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23 publications mentioning mmu-mir-295

Open access articles that are associated with the species Mus musculus and mention the gene name mir-295. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 198
mir-295 cluster predicted targets”  =  predicted TargetScan targets of the miR-295 cluster; “295 KO”  =  genes that showed a 1.2 fold upregulation on mir-295 cluster loss; “Dcr KO”  =  genes that showed a 1.2 fold upregulation on Dicer loss. [score:13]
Relative to a control set of genes (control) matched for 3' UTR length, dinucleotide composition, and expression level, the mir-295 cluster target set (targets) was more derepressed upon Dcr loss (Figure 1C). [score:7]
To confirm that targets of the mir-295 cluster show a transcriptome-wide signature in this dataset, we calculated a cumulative density function (cdf) plot comparing expression differences for the set of all mir-295 cluster targets as determined by Targetscan 5.1 [16]. [score:7]
targets include ∼3000 predicted TargetScan targets of the miR-295 cluster. [score:7]
An even larger derepression was seen for conserved mir-295 cluster targets (conserved targets), suggesting further enrichment of genuine targets in this set (Figure 1C). [score:7]
Using a combination of target prediction data with microarrays of mESCs before (Dcr WT) and after (Dcr KO) miRNA loss, as well as before (295 WT) and after (295 KO) specific deletion of the mir-295 cluster (Medeiros et al., manuscript in preparation), we have identified novel targets of the mir-295 cluster in ES cells. [score:5]
Microarray data and Targetscan predictions identify candidate miR-295 targets in mESCs. [score:5]
Interestingly, these genes as well as several previously identified miR-295 family targets are known to be directly or indirectly associated with p53. [score:5]
A. Venn diagram of microarray and target prediction data used to generate mir-295 cluster target candidates. [score:5]
1002054.g002 Figure 2 A. Venn diagram of microarray and target prediction data used to generate mir-295 cluster target candidates. [score:5]
Plots include conserved targets (red line), all predicted miR-295 targets (blue line), and control mRNAs (grey line). [score:5]
Validated targets of miR-295 are shown in red and computationally predicted targets are shown in orange. [score:5]
Taken together, these data suggest that direct miRNA -mediated repression of Casp2 leads to approximately 5-fold repression, making it one of the most potently repressed mir-295 cluster targets identified to date. [score:4]
Predicted targets of the mir-295 cluster are enriched in pathways regulating apoptosis. [score:4]
Originally identified as a direct p53 transcriptional target that binds Bcl2 [18], [19], the Ei24 3' UTR contains one 7mer miR-295 site. [score:4]
Activity of luciferase reporters of predicted targets were assayed in WT, Dcr KO ES cells, as well as in Dcr KO ES cells after over expression of 20 nM miR-295. [score:4]
Caspase 2 and Ei24, key apoptotic mediators, are direct targets of the mir-295 cluster. [score:4]
Over 40% of upregulated transcripts were shared between the Dcr KO and 295 KO lines, consistent with the finding that the mir-295 cluster contributes around half of all miRNAs in ES cells. [score:4]
The pro-apoptotic genes Caspase 2 (Casp2) and Ei24 are direct targets of the mir-295 cluster. [score:4]
Ingenuity Pathway Analysis (IPA) of miR-295 targets. [score:3]
Acute Dicer deletion and specific mir-295 cluster deletion show global target derepression signatures. [score:3]
Because deletion of Dcr involves global miRNA loss, and three additional clusters containing the same or similar hexamer seed, mir-302, mir-467, and mir-17-92, are expressed in ESCs (Table S2), we examined the 295 KO line to determine the specific contribution of the mir-295 cluster to cell survival. [score:3]
