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27 publications mentioning mmu-mir-298

Open access articles that are associated with the species Mus musculus and mention the gene name mir-298. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 173
We identified 1 validated target of miR-296-3p; 5 validated targets of miR-298-5p; 207 predicted targets of miR-296-3p; 707 predicted targets of miR-298-5p. [score:9]
Four of them (HMX2, HNF4A, LEF1, MAFB) are known to be expressed in the islets of Langerhans, and MAFB is known to be expressed only in rodent islet α cells within adult pancreas [25]; the presence of binding sites for this TF within the promoter of the genes encoding miR-296-3p and miR-298-5p suggests that it may regulate the expression of both miRNAs. [score:8]
Altogether, high-throughput microRNA profiling, functional analysis with synthetic mimics and molecular characterization of modulated pathways strongly suggest that specific downregulation of miR-296-3p and miR-298-5p, coupled to upregulation of their targets as IGF1Rβ and TNFα, is a major determinant of mammalian pancreatic α cells resistance to apoptosis induction by cytokines. [score:7]
HT miRNA profiling data, functional analysis with synthetic mimics and molecular characterisation of modulated pathways strongly suggest that specific downregulation of miR-296-3p and miR-298-5p in pancreatic α cells, coupled to upregulation of their targets as IGF1Rβ and TNFα and activation of the corresponding signaling pathways, is a major determinant of their resistance to apoptosis induction by cytokines. [score:7]
Among them, Bcl2, Ccna2, Irs2, Nr4a2 are transcriptionally regulated by CREB1, which is a validated target of miR-296-3p [22]; Tnf and Vdr are validated targets of miR-298-5p [23, 24]. [score:6]
We focused our study on two microRNAs, miR-296-3p and miR-298-5p, which were: (1) specifically expressed at steady state in αTC1-6, but not in βTC1 or INS-1 cells; (2) significantly downregulated in αTC1-6 cells after treatment with cytokines in comparison to untreated controls. [score:6]
Within the network of genes regulated by α-miRNAs, insulin-like growth factor receptor signaling pathway is a biological process significantly enriched among the genes interacting with targets of miR-296-3p and miR-298-5p, with respect to the genes linked to the targets of the other miRNAs (p-value = 0.039, Fisher’s exact test). [score:6]
To verify whether in vitro modulation of miR-296-3p and miR-298-5p affected the expression of their targets, we performed transient transfection experiments of αTC1-6 cells with their mimics. [score:5]
Modulation of miR-296-3p and miR-298-5p also alters expression of their targets. [score:5]
Although its biological effect was potentiated when also miR-296-3p was expressed, our results suggest that the role of miR-298-5p is more important in this process than that of miR-296-3p (Figure  3): this would highlight the role of one or a few specific miR-298-5p targets. [score:5]
Bar graph showing changes in gene expression of a selected set of miR-296-3p and miR-298-5p targets for each of three different experimental conditions: (i) αTC1-6 treated with cytokines with respect to matched untreated control cells at the time points 24 and 48 h; (ii) untreated αTC1-6 transfected with mimics of miR-296-3p with respect to scramble -transfected control cells at the time points 24 and 48 h; (iii) untreated αTC1-6 transfected with mimics of miR-298-5p with respect to scramble -transfected control cells at the time points 24 and 48 h. Data are reported as LOG of 2^ [-ΔΔCt] values. [score:5]
Our computational analysis suggests that MAFB (a transcription factor exclusively expressed in pancreatic α cells within adult rodent islets of Langerhans) controls the expression of miR-296-3p and miR-298-5p. [score:5]
Figure 4 Modulation of miR-296-3p and miR-298-5p alters expression of their targets. [score:5]
Mir-298-5p resulted significantly downregulated starting at 12 h PT and reached a highly significant downregulation at 48 h PT, compared to matched untreated controls: Student’s t-test, Bonferroni adjusted p-values, were <0.05 and <0.01, respectively (Figure  2B). [score:5]
