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32 publications mentioning mmu-mir-379

Open access articles that are associated with the species Mus musculus and mention the gene name mir-379. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 190
These results suggest that reduction of hlnc-MGC by HMGC10 can suppress the miR-379 cluster miRNAs, restore the expression of their targets and inhibit the profibrotic genes in HMC treated with TGF-β1 or HG, highlighting the potential translational significance. [score:11]
These results suggest that MGC10 is effective in reducing the expression of not only lnc-MGC and miR-379 cluster miRNAs in vivo in diabetic mice, but also restores the expression of the cluster miRNA targets, inhibits profibrotic genes and prevents glomerular fibrosis, podocyte death, and hypertrophy in diabetic mice. [score:9]
When Chop- KO MMC were transfected with miR-379 mimic, significant increase of miR-379, profibrotic genes but decrease of targets were observed (Supplementary Fig. 24d–i), confirming that ectopic expression of decreased miRNAs in Chop- KO MMC reverses the expression of targets and profibrotic genes. [score:9]
Our data suggest that diabetic conditions (HG), which also induce TGF-β1, upregulates ∼40 miRNAs within the miR-379 megacluster that target regulators of ER stress and protein synthesis resulting in hypertrophy and fibrosis related to DN (Fig. 9a). [score:7]
siRNAs targeting Chop inhibited the induction of lnc-MGC and miR-379 cluster miRNAs as well as parameters (ECM gene expression and cellular hypertrophy) of DN in vitro. [score:7]
Furthermore, targets (Edem3, Tnrc6b and Bhc80) of the miR-379 cluster were upregulated by MGC10 (Supplementary Fig. 31d–g). [score:6]
Because MGC10 is fully phosphorothioated, it is efficiently transported into the nucleus where it cleaves lnc-MGC RNA and thereby suppresses the expression of the miR-379 cluster (Supplementary Fig. 33). [score:5]
TM reciprocally decreased several targets of the miR-379 cluster including Edem3, a target of miR-379 (Supplementary Fig. 26a–g). [score:5]
miR-379 mimics also inhibited the luciferase activity of this reporter compared to negative control mimics (CTR), suggesting Edem3 is a direct target of miR-379. [score:5]
Key targets (Edem3, Atf3, Tnrc6B, Cpeb4, Pum2) of the miR-379 cluster were reduced in kidneys from diabetic mice but their expression was restored in the kidney cortex and glomeruli of diabetic mice injected with MGC10 (Fig. 6g,h and Supplementary Fig. 36d–f). [score:5]
Inhibition of lnc-MGC by in vitro and in vivosiRNAs designed to target lnc-MGC regions located upstream of miR-379 were effective to silence lnc-MGC and cluster miRNAs (Supplementary Fig. 29a,b). [score:5]
For each miR-379 cluster miRNA, the potential human or mouse target genes containing at least 3 conserved binding sites were identified using the online bioinformatics tool TargetScan (http://www. [score:5]
miR-379 and miR-200b mimics had no effect on reporters containing partial deletion of the region harbouring miR-379 and miR-200b/c target sites in the 3′UTR of Edem3, verifying these sites to be bonafide targets of miR-379 and miR-200b/c (Supplementary Fig. 28c). [score:5]
miR-379 cluster expression depends on the expression of the host lnc-MGC from its promoter. [score:5]
These results suggest that TM (ER stress) increases lnc-MGC and the miR-379 cluster miRNAs, and enhances ER stress and DN phenotypes (hypertrophy and fibrosis) by inhibiting the miR-379 cluster targets. [score:5]
Pre-ranked gene set analysis (GSEA) applied on the gene set using the ranked list of all the miRNAs revealed that miRNAs in the miR-379 cluster were significantly enriched within the miRNAs upregulated in the STZ diabetic mice, with normalized enrichment score of 1.56 (P=0.004). [score:4]