Here, we provide the first demonstration that the mir-295 cluster can suppress apoptosis in mESCs following exposure to the genotoxic stressors ionizing irradiation and doxorubicin. [score:3]
When we applied siRNAs specific to each validated target, or to Bim, a well-characterized proapoptotic factor, cells exhibited a decrease of 5–10% in Casp3 activation 24 h after irradiation, a level similar to mir-295 cluster miRNA overexpression (Figure 4B, Figure S6A and S6B). [score:3]
Transfection of miR-295 also strongly repressed an intact Casp2 reporter in these cells, but not a reporter in which the four target sites were mutated (Figure 3C). [score:3]
Consistent with their high expression, these miRNAs (which we shall refer to as the mir-295 cluster) have been linked to a number of functions in ES cells including maintenance of pluripotency and proliferation. [score:3]
The magnitude of repression for the previously identified miR-295 targets Lats2 and p21 was comparable to that observed previously [12]. [score:3]
Table S3 Predicted targets of the mir-295 cluster. [score:3]
We further refined our candidate list using available array data from the 295 KO line, which also showed cdf plot signature changes for mir-295 cluster targets (Figure 1C) (Medeiros et. [score:3]
Again, overexpression of two miRNAs in the cluster, miR-290-3p and miR-295, reduced the rate of apoptosis (Figure 5D, Figure S7A and S7B). [score:3]
IPA was performed for validated targets of miR-295 from this and prior studies [10], [11], [12], and identified the network, “Cell Death, Cell Cycle, Cellular Function and Maintenance,” which centers around p53. [score:3]
These in vitro results support the enrichment of our candidate list for true miR-295 targets. [score:3]
1002054.g006 Figure 6IPA was performed for validated targets of miR-295 from this and prior studies [10], [11], [12], and identified the network, “Cell Death, Cell Cycle, Cellular Function and Maintenance,” which centers around p53. [score:3]
We additionally confirmed two previously identified miR-295 targets, p21 (also known as Cdkn1a) and Lats2 [29]. [score:3]
Ingenuity Pathway Analysis (IPA) was performed on the set of validated miR-295 targets to identify the most strongly associated canonical pathways. [score:3]
Thus, miR-295 family miRNAs target a number of p53 associated genes and in all cases antagonizing p53 activation, consistent with the protective effect we have identified here. [score:3]
Figure S2 Repression of predicted targets of the miR-295 cluster in Dcr WT and Dcr KO ES cells. [score:3]
Table S1Sequences and expression level of the mir-295 cluster in ES cells. [score:3]
Consistent with these findings, the mir-295 cluster itself has been speculated to be an “oncomir” cluster, as overexpression of its human homolog, the mir-371-373 cluster, has been found in various human tumors [36], [37], [38] and may promote malignant transformation [39]. [score:3]
Given that ESCs are highly sensitive to DNA damage [20] and both validated targets have been implicated in the DNA damage response, we hypothesized that the mir-295 cluster may be specifically protective in the context of genotoxic stress. [score:3]
B. Activity of luciferase reporters of predicted targets of the mir-295 cluster were assayed in Dcr WT and Dcr KO ES cells. [score:2]
50 nM miR-295, miR-467a, Bim siRNA, Casp2 siRNA and Ei24 siRNA were transfected into Dcr KO ES cells, and Casp2 protein expression was assayed 24 hours later. [score:2]
In support of the reporter assay, Dcr KO cells showed a comparable increase in Casp2 at the protein level, which could be partially rescued by transfection of either miR-295, miR-467a (which shares the same hexamer seed), or a Casp2 siRNA, but not by siRNAs against other unrelated targets (Figure 3B). [score:2]