By exploiting specific microRNA mimics, we demonstrated that experimental upregulation of miR-296-3p and miR-298-5p raised the propensity to apoptosis of transfected and cytokine -treated αTC1-6 cells with respect to αTC1-6 cells, treated with cytokines after transfection with scramble molecules. [score:4]
Figure 5 Expression of IGF1Rβ and TNFα proteins is regulated by miR-296-3p and miR-298-5p in αTC1-6. (A) of IGF1Rβ in (1) untreated αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p (left); (2) αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p and treated with cytokines for further 24 h (middle); (3) αTC1-6 treated with cytokines for 24 h and their matched untreated controls (right). [score:4]
Figure 3 Upregulation of miR-296-3p and miR-298-5p reduces αTC1-6 resistance to apoptosis induced by cytokines. [score:4]
Expression of a macro-noncoding RNA (precursor of miR-296, miR-298, Nespas) is predicted to be controlled by two groups of CpG islands (one comprising two CpG islands, from 17.5 to 18.8 kb upstream the first nucleotide of pre-miR-296; the other made of three CpG islands, from 30.1 to 33.6 Kb upstream the first nucleotide of pre-miR-296). [score:3]
Figure 2 Expression of miR-296-3p and miR-298-5p in αTC1-6 and βTC1. [score:3]
Expression of IGF1Rβ and TNFα is controlled by miR-296-3p and miR-298-5p in αTC1-6 cells. [score:3]
Through western analysis, we confirmed our computational prediction that IGF1Rβ and TNFα are common targets to both miRNAs and that miR-296-3p and miR-298-5p also control IRS-1 and ERK-1 within the IGF1R signaling pathway. [score:3]
In αTC1 transfected with mimics of miR-296-3p or miR-298-5p, real-time PCR showed altered expression of different genes with respect to scramble -transfected cells, including Igf1r, Tnf, Vdr (Figure  4). [score:3]
Identification of miR-296-3p and miR-298-5p targets. [score:3]
Decreased expression of mir-296-3p and miR-298-5p and the corresponding activation of survival and proliferation signals, mediated by IGF1R and its downstream nodes (e. g., IRS-1 and ERK-1), may thus explain why αTC1-6 cells are resistant to death induction by cytokines (see Additional file 13). [score:3]
Scatter plot showing correlation between miR-296-3p (x-axis) and miR-298-5p (y-axis) expression in αTC1-6, during a 6-12-24-48 h time-course experiment. [score:3]
Click here for file Scatter plot showing correlation between miR-296-3p (x-axis) and miR-298-5p (y-axis) expression in αTC1-6, during a 6-12-24-48 h time-course experiment. [score:3]
A selection of validated and predicted targets of miR-296-3p and miR-298-5p was chosen according to their involvement in apoptosis, cell cycle progression, cell differentiation and hormone secretion. [score:3]
We focused our attention on 7 targets of miR-296-3p, 4 of miR-298-5p, 2 common to both miRNAs: they were chosen according to their involvement in apoptosis, cell cycle progression, cell differentiation and hormone secretion (see Additional file 8). [score:3]
The expression of phospho-IRS-1 didn’t change in untreated αTC1-6 transfected with mimics of each miRNA alone, while it decreased about 1.5 folds in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p (Figure  6A, left panel). [score:3]
Following transfection of αTC1-6 with either mimics of miR-296-3p or miR-298-5p, TNFα protein was about 1.2 folds less expressed with respect to scramble -transfected controls; this decrease was more pronounced (1.6 folds) when cells were transfected with both mimics (Figure  5B, left panel). [score:3]
Click here for file Validated and predicted targets of miR-296-3p and miR-298-5p. [score:3]
Validated and predicted targets of miR-296-3p and miR-298-5p. [score:3]
Interestingly, also the activation of ERK-1 appears to be regulated by miR-296-3p and miR-298-5p: in the absence of treatment with cytokines, αTC1-6 cells transfected with mimics of miR-296-3p showed levels of phospho-ERK-1 (Thr202) similar to those found in scramble -transfected αTC1-6 cells; the transfection with mimics of miR-298-5p or of both miRNAs led instead to a decrease of the protein (1.2 and 1.3 folds, respectively) (Figure  6B, left panel). [score:2]
