[+] score: 3
Influenza virus infection modulates multiple cellular miRNAs, and miR-323, miR-491, and miR-654 have been shown to inhibit viral replication by binding to the viral PB1 gene [48], while miR-507 and miR-136 have potential binding sites within the viral PB2 and HA genes [49]. [score:3]
[1 to 20 of 1 sentences]
51
[+] score: 3
In summary, the ceRNA network suggested that novel_circRNA_007362 and novel_circRNA_032232 might interact with 24 miRNAs (Fig. 6A) as well as tch-let-7a-3p, tch-miR-136-5p, tch-miR-146a-5p, tch-miR-17-5p, tch-miR-183-5p, tch-miR-188-5p, tch-miR-23b-3p, tch-miR-326, and tch-miR-93-5p (Fig. 6B) to regulate development and aging of the cerebellum and hippocampus. [score:3]
[1 to 20 of 1 sentences]
52
[+] score: 3
In the Dlk1-Dio3 region, the maternally expressed genes can produce non-coding RNAs, including mir-431, mir-433, mir-127, mir-432 and mir-136. [score:3]
[1 to 20 of 1 sentences]
53
[+] score: 3
Gao H Long noncoding RNA CRNDE functions as a competing endogenous RNA to promote metastasis and oxaliplatin resistance by sponging miR-136 in colorectal cancerOncoTargets Ther. [score:3]
[1 to 20 of 1 sentences]
54
[+] score: 3
The first significant study of miRNAs in chondrosarcoma tissue samples and cell lines revealed downregulation of let-7a, miR-100, miR-136, miR-222, miR-335, and miR-376a compared to normal chondrocytes (Yoshitaka et al., 2013; Nugent, 2014). [score:3]
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55
[+] score: 3
MiR-507 and miR-136 could restrict the virus replication by targeting the genes of influenza virus Polymerase B2 (PB2) and Hemagglutinin (HA), respectively [15]. [score:3]
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56
[+] score: 2
Namely, pregnant rats fed SO and FO diets during the first 12 days of pregnancy showed significant lower expression of miR-449c-5p, miR-134–5p, miR-188, miR-32, miR130a, miR-144–3p, miR-431, miR-142–5p, miR-33, miR-340–5p, miR-301a, miR-30a, miR-106b, and miR-136–5p, as compared with OO, LO, and PO diets. [score:2]
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57
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-18b, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Mir-136 and mir-718 were not detectable in the adipocyte cultures using the Taqman assays-on-demand, while mir-346, mir-298, mir-330 and mir-501 were expressed at low levels (Ct levels above 33), see Table 1. This suggests that currently there is no gold standard method (when RNA is limiting) to validate miRNA data profiles. [score:2]
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58
[+] score: 2
It has been previously reported that some dysregulated miRNAs, such as miR-106a, miR-141, miR-143, miR-145, miR-218, miR-31, Let-7a, miR-17-5p, miR-221, miR-93, and miR-136 are altered in gastric cancer (18– 24), which is in concordance with our results. [score:2]
[1 to 20 of 1 sentences]
59
[+] score: 2
Three microRNAs in this region, miR-431, miR-127, and miR-136, were shown previously to regulate Peg11 through a siRNA-like mechanism [52]. [score:2]
[1 to 20 of 1 sentences]
60
[+] score: 2
Member(s) of the hsa-miR-181 14 and hsa-miR-29 families 15 exhibit both anticancer and pro-cancer regulation under different clinical conditions, while members of hsa-miR-126 16, hsa-miR-129 17, hsa-miR-136 18, hsa-miR-204 19, hsa-miR-663 20, hsa-miR-99 21, hsa-miR-378 22, hsa-miR-92 23, and hsa-miR-409 24 families are recognized as having anticancer properties under different clinical conditions. [score:2]
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61
[+] score: 2
Circ-Foxo3, originated from one of the forkhead family of transcription factors Foxo3, could both act as miRNA sponges for miR-136, miR-138, miR-433, miR-762, miR-3614-5p and influencing their function [50]. [score:1]
osteoarthritis Circ-CER ↓ CircRNA-CER/MMP13-miR-136- chondrocyte ECM degradationLiu, Q. [43]. [score:1]
[1 to 20 of 2 sentences]
62
[+] score: 1
The highest degree of miRNA was hsa-miR-136-5p (D = 60), indicating that it interplayed with 60 different circRNAs in this network. [score:1]