50 nM miR-295, miR-467a, and miR-20a were transfected into 295 KO ES cells, and Casp2 protein expression was assayed 24 hours after the transfection. [score:2]
Within the mir-290-295 cluster, the ‘AAGUGC’ seed is found in miR-290-3p, miR-291a-3p, miR-291b-3p, miR-292-3p, miR-294, and miR-295. [score:1]
The 3' UTR of Ei24 fused to a luciferase reporter conferred approximately 2-fold repression in Dcr WT cells relative to Dcr KO cells, an effect that could be restored following transfection of miR-295 (Figure 3C). [score:1]
Importantly, mature miRNA levels from the mir-295 cluster were unchanged by these stressors (Figure S3D). [score:1]
This partial derepression in the mir-295 cluster deletion probably reflects the quantitative change in the total level of AAGUGC seed miRNAs, as exogenous miR-295 could further repress Casp2 protein levels (Figure 5B). [score:1]
In conclusion, these data expand our understanding of ESC miRNA function, linking the ES cell specific miR-295 family to key players in cell death. [score:1]
In this context, the Casp2 reporter was derepressed approximately half as strongly as it was in Dcr KO cells, suggesting that the miR-302 and miR-467a families of miRNAs incompletely compensate for loss of the mir-295 cluster (Figure 5A). [score:1]
Microarrays for the mir-295 cluster deletion were performed on two deletion and two wild-type lines independently derived. [score:1]
Mir-295 cluster miRNAs promote survival of ES cells during genotoxic stress. [score:1]
miR-467a shares the same hexamer seed with miR-295, and Bim siRNA and Ei24 siRNA served as negative controls. [score:1]
Indeed, Pathway Analysis of well-characterized miR-295 targets brought up a single significant network (p = 10 [−14]), “Cell Death, Cell Cycle, Cellular Function and Maintenance,” which prominently featured p53 (Figure 6). [score:1]
A. Dcr KO cells were treated with 5-Gy radiation 24 hours after transfection of 50 nM miR-295 or miR-290-3p. [score:1]
mESCs cells containing a floxed and excised mir-295 cluster were generated in a similar manner and will be described in an upcoming publication (Medeiros et. [score:1]
A. 295 KO cells were treated with 5-Gy radiation 24 hours after transfection of 50 nM of miR-295 or miR-290-3p. [score:1]
Loss of the mir-295 cluster derepresses Casp 2 and Ei24 3' UTRs and enhances sensitivity to DNA damaging agents. [score:1]
Therefore, deletion and restoration of mir-295 cluster miRNAs recapitulate the modulation of apoptosis rates seen in a Dcr null context. [score:1]
B. Dcr KO cells were treated with 5-Gy radiation 24 hours after transfection of 50 nM miR-295, miR-290-3p, Bim siRNA, Casp2 siRNA or Ei24 siRNA. [score:1]
To examine whether the miR-295 targets modulated apoptosis, we transfected a series of siRNAs into Dcr KO cells and evaluated cell death following irradiation. [score:1]
Specific deletion of the mir-295 cluster enhances susceptibility to apoptosis upon DNA damage. [score:1]
Based on these repression data as well as the earlier informatic predictions, we tested whether mir-295 cluster miRNAs could modulate apoptosis in mESCs. [score:1]
Relative to control siRNAs, transfection of miR-290-3p or miR-295 drastically decreased the apoptosis response of Dcr KO cells to gamma irradiation (Figure 4B, Figure S6A and S6B). [score:1]
D. Northern analysis for miR-295 in Dcr KO ES cells, WT ES cells, and WT ES cells 6 hours after 2 μM doxorubicin treatment. [score:1]
Like p53, the mir-295 cluster affects both arms of cellular proliferation, namely cell death and cell cycle progression [12], [29]. [score:1]
Additional transfection studies confirmed that repression could be conferred specifically by miR-295 in a Dcr KO background (Figure S2). [score:1]
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2
[+] score: 25
The incorporation of 3-7CG-S, 4-7CGC-S and 3-7UA-S seed only target sites, designed to interact with miR-292-3p+1, miR-293-3p+2 and miR-295-3p+1 respectively resulted in either no silencing or very inefficient silencing of the reporters (Figure 4E). [score:3]