Click here for file 3 Hypothetical mo del of regulation of miR-296-3p and miR-298-5p biomolecular activity in αTC1-6 at steady state (left) and after treatment with cytokines (right). [score:2]
Hypothetical mo del of regulation of miR-296-3p and miR-298-5p biomolecular activity in αTC1-6 at steady state (left) and after treatment with cytokines (right). [score:2]
Their assignment to specific families is shown in Additional files 2 and 3. After treatment with cytokines for 48 h, 3 miRNAs (miR-146a, miR-203, miR-298-5p) were significantly differentially expressed in αTC1-6 as compared to matched untreated controls (Limma test, Benjamini-Hochberg adjusted p-values < 0.05) (see Additional file 4). [score:2]
Phospho-IRS1 (Tyr612) and Phospho-ERK-1 (Thr202), which we demonstrated to be controlled by miR-296-3p and miR-298-5p, are known to regulate the response to insulin and to be involved in survival and proliferation processes [30]. [score:2]
By using the same controls, we detected a slight decrease of phospho-IRS-1 (1.2 folds) in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p and treated with cytokines (Figure  6A, right panel). [score:1]
CpG islands upstream genes encoding miR-296, miR-298, Nespas were identified through UCSC Genome Browser (http://genome. [score:1]
Activation of IRS-1 and ERK-1 is also under control of miR-296-3p and miR-298-5p. [score:1]
Click here for file On scale representation of the genome segment comprising Nespas, miR-296, miR-298. [score:1]
The decrease of IGF1Rβ was not detectable in αTC1-6 transfected with either mimic of miR-296-3p or miR-298-5p and then treated with cytokines for 24 h. In αTC1-6 treated with cytokines for 24 h, after transfection with mimics of both miRNAs 296-3p and 298-5p, it was instead lower than at steady state (1.4 folds). [score:1]
Genomics of genes encoding miR-296-3p, miR-298-5p, Nespas and identification of upstream CpG islands. [score:1]
Among them, miR-296-3p and miR-298-5p stood out clearly as potentially critical nodes, responsible for α cells resistance to cytokine -induced cell death. [score:1]
For analysis of correlation between the expression of miR-296-3p and miR-298-5p in αTC1-6, Pearson correlation coefficient was calculated. [score:1]
Transfections were performed using siPORT™ NeoFX™ (Lifetechnologies™) with 30 nM mimics of miR-296-3p/miR-298-5p/scrambled sequence (Pre-miR™ miRNA Precursor Molecules—Negative Control #1, Lifetechnologies™). [score:1]
At 24 h PT, αTC1-6 transfected with mimics of miR-298-5p show a highly significant increase of the number of apoptotic cells with respect to scramble -transfected control; at the same time point, in αTC1-6 transfected with mimics of both miR-296-3p and miR-298-5p a highly significant increase of the number of apoptotic cells is detected with respect to all the other experimental conditions. [score:1]
For each time point DCt values of miR-296-3p and miR-298-5p were correlated, both from untreated and cytokines -treated αTC1-6 cells (r-value = 0.88, p-value = 1.15e-08, Pearson’s correlation test). [score:1]
Their assignment to specific families is shown in Additional file 5. To identify miRNAs whose functions could explain the differential response to cytokines of pancreatic α and β cells, we specifically focused our attention on miR-296-3p and miR-298-5p. [score:1]
Finally, χ [2]-square test was used to establish if miR-296-3p and miR-298-5p have more common targets than expected by chance; Fisher’s exact test was applied to evaluate the enrichment in specific gene ontologies. [score:1]
Our results suggest that miR-296-3p and miR-298-5p play a pivotal role in determining this trait. [score:1]
In the genomic region comprising the genes encoding miR-296-3p, miR-298-5p and Nespas, MatInspector identified Transcription Factor Binding Sites (TFBS) for sixty seven Transcription Factors (TFs). [score:1]
org predicts two binding sites for mmu-miR-296-3p and mmu-miR-298-5p on Mafb mRNA 3’ UTR. [score:1]