These results also suggest that one of the mechanisms by which the miR-379 cluster upregulated in diabetes contributes to DN is through ER stress promoted by loss of Edem3. [score:4]
This illustrates two independent modes of Edem3 regulation, loss of N-glycosylation and decrease of expression through miR-379 induction (Supplementary Fig. 26g–i). [score:4]
In addition, the expression of candidate target genes of the miR-379 cluster was significantly higher in MMC from Chop- KO mice as compared to WT (basal and after TGF-β1 treatment) (Supplementary Fig. 23b). [score:4]
In addition, key miRNAs in the miR-379 megacluster were downregulated by MGC10 (Supplementary Fig. 31a–c). [score:4]
siRNAs designed to target lnc-MGC regions located upstream of miR-379 were effective to silence lnc-MGC and cluster miRNAs (Supplementary Fig. 29a,b). [score:3]
Expression of the cluster miRNAs, (miR-379, -494, -495, -377) but not miR-882, and Mirg depicted a similar pattern as lnc-MGC, demonstrating specificity to this cluster (Fig. 6a–f). [score:3]
On the other hand, TGF-β1 treatment decreased Edem3 expression likely through induction of miR-379 since miR-379 mimic oligonucleotides (oligos) reduced Edem3 levels (Supplementary Fig. 26h,i). [score:3]
Chop siRNA significantly attenuated HG- and TGF-β1 -induced expression of miR-379 and lnc-MGC in MMC (Fig. 4b,c). [score:3]
The levels of key targets of the miR-379 cluster were significantly lower in diabetic mice. [score:3]
Similar trends were observed for miR-379, miR-494, miR-495 and miR-377, but not miR-822, suggesting that inhibition of hlnc-MGC (host RNA) by HMGC10 reduces the cluster miRNAs in HMC treated with TGF-β1 (Fig. 8a). [score:3]
No significant change was detected in the expression of miR-882 (outside of the miR-379 cluster). [score:3]
The expression of each detectable miRNA within the miR-379 cluster in the two samples (CTR and STZ) were ordered by log2 fold change from low to high, mean-centered and shown in the heatmap. [score:3]
Because MGC10 was effective in reducing the expression of lnc-MGC and key miR-379 cluster miRNAs in MMC in vitro, we next tested its actions in mouse kidneys in vivo (Supplementary Fig. 32). [score:3]
Expression of miR-379 cluster miRNAs in human kidney tissue. [score:3]
Chop siRNA inhibited TGF-β1 or HG mediated increase of miR-379 in MMC but had no effect on basal levels of miR-379. [score:3]
Together with ChIP data, the CHOP binding site (−1.6 kb) is essential for the expression of lnc-MGC and miR-379 cluster. [score:3]
With respect to ER stress, immunostaining of Edem3, a target of miR-379, showed significant decrease in glomeruli of diabetic mice and this was reversed in glomeruli of diabetic mice injected with MGC10 (Fig. 7d,e). [score:3]
Edem3 is as a target of miR-379. [score:3]
The E-box binding region might contribute to the regulation of the miR-379 cluster by mechanisms (miRNA -mediated increase of E-box activators and decrease of E-box repressor) similar to those identified in the regulation of collagens in MC under diabetic conditions 16 45. [score:3]
To verify the role of ER stress, MMC were treated with tunicamycin (TM), a known ER stress inducer, and the expression of miR-379 cluster miRNAs examined. [score:3]
To test if the miR-379 cluster is similarly regulated in human cells, human MC (HMC) were treated with TGF-β1 or HG. [score:2]
To identify a putative promoter that drives the expression of this genomic region, we carried out 5′ RACE experiments using primers spanning the miR-379 upstream region (Fig. 2b). [score:2]
We also identified binding sites for CHOP, a transcription factor associated with the ER stress response, and an overlapping E-box ∼1.6 kb upstream of miR-379 (Fig. 3a), suggesting that the identified promoter of the lncRNA-MGC-miRNA cluster may be regulated by CHOP. [score:2]