In this case pre-miR-295 and pre-miR-372 would express the same single 2-7U 7mer seed, which is shared with pre-miR-291a, pre-miR-294 and pre-miR373 and, importantly, is represented in all homologous miR-290–295/miR-371–373 loci. [score:3]
Thus, similarly to its interaction with the mouse miR-291-3p0, miR-294-3p0 and/or miR-295-3p0, the 2-7C-S target appears to interact via G:U wobble base pairing with miR-372-3p0 and/or miR-373-3p0 which also have a 2-7U seed. [score:3]
Nevertheless, we note that the 3-7UA-S seed only reporter, which corresponds to the putative miR-295-3p+1 isoform, had the same activity in wild type and miR-290-295 knockout ES cells, whereas silencing of the 3-7CG-S and 4-7CGC-S reporters, which correspond to the active miR-292-3p+1 and miR-293-3p+2 isomiRs was consistently lower in the wild type ES cells (Figure 4E). [score:2]
The 7mer seed regions that correspond to the putative miR-295-3p+1 and miR-372-3p+1 isoforms are not conserved in the miR-290–295/miR-371-373 cluster family (Figure 1A). [score:1]
In addition, several hairpins yield two miRNA isoforms with alternative 5′-ends represented by similar numbers of reads in the sequencing libraries (Figure 2, pre-miR-292, pre-miR-295, pre-miR-372). [score:1]
miR-295-3p+1 -AGUGCUG a (3p)3-7UG? [score:1]
With the caveat that miR-295-3p+1 and miR-372-3p+1 might perform species specific functions, the remainder of the miR-290-295/miR-371-373 pre-miRNAs appear to be functionally equivalent since they only produce mature 3p0 miRNAs with identical 2-7U seeds. [score:1]
The activities of miR-295-3p+1 and miR-372-3p+1 are unknown (Active?). [score:1]
Such isoforms have identical 6mer 3-7U seeds, but their 7mer seeds are different (3–7A for miR-295-3p+1 and 3-7U for miR-372-3p+1, Figure 1A, Figure S2). [score:1]
Sequencing data suggest that pre-miR-295 and pre-miR-372 might produce additional 3p+1 isoforms (Figure 2). [score:1]
The reporter silencing experiments presented in this study neither confirm nor confidently rule out the existence of the miR-295-3p+1 and miR-372-3p+1 isoforms implied by sequencing as that requires studying the silencing of the corresponding bulge reporters, which we did not pursue. [score:1]
Thus, given the conservation of all other miR-290–295/miR-371–373 seeds we favor a mo del in which both miR-295-3p+1 and miR-373-3p+1 are not active. [score:1]
The 2-7C-S miRNA binding site might be recognized by 3p0 miRNAs with 2-7U seeds (miR-291a-3p0, miR-294-3p0 and miR-295-3p0, Figure 4A) via a G:U wobble at position 8 of the miRNA seed. [score:1]
This observation is consistent with absence of miR-295-3p+1 activity. [score:1]
Note that in this scenario, the putative species-specific miR-295-3p+1 and miR-372-3p+1 isoforms are processed from different paralogous pre-miRNA families. [score:1]
Therefore, pre-miR-291a, pre-miR-291b and pre-miR294 are likely co-orthologs of pre-miR-372 and pre-miR-295 is an ortholog of the promoter distal pre-miR-373. [score:1]
Furthermore, as discussed below, pre-miR-295 and pre-miR-372 do not appear to be bona fide orthologs. [score:1]
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3
[+] score: 14
By 12 d post-tamoxifen treatment, miR-295 was below detection levels of quantitative qRT-PCR, indicating full depletion of DCR activity, also confirmed by quantitation of previously validated mESC miRNA target transcripts (Figure 1C and Figure S1C). [score:3]
qRT-PCR analysis of L1_ORF2 mRNA levels (C), miR-295 and miR-16 levels (D), and Hmga2 and Btg2 mRNA levels (established targets of mmu-miR-196a and mmu-let-7a and mmu-miR-132, respectively) in the various cell lines depicted in (E). [score:3]
MiR-295 levels were strongly reduced at 2 d, and at 5 d post-tamoxifen treatment; a corresponding increase in microRNA target levels confirmed cellular depletion of hAgo2, as reported [38] (Figure 4G and S4G). [score:2]