Figure 6 Activation of IRS-1 and ERK-1 is under control of miR-296-3p and miR-298-5p in αTC1-6. (A) of phospho-IRS-1 (Tyr612) in (1) untreated αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p (left); (2) αTC1-6 transfected for 24 h with (i) scramble molecules (NC); (ii) mimics of miR-296-3p; (iii) mimics of miR-298-5p; (iv) mimics of both miR-296-3p and miR-298-5p and treated with cytokines for further 24 h (right). [score:1]
αTC1-6 transfection with mimics of miR-296-3p and miR-298-5p increases apoptosis levels induced by cytokines. [score:1]
Sequences of mature miR-296-3p are 100% conserved between rodents and humans, whereas those of miR-298-5p are 74% identical. [score:1]
On scale representation of the genome segment comprising Nespas, miR-296, miR-298. [score:1]
Genomics of genes encoding miR-296-3p, miR-298-5p, Nespas and identification of upstream CpG islandsGenes encoding miRNAs 296-3p and 298-5p are clustered in a genomic region, which also comprises the gene for the noncoding transcript Nespas and is imprinted in mice and humans [21]. [score:1]
Transient transfection of αTC1-6 cells with mimics of miR-296-3p and miR-298-5p. [score:1]
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2
[+] score: 41
By contrast miR-292-5p and miR-298 have weaker seed sequence enrichments amongst significantly down-regulated genes following transfection and their proposed targets are not enriched among the genes up-regulated by Dgcr8 depletion. [score:9]
In the case of miR-298, it is not highly expressed in mouse ES cells so we were not expecting to identify a large number of in vivo targets that would be up-regulated upon miRNA depletion. [score:8]
In all cases except miR-292-5p and miR-298 there is clear enrichment of the miRNA targets of each miRNA in the genes up-regulated when miRNAs are depleted, confirming that the gene lists represent the effects of a reversal of Dgcr8 depletion. [score:6]
Briefly, 1500 ng of biotinylated cRNA was hybridised to Illumina expression BeadChips (Mouse-6 v1.1 for mmu-miR-291-3p and mmu-miR-25 mimics and cell line expression profiles, and Mouse-6 v2 for mmu-miR-302, mmu-miR-292-5p, mmu-miR-106a, mmu-miR-21 and mmu-miR-298 mimics. [score:5]
For a full description see Figure 3. B: GSEA enrichment plots [29] judging the enrichment of the transcripts within the miRNA target lists for miR-25, miR-291a-3p, miR-292-5p or miR-298 within regions of a list of transcripts ordered according to log fold change following the depletion of Dgcr8 in homozygous mutant cell lines. [score:3]
In addition miR-298, miR-302a, miR-21 and miR-291a-3p appear to target genes in these pathways to varying degrees. [score:3]
A: Sylamer plots comparing the expression profiles of Dgcr8 [gt1/tm1] cells transfected with a miRNA mimic (miR-25, miR-291a-3p, miR-292-5p or miR-298) and a cel-miR-239b control miRNA. [score:3]
miRIDIAN Negative Control #2 (Dharmacon CN-002000-01-05) miRIDIAN mmu-miR-291-3p mimic (Dharmacon C-310470-01-0005) miRIDIAN mmu-miR-25 mimic (Dharmacon C-310564-01-0005) miRIDIAN mmu-miR-302 mimic (Dharmacon C-310483-05-0005) miRIDIAN mmu-miR-292-5p mimic (Dharmacon C-310471-03-0005) miRIDIAN mmu-miR-106a mimic (Dharmacon C-310488-07-0005) miRIDIAN mmu-miR-21 mimic (Dharmacon C-310515-05-0005) miRIDIAN mmu-miR-298 mimic (Dharmacon C-310479-07-0005) Trizol purified RNA was cleaned up with an RNeasy MiniElute Cleanup Kit (Qiagen). [score:1]
This large overlap is contrasted with the much lower overlap (0–11%) seen between these two miRNAs and miR-298, miR-21, miR-25 and miR-292-5p (Figure S8). [score:1]
miRIDIAN Negative Control #2 (Dharmacon CN-002000-01-05) miRIDIAN mmu-miR-291-3p mimic (Dharmacon C-310470-01-0005) miRIDIAN mmu-miR-25 mimic (Dharmacon C-310564-01-0005) miRIDIAN mmu-miR-302 mimic (Dharmacon C-310483-05-0005) miRIDIAN mmu-miR-292-5p mimic (Dharmacon C-310471-03-0005) miRIDIAN mmu-miR-106a mimic (Dharmacon C-310488-07-0005) miRIDIAN mmu-miR-21 mimic (Dharmacon C-310515-05-0005) miRIDIAN mmu-miR-298 mimic (Dharmacon C-310479-07-0005) Trizol purified RNA was cleaned up with an RNeasy MiniElute Cleanup Kit (Qiagen). [score:1]
A set of miRNAs was transfected including miR-25, miR-291a-3p, miR-292-5p, miR-106a, miR-21, miR-302a and miR-298. [score:1]
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3
[+] score: 38