[1 to 20 of 1 sentences]
63
[+] score: 1
A greater than 1.5 fold increase was observed for 36 miRNAs, including miR-136-5p and miR-34a-5p, and a lower than 1.5 fold decrease was seen for 85 miRNAs including miR-7-5p and miR-34b-3p in spheroids cultured on concave microwell plates. [score:1]
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64
[+] score: 1
Among the miRNAs, seven of them (miR-16-2, miR-93, miR-95, miR-136, miR-153, miR-195, and miR-199a-3p) were mainly associated with esophageal adenocarcinoma, breast cancer and colorectal carcinoma, suggesting the role of these miRs in cell-proliferation and cell-signaling. [score:1]
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65
[+] score: 1
For example, mir-182 and mir-183 (both amongst the most islet-specific transcripts) originate from the same cluster on chromosome 7q32.2, whilst mir-136 and mir-127 map together on chromosome 14q32.2. [score:1]
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66
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-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-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
26E-0212mmu-miR-101b-3pmir-1010.297.791.72E-059.11E-0437mmu-miR-101a-3pmir-1010.2410.121.17E-031.92E-0250mmu-miR-107-3pmir-1030.228.773.24E-034.12E-0264mmu-miR-124-5pmir-1240.156.327.13E-037.09E-0233mmu-miR-301a-3pmir-1300.228.396.90E-041.29E-0259mmu-miR-130a-3pmir-1300.168.305.94E-036.44E-0252mmu-miR-135b-5pmir-1350.227.924.08E-034.99E-0274mmu-miR-136-5pmir-1360.229.061.09E-029. [score:1]
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67
[+] score: 1
miR-127 is located in chromosome region 14q32.2 and belongs to a cluster that includes miR-431, miR-433, miR-127, miR-432, and miR-136 [10]. [score:1]
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68
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-217, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-328, hsa-mir-335, hsa-mir-133b, hsa-mir-409, hsa-mir-484, hsa-mir-485, hsa-mir-486-1, hsa-mir-490, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-506, hsa-mir-509-1, hsa-mir-532, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-33b, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-1224, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-802, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-4262, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-486-2, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
A recent study in rats fed with ad lib liquid 6.7% ethanol-containing diet for 3 weeks showed increased miR-127, miR-136, miR-378 and miR-150.3p. [score:1]
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69
[+] score: 1
We detected a number of miRNAs processed from both the 5p and 3p arms of their respective pre-miRNAs, such as miR-136, miR-151, miR-140, and miR-330 (Table S2, S3). [score:1]
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70
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Yang et al. found that the two RNAs can both act as miRNA sponges for miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614-5p, and miR-3622b-5p, influencing their function by binding to them. [score:1]
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MiRNAs associated with TMZ resistance in glioblastoma include miR-195 [8], miR-9 [9], miR-125b [10], miR-136 [11], miR-181b [12], and miR-221/222 [13]. [score:1]
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Based on computational prediction, human miR-136 and miR-507 have potential binding sites at the polymerase basic 2 (PB2) and hemmagglutinin (HA) proteins of H5N1 AIV, and those two miRNAs may modulate AIV infection in humans [19]. [score:1]
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In addition to this, 25 binding sites were detected in circ-Foxo3 for eight miRs, including miR-22, miR-136, miR-138, miR-149, miR-433, miR-762, miR-3614-5p, and miR-3622b-5p [21]. [score:1]
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