qRT-PCR analysis of miR-295 (G) and L1_ORF2 mRNA (H) levels upon hAgo2 deletion in Tamoxifen -treated Ago1,2,3,4_ KO mESCs. [score:1]
C. qRT-PCR analysis of miR-295 levels in the tamoxifen treated mESCs, as depicted in (B). [score:1]
B. Accumulation of miR-295, miR-302d, miR-21 and miR-16 analyzed by qRT-PCR before and 10 days after differentiation of Dcr [Flx/Flx], Dcr [−/−] and h Dcr-complemented Dcr [−/−] mESCs. [score:1]
To address this, we examined Dgcr8_ KO mESCs, in which production of even the most abundant mESC miRNAs, including miR-295, is abrogated [37] (Figure 4D). [score:1]
qRT-PCR analysis of miR-295 (D) and L1_ORF2 mRNA (E) levels in WT and Dgcr8_ KO mESCs. [score:1]
Although Dcr deletion was already achieved 24 h post-tamoxifen treatment (Figure 1B), reduced accumulation of miR-295, one of the most abundant mESC miRNAs, was only visible 6 days post-tamoxifen treatment, presumably reflecting the high DCR protein stability [22]. [score:1]
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4
[+] score: 13
Incidentally, the enzyme is a predicted target (TargetScan) of miR-295, of which the expression is high in the dormant blastocysts. [score:7]
It is interesting to note that integrin α [v] subunit is one of the target genes of the miR-295 cluster [58], which is also down-regulated in the activated blastocysts. [score:6]
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5
[+] score: 11
ch/ElMMo2/) of predicted target transcripts revealed a consensus set of regulated cellular functions for miR-291a-3p, miR-292-3p, miR-294 and miR-295, but not for miR-293 (Dataset S2 for the EIMMo target prediction software and Dataset S3 for the Pictar target prediction software). [score:8]
In agreement with these previous studies, separate time-course analyses of each member revealed that only 4 miRNAs, which share the same AAAGUGC 5′ seed sequence (miR-291a-3p, miR-292-3p, miR-294, miR-295, Figure 2A, blue), likely contribute significantly to the global trend of miR-290 cluster expression (reduced throughout differentiation, PAM class A; Figure 2A, grey). [score:3]
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6
[+] score: 11
Zovoilis et al. demonstrated that the Dkk-1 was a direct target of miR-294 and miR-295, and the other members of the miR-290-295 cluster controlled Wnt or Dkk-1 activation indirectly [48]. [score:5]
The other miRNAs of the miR-290-295 cluster (miR-290-5p, miR-291a-5p, miR-291b-5p, miR-292-5p, miR-293, miR-293 [*], miR-294 [*], and miR-295 [*]) differing in their seed sequences, are still highly expressed in ESCs with the exception of the hardly detectable [22] minor forms of miR-293, miR-294, and miR-295 (miR-293 [*], miR-294 [*], and miR-295 [*]). [score:3]
miR-290-291a unit replication formed miR-292-291b, and then miR-290, miR-291a and miR-292 (as the same unit) replication resulted in the formation of miR-293, miR-294 and miR-295 ESC and iPSC self-renewals need to eliminate differentiation signal and obtain the pluripotency signal, in addition, the differentiation process trigger the closure of pluripotency procedure and the induction of lineage specification. [score:1]
Within the miR-290-295 cluster, the seed sequences of ‘AAGUGC’ hexamer are found in miR-290-3p, miR-291a-3p, miR-291b-3p, miR-292-3p, miR-294, and miR-295. [score:1]
The miR-290-291 unit replication forms miR-292-291b, and then the miR-290, miR-291a and miR-292 (as the same unit) replication results in the formation of miR-293, miR-294 and miR-295, finally forming the present miR-290-295 cluster [21] (Fig.   1). [score:1]
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7
[+] score: 11