In miR-153 transfected ALCs compared with negative control siRNA transfected ALCs, the expression of miR-3085 and miR-346 was upregulated, while the expression of miR-298, miR-135a, miR-376b and miR-203 was downregulated. [score:10]
Specifically, in miR-153 transfected ALCs, the expression of miR-3085 and miR-346 was upregulated compared with negative control siRNA, while the expression of miR-298, miR-135a, miR-376b and miR-203 was downregulated (P < 0.05) (Fig. 3b and). [score:10]
In LS8 cells, the increased intracellular level of miR-153 induced similar directional changes (as in ALCs) in the expression of miR-3085, miR-298, miR-135a and miR-376b. [score:4]
In both ALCs (a) and LS8 cells (b), treatment with EMD elicited significant downregulation of miR-3085, miR-298, miR-138, miR-135a and miR-376b. [score:4]
Within both ALCs and LS8 cells, addition of EMD elicited significant downregulation of miR-3085, miR-298, miR-138, miR-135a and miR-376b (P < 0.05) (Fig. 6a,b and). [score:4]
In LS8 cells, intracellular overloading of miR-153 induced similar changes in the expression of miR-3085, miR-298, miR-135a and miR-376b as those in ALCs. [score:3]
In the significantly enriched functional categories, such as those labeled with ‘endosome membrane’ or ‘lysosomal lumen’, miR-153 together with miR-3085, miR-298, miR-138, miR-135a, miR376b, miR-203 and miR-346 were predicted to be epigenetic regulators involved in endocytosis and endosomal/lysosomal pathways 11. [score:2]
In order to identify that ALCs and LS8 cells are suitable mo dels for investigating the functional role of miR-153, the baseline expression of miR-153 (along with miR-31, miR-21, miR-223, miR-410, miR-3085, miR-298, miR-135a, miR-138, miR376b, miR-203 and miR-346) was quantified by real-time PCR. [score:1]
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4
[+] score: 34
However, Barbagallo et al. reported that the downregulation of miR-296-3p and miR-298-5p, which consequently led to the upregulation of their respective targets IGF1Rβ and TNFα, was a major determinant of the resistance of mammalian pancreatic α cells to cytokine -induced apoptosis [27]. [score:9]
Seven of these miRNAs were found to be significantly downregulated (miR-449a-3p, miR-298-5p, miR-92a-1-5p, miR-423-5p, miR-423-3p, miR-128-3p, miR-340-3p), and 1 was found to be significantly upregulated (miR-21a-3p) at 6 hours after transient scrotal heat treatment. [score:7]
MiR-449a-3p, miR-298-5p, miR-92a-1-5p, miR-423-5p, miR-423-3p, miR-128-3p and miR-340-3p were found to be significantly downregulated (A-G, all p < 0.05), and miR-21a-3p was found to be significantly upregulated at 6 hours after heat treatment (J, p = 0.006). [score:7]
Our observation that miR-298-5p was downregulated after scrotal hyperthermia was not previously reported in studies of testicular miRNA expression. [score:6]
Furthermore, our observation of a non-significant association between the relative miR-298-5p level and the germ cell AI in the correlation analysis suggests that the downregulation of miR-298-5p alone may not be sufficient to induce germ cell apoptosis. [score:4]
The relative levels of miR-298-5p (B), miR-423-5p (D) and miR-340-3p (G) were not significantly correlated with germ cell AI. [score:1]
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5
[+] score: 29
Microarray data revealed that several microRNAs were dysregulated in Cs1-ko mice (S1 Table), including miR301a, which was maximally downregulated, whereas, miR-298 was highly upregulated in Cs1-ko mouse hearts (schematically depicted in Fig 2A). [score:8]
MiR-301a was identified the most downregulated microRNA, whereas, miR-298 was highly upregulated (N = 4 each), which was confirmed in independent cohort by quantitative real-time PCR for miR-301a (B), and miR-298 (C) (N = 5 (WT), and 6 (Cs1-ko)). [score:7]
We further validated the expression of miR-301a and miR-298 by quantitative real-time PCR (qPCR) in independent set of mouse cohort to confirm its downregulation (Fig 2B and 2C). [score:6]
Few of the highly upregulated microRNAs were: miR-79, miR-183, miR-206, miR-207, miR-296-3p, miR-298, miR-380-5p, miR-433, miR-449b, miR-705, miR-761 (S1 Table). [score:4]
MiR-206 and miR-298 are previously shown to be upregulated in rat mo del of post-infarction heart failure [50]. [score:4]
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6
[+] score: 26
This bioinformatic approach [8] revealed 164 potentially downregulated target genes for the upregulated mmu-miR-298 in the ileum (Table S3). [score:9]
Table S1 Genes potentially targeted by mmu-miR-298, which is up-regulated in the ileum upon colonization, predicted by MiRanda, TargetScan or PicTar algorithms. [score:8]
Table S3 Target genes of mmu-miR-298 predicted by at least two of the three algorithms MiRanda, TargetScan and PicTar. [score:5]
qRT-PCR was performed using SYBR Green qPCR Master Mix (Fermentas) on a Mastercycler Realplex [4] (Eppendorf) using the following primers:For mature miRNA expression: the universal primer provided in the NCode [TM] miRNA first-strand cDNA synthesis kit was used together with one of the following forward primer: mmu-miR-665: 5′-ACCAGG AGG CTG AGG TCC CT-3′mmu-miR-128: 5′-TCACAGTGAACCGGTCTCTTT-3′ mmu-mir-200c*: 5′-CGTCTTACCCAGCAGTGTTTGG-3′ mmu-miR-342-5p: 5′-AGGGGTGCTATCTGTGATTGAG-3′ mmu-miR-466d-3p: 5′-TATACATACACGCACACATAG-3′ mmu-miR-466d-5p: 5′-TGTGTGTGCGTACATGTACATG-3′ mmu-miR-465c-5p: 5′-TATTTAGAATGGCGCTGATCTG-3′ mmu-miR-683: 5′-CCTGCTGTAAGCTGTGTCCTC-3′ mmu-miR-665: 5′-ACCAGGAGGCTGAGGTCCCT-3′ mmu-miR-298: 5′-GGCAGAGGAGGGCTGTTCTTCCC-3′ For Abcc3 expression:Forward 5′-CTT CTT TTC CCG CTT GTC TTT-3′;Reverse 5′- CCT CCT CAG ACA GAG ACC AGA-3′. [score:2]
qRT-PCR was performed using SYBR Green qPCR Master Mix (Fermentas) on a Mastercycler Realplex [4] (Eppendorf) using the following primers: For mature miRNA expression: the universal primer provided in the NCode [TM] miRNA first-strand cDNA synthesis kit was used together with one of the following forward primer: mmu-miR-665: 5′-ACCAGG AGG CTG AGG TCC CT-3′ mmu-miR-128: 5′-TCACAGTGAACCGGTCTCTTT-3′ mmu-mir-200c*: 5′-CGTCTTACCCAGCAGTGTTTGG-3′ mmu-miR-342-5p: 5′-AGGGGTGCTATCTGTGATTGAG-3′ mmu-miR-466d-3p: 5′-TATACATACACGCACACATAG-3′ mmu-miR-466d-5p: 5′-TGTGTGTGCGTACATGTACATG-3′ mmu-miR-465c-5p: 5′-TATTTAGAATGGCGCTGATCTG-3′ mmu-miR-683: 5′-CCTGCTGTAAGCTGTGTCCTC-3′ mmu-miR-665: 5′-ACCAGGAGGCTGAGGTCCCT-3′ mmu-miR-298: 5′-GGCAGAGGAGGGCTGTTCTTCCC-3′ For Abcc3 expression: Forward 5′-CTT CTT TTC CCG CTT GTC TTT-3′; Reverse 5′- CCT CCT CAG ACA GAG ACC AGA-3′. [score:2]
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7
[+] score: 16
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-27b, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-182, mmu-mir-199a-1, mmu-mir-122, mmu-mir-143, mmu-let-7d, 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-15a, mmu-mir-23a, mmu-mir-27a, mmu-mir-31, mmu-mir-98, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-181b-1, mmu-mir-379, mmu-mir-181b-2, mmu-mir-449a, mmu-mir-451a, mmu-mir-466a, mmu-mir-486a, mmu-mir-671, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-491, mmu-mir-700, mmu-mir-500, mmu-mir-18b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-466d, mmu-mir-466l, mmu-mir-669k, mmu-mir-669g, mmu-mir-669d, mmu-mir-466i, mmu-mir-669j, mmu-mir-669f, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-669e, mmu-mir-669l, mmu-mir-669m-1, mmu-mir-669m-2, mmu-mir-669o, mmu-mir-669n, mmu-mir-466m, mmu-mir-669d-2, mmu-mir-466o, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-466b-7, mmu-mir-669p-2, mmu-mir-669a-10, mmu-mir-669a-11, mmu-mir-669a-12, mmu-mir-466p, mmu-mir-466n, mmu-mir-486b, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-145b, mmu-let-7j, mmu-mir-451b, mmu-let-7k, mmu-mir-126b, mmu-mir-466c-3
For example, miR-127 has been shown to participate in cancer development [85], miR-145 has been shown to control c-Myc expression through p53 [86], miR-199a regulates MET protooncogene and affects NF-KB expression [54], miR-379 affects brain neuronal development [87], [88], miR-451 affects erythroid differentiation [89], miR-126 affects angiogenic signaling and controls blood vessel development [90], miR-143 regulates ERK5 signaling and targets KRAS gene [91], miR-298 regulates CYPA3 expression [92] and miR-486 regulates kinase activity and tumor progression [93]. [score:16]
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8
[+] score: 13