We chose to profile the ubiquitously expressed miR-16, five ESC-specific miRNAs (miR-290, miR-291-3p, miR-292-3p, miR-294, and miR-295) [23], [24], and two miRNAs that are upregulated in ESCs undergoing differentiation (miR-21 and miR-22) [23], [24]. [score:6]
The difference in Ct values between the negative control (MEFs alone) and each experimental group (miR-290, miR-291-3p, miR-292-3p, miR-294, miR-295, miR-16, and RNU6b) is shown. [score:1]
The majority of miRNAs tested do not differ significantly from one another except for miR-295, which is significantly more abundant than miR-290 and miR-291. [score:1]
The abundance of several miRNAs (miR-290, miR-291-3p, miR-292-3p, miR-294, and miR-295) increased in MEFs as early as 1 hour after incubation, suggesting transfer. [score:1]
The relative abundance of all tested miRNAs overlaps except for that of miR-295, which is significantly more abundant than miR-290 and miR-291 (Figure 5B). [score:1]
The miRNAs tested include miR-16 (lane 1), miR-21 (lane 2), miR-22 (lane 3), miR-290 (lane 4), miR-291-3p (lane 5), miR-292-3p (lane 6), miR-294 (lane 7), miR-295 (lane 8), and the small nuclear RNA, RNU6b (lane 9). [score:1]
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8
[+] score: 10
Expression of miR-295-3p was observed in rat PSCs and absent in rat EFs, which was consistent with its expression pattern in the mouse [51] (Fig.   4a). [score:5]
We found that rat miR-295-3p, miR-741-3p and miR-743a-3p expression was significantly decreased during ESC and iPSC differentiation (Fig.   4b). [score:3]
A pluripotency -associated miRNA, miR-295-3p, was used as a positive control. [score:1]
Some miRNAs, such as miR-291, miR-294 and miR-295, can enhance reprogramming that is induced by OSK factors [22]. [score:1]
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9
[+] score: 10
In addition, Zheng et al. [36] have reported that hsa-miR-295-5p expression is upregulated by and that this miRNA suppresses viral replication by targeting the VP1 and VP3 coding regions. [score:10]
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10
[+] score: 6
Analysis of miRSystem revealed among the eight miRNAs, four miRNAs (miR-291a-3p, miR-295-3p, miR-302b-3p and miR-302d-3p) have apoptosis -associated target genes (PI3K, NIK and Cn) or a DNA-damage repair -associated target gene (RAD23B). [score:5]
173 (miR-186-5p, miR-208a-5p, miR-291a-3p, miR-294-3p, miR-295-3p, miR-302a-3p, miR-302b-3p, miR-302c-3p and miR-302d-3p). [score:1]
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11
[+] score: 6
This was also the case for miR-295*, for which both Affymetrix and detected a down-regulation during the differentiation process. [score:4]
miR-295* represented those miRNAs only being identified as being regulated by the Affymetrix platform. [score:2]
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12
[+] score: 4
The qRT–PCR analysis of differentially expressed microRNA candidates mmu-miR-7a, mmu-miR-19b, mmu-miR-30c, mmu-miR-103, mmu-miR-107 and mmu-miR-467 that are presented in Tables 2 and 3. The expression of each miRNA was measured and normalized to that of miR295 as a control. [score:3]
We also showed quantification of a microRNA (miR295: MI0000393) not submitted to imprint as control. [score:1]
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13
[+] score: 4
These miRNAs, which include miR-291-3p, miR-294 and miR-295, are thus named ES cell-specific cell cycle -regulating (ESCC) miRNAs based on their ability to regulate G1-S transition [39]. [score:3]
Although miR-290 itself was not known to promote reprogramming, several members of the miR-290 family, miR-291-3p, miR-294 and miR-295, enhance reprogramming of MEFs in the absence of c-Myc [41]. [score:1]
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14
[+] score: 3
miRanda algorithm showed that, activin receptor 1 (ACVR1) is predicted target gene for mmu-mir-193, mmu-mir-294, mmu-mir-295 and mmu-mir132. [score:3]
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15