Other miRNAs from this paper: mmu-mir-328, hsa-mir-328, hsa-mir-298
In vivo, we observed decreased expression levels of miR-298 and miR-328 in the hippocampus of aging APPSwe/PS1 mice [8], which supports further the possibility that the loss of miRNA regulation of BACE1 mRNA translation may lead to higher BACE1 protein expression, an enhanced Aß formation and the development of AD. [score:9]
In a recent study from our laboratory, we reported similar observations in an animal mo del of AD (APPSwe/PS1 mice) and demonstrated a role for two miRNAs, i. e. miR-298 and miR-328, in the regulation of BACE1 expression, using mainly transiently transfected murine neuronal N2a cells in culture [8]. [score:4]
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9
[+] score: 12
Other miRNAs from this paper: mmu-mir-150, mmu-mir-1943, mmu-mir-5099
miR-298 and -1943 have been reported to have a suppressive role against tumour progression (Supplementary Fig.   12e). [score:3]
miR-298–5p in CD8 [+] T cell EVs is one of the molecules involved in the depletion of tumoural mesenchymal cell populations, although it is necessary to elucidate the mechanism of action including identification of target genes. [score:3]
After comparison of global-normalised law data from microarray analysis (3D-gene: Toray) among miRNAs from DUC18 CD8 EVs, BALB CD8 EVs, BALB TB CD8 EVs, bone-derived MSCs, CMS5a and B16, we selected miR-298, 1943 and 5099 and miR-150, 223 and 3470b as both DUC18 CD8 EV- and BALB CD8 EV-dominant miRNAs and BALB TB CD8 EV-dominant miRNAs, respectively (Supplementary Table  1). [score:1]
These results indicate that CD8 [+] T cells from normal mice, but not tumour-bearing mice, release cytotoxic miRNA (miR-298-5p)-embedded EVs to kill MSCs. [score:1]
In addition, the levels of miR-298-5p in BALB CD8 EVs were confirmed to be higher than those in TB CD8 EVs from B16F10-bearing mice or tumour cell-derived EVs (Supplementary Fig.   10e). [score:1]
c Selected miR-298-5p, -1943-3p and -5099 as both DUC18 CD8 EV- and BALB CD8 EV-dominant miRNAs were synthesised and transfected alone or in a mixture by lipofection into bone-derived MSCs (n = 4 per group). [score:1]
According to the RNA sequences from miRBase, selected DUC18 CD8 EV-dominant miR-298–5p, 1943-5p and 5099; and BALB TB CD8 EV-dominant miR-150-5p, 223-3p and 3470b were synthesised (Hokkaido System Science). [score:1]
The number of MSCs was reduced by introduction of miR-298 in an activated caspase-3 -mediated manner (Supplementary Fig.   10d), but not by introduction of miR-1943 or miR-5099 (Fig.   2c, d). [score:1]
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[+] score: 10
On the other hand, miR-298 expression was not found in ES cells [47]. [score:3]
The other two miRNAs identified in this screen, miR-25 and miR-298, were not previously reported for their role in ES cells or in reprogramming when the project started. [score:1]
Table S3 Conservation of miR-25 and miR-298 mature sequences. [score:1]
0040938.g002 Figure 2 a. Four microRNAs: miR302 (cluster), miR-25/93, miR-290 and miR-298 were able to improve reprogramming. [score:1]
Two candidates, miR-25 and miR-298, were found to substantially improve reprogramming with the four Yamanaka factors. [score:1]
All mature sequences of miR-25 and miR-298 are obtained from miRBase database. [score:1]
a. Four microRNAs: miR302 (cluster), miR-25/93, miR-290 and miR-298 were able to improve reprogramming. [score:1]
Four out of the 52 tested miRNAs or miRNA clusters: the miR-302 cluster, miR-25, miR-290 and miR-298, gave substantially more Puro [r] iPSC colonies (2–4 fold) than the control where only the four factors were used (PB-CAG-OCKS) (Fig. 2a). [score:1]
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[+] score: 10
Thus, reduction of miR-298 and miR-195 results in increased expression of their predicted targets. [score:5]
Decreased expression of miR-298 and miR-195 is predicted to result in increased protein expression of Myf5 and Smad2, respectively, in emerin -null myogenic progenitors. [score:5]
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12
[+] score: 8