[+] score: 2
qRT-PCR analysis of miR-295 (D) and L1_ORF2 mRNA (E) levels in WT and Dgcr8_ KO mESCs. [score:1]
qRT-PCR analysis of miR-295 (G) and L1_ORF2 mRNA (H) levels upon hAgo2 deletion in Tamoxifen -treated Ago1, 2, 3, 4_ KO mESCs. [score:1]
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16
[+] score: 2
To validate the microarray results, eight miRNAs were selected for further experimental confirmation: miR-126-5p, miR-99a, miR-324-5p, miR-762, miR-29a, miR-302c, miR-295, miR-20b. [score:1]
Eight miRNAs (miR-126-5p, miR-99a, miR-324-5p, miR-762, miR-29a, miR-302c, miR-295, miR-20b) were randomly selected to confirm the microarray results using real-time RT-PCR. [score:1]
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17
[+] score: 1
Other miRNAs from this paper: mmu-mir-294
On day 2 and day 5, a 25 µM miR-294 and miR-295 cocktail (Dharmacon) was transfected using DharmaFECT 1 (Dharmacon) according to the manufacturer’s instructions. [score:1]
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18
[+] score: 1
Only miR-291-3p, miR-294 and miR-295 can promote the G1-S transition of the cell cycle and the induction of pluripotency [13], [14]. [score:1]
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19
[+] score: 1
Since the high number of predicted miRNA–mRNA interactions impeded their comprehensive experimental validation, we focused on the effects of the miRNAs showing the strongest predicted interaction with Kdm2b (mmu-miR-150-5p and mmu-miR-27b-5p), SmarcA4 (mmu-miR-181c-5p and mmu-miR-425-5p), and Dnmt3b (mmu-miR-295-5p) (Additional file 5: Table S5). [score:1]
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20
[+] score: 1
The same SNP i. e. rs3657112 also showed statistical interaction with chromosome 9 loci 67–72 Mb for miR-295. [score:1]
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21
[+] 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-27a, hsa-mir-29a, hsa-mir-101-1, dme-mir-1, dme-mir-2a-1, dme-mir-2a-2, dme-mir-2b-1, dme-mir-2b-2, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-101a, mmu-mir-124-3, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-137, mmu-mir-140, mmu-mir-142a, mmu-mir-155, mmu-mir-10b, mmu-mir-183, mmu-mir-193a, mmu-mir-203, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-183, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-222, hsa-mir-223, dme-mir-133, dme-mir-34, dme-mir-124, dme-mir-79, dme-mir-210, dme-mir-87, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, dme-let-7, dme-mir-307a, dme-mir-2c, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-193a, 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-29a, mmu-mir-27a, mmu-mir-34a, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-210, mmu-mir-223, mmu-mir-222, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-411, hsa-mir-193b, hsa-mir-411, mmu-mir-193b, hsa-mir-944, dme-mir-193, dme-mir-137, dme-mir-994, mmu-mir-1b, mmu-mir-101c, hsa-mir-203b, mmu-mir-133c, mmu-let-7j, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, mmu-mir-124b
The most prominent examples include hsa-miR-944 in human (14% of reads correspond to miR-944 5′-isomiRs, Supplementary Table S2), mmu-miR-295 in mouse (24%, Supplementary Table S3), dme-miR-994 in fruitfly (38%, Supplementary Table S4), which has been previously annotated as a prominent miRNA with highly imprecise 5′ ends (7). [score:1]
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The top-ranked miRNAs for cluster B were mmu-miR-134–5p, mmu-miR-136–5p, mmu-miR-214–3p and mmu-miR-295–5p. [score:1]
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Additionally, seven miRNAs exhibited a consistent pattern of no amplification in TEC from infected animals (miR-144, miR-208b, miR-291b-3p, miR-295, miR-302a, miR-488, and miR-654-3p, Figure S4 in). [score:1]
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