Mir-29a, miR-219, miR-338 and miR-132 were the miRNAs undergoing the strongest upregulation during development, a result confirmed by reverse transcription PCR (Supplementary Fig. 1) and in agreement with previous data 8, whereas miR-298, miR-149 and miR-331 were the top downregulated miRNAs. [score:8]
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13
[+] score: 8
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 A. Scatterplot showing relative expression of miRNAs by macroarray. [score:4]
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 Because miRNAs typically regulate translation in animal cells, we compared CXCL10 and STAT1 protein levels in both control and Dicer [d/d] animals and cells. [score:4]
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14
[+] score: 7
The highest fold-changes were 5.8 for mmu-miR-298 in colon (up-regulation) and 0.164 for mmu-miR-207 in forestomach (down-regulation). [score:7]
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15
[+] score: 6
Both SA1 and SA2 infection led to expression of mmu-miR-298 that targets IKKi/IKKϵ [24] and thus regulates NF-κB pathway [25]. [score:6]
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16
[+] score: 5
Indeed, several miRNAs target BACE1, including miR-9, miR-29, miR-107, miR-186, miR-188, miR-298, and miR-328, some of which are closely related to synaptic and cognitive function [40, 41]. [score:3]
Previously, several miRNAs have been demonstrated to be involved in post-transcriptional regulation of BACE1, including miR-9, miR-29, miR-107, miR-186, miR-188, miR-298, and miR-328 [40, 41]. [score:2]
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17
[+] score: 4
Of which, let-7f, let-7d, let-7e, let-7i, miR-20a, miR-298, let-7g, miR-21, and let-7a are up-regulated in activation group. [score:4]
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18
[+] score: 4
Mir296 and Mir298 are paternal allele-specifically expressed and their transcription in the paternal chromosome depends on the unmethylated allele of the germline DMR located at the Nespas promoter 27 kb away (8). [score:2]
The paternally expressed Nespas RNA (28, 29) extended beyond the Mir296 and Mir298 microRNAs (Supplementary Figure S1C). [score:2]
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19
[+] score: 4
MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1. J. Biol. [score:4]
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20
[+] score: 4
MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1. J. Biol. [score:4]
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21
[+] score: 3
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-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-136, 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]
5 miR-298 33.2 ±0.2 33.8 ±0.2 33.5 ±0.6 33.5 ±0.4 miR-346 35.7 ±1.1 36.4 ±0.8 35.7 ±0.6 34.7 ±0.4 miR-501 34.5 ±0.9 34.4 ±0.9 34.6 ±0.1 34.4 ±0.4 miR-718 ND ND ND ND miR-720 22.5 ±0.3 22.9 ±0.1 23.4 ±0.4 22.9 ±0. [score:1]
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22
[+] score: 3
Nrf2 (+/+) Saline—Nrf2(–/–) Saline miR-128, miR-7a, miR-669c, miR-298, miR-543, miR-770-5p, miR-669b* and miR-544-5p S1 Changes in miRNA expression profile after exposure to paraquat. [score:3]
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[+] score: 3
MiR-335-3p, miR-223-3p, miR-340-5p, miR-298-5p and miR-224-5p had higher expression in SAT and VAT than in BAT (Supplementary Table 4). [score:3]
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24
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
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25
[+] score: 1
On the other hand, Gnas-Nespas cluster encode miR-296 and miR-298 which are derived from non-coding Nespas gene transcript. [score:1]
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26
[+] score: 1
Typical cardio-specific miRNAs (such as miR-143) could be found in this cluster, as well as some embryo-related miRNAs (such as miR-298) [25]. [score:1]
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[+] score: 1
The highest -log P value of 6.57 was observed for miR-298 on chromosome 9 explaining 20.76 % of the variance. [score:1]
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