CAGA repeats (Smad -binding elements) were found ∼3 kb upstream of miR-379 (Fig. 3a), suggesting regulation by TGF-β1. [score:2]
TGF-β1 and HG significantly increased the expression of miR-379, miR-494, miR-495 and miR-377 as well as lnc-MGC, but not miR-882, compared with serum depleted (SD) or normal glucose (NG) controls respectively in cultured mouse MC (MMC; Fig. 2d). [score:2]
Smad2/3 occupancy peaked at 1 h, and returned to normal by 24 h, suggesting the miR-379 cluster is regulated by TGF-β1 through rapid enrichment of Smad2/3 at the upstream region. [score:2]
43), a miRNA in the miR-379 cluster that we confirmed to be increased in diabetic mice glomeruli. [score:1]
miR-379 is located at the 5′ end, miR-494 and miR-495 in the middle, and miR-377 downstream (Fig. 1c). [score:1]
miRNAs in the miR-379 cluster were presented in red. [score:1]
miR-882 was plotted in blue as a negative control (outside the miR-379 cluster). [score:1]
The fragment of upstream of lnc-MGC (miR-379 cluster) digested with SacI and HindIII was cloned into pGL4 luciferase vector (Promega). [score:1]
hlnc-MGC and miR-379 cluster miRNAs were increased by TGF-β1 or HG in HMC, with miR-882 showing no significant difference (Fig. 8a,b). [score:1]
The increases of lnc-MGC, miR-379, miR-494, miR-495 and miR-377 noted in glomeruli from diabetic WT mice were not observed in glomeruli from diabetic Chop- KO mice (five mice in each group). [score:1]
miR-882 is located far-upstream of the miR-379 cluster and not covered by lnc-MGC. [score:1]
We used 5′ RACE to identify the putative upstream promoter region of the miR-379 megacluster and host lncRNA-MGC. [score:1]
Smad -binding elements (CAGA repeats) and CHOP binding consensus and E-box sequences were found upstream of miR-379. [score:1]
Edem3 protein levels were decreased in MMC treated with TGF-β1, or in MMC transfected with miR-379 mimics (Supplementary Fig. 26h,i). [score:1]
43), a miR-379 cluster miRNA confirmed to be increased in diabetic glomeruli. [score:1]
CAGA repeats (potential Smad -binding elements) were identified at ∼3 kb upstream of miR-379 and CHOP binding element and E-boxes were found close to a SacI restriction enzyme site at ∼1.6 kb upstream of miR-379. [score:1]
The miR-379 miRNA megacluster is increased in the glomeruli of diabetic mice. [score:1]
miR-379, -495 and -377 (but not miR-882), were also reduced in the same samples (Supplementary Fig. 32c–f). [score:1]
A reporter plasmid encompassing the full 3′UTR of mouse Edem3 gene (Full) was cotransfected into MMC along with miR-379 mimics (Supplementary Fig. 28a,b). [score:1]
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2
[+] score: 57
We also showed that while antagomir-379 reduced miR-379 expression (S3D Fig) significantly, it has no effect on miR-127 expression (S3F Fig), suggesting the specificity of antagomirs. [score:5]
While did not induce any DLK1-Dio3 miRNA expression in unstimulated splenocytes (medium, Fig 3A), it did induce the expression of DLK1-Dio3 miRNAs including miR-154, miR-127, miR-379, miR-382, miR-433, and miR-300 substantially in Con A activated splenocytes (Con A, Fig 3A). [score:5]
miR-154, miR-379, and miR-300 have been shown to be decreased in different types of cancer cells, and they function as tumor suppressors by targeting TLR2, Cyclin B1, and Twist, respectively [46– 48]. [score:5]
However, for unknown reason, 5-aza-CdR treatment increased miR-154, miR-127, and miR-379 expression even in inactivated CD4 [+] T cells from MRL mice (medium, Fig 3B), and Con A activation did not further promote the effect of 5-aza-CdR on DLK1-Do3 miRNA expression in CD4 [+] T cells. [score:5]
The dysregulated expression of selected DLK1-Dio3 miRNAs such as miR-134, miR-433, miR-494, and miR-379 has also been noticed in human lupus [21, 29]. [score:4]
Impressively, of the 17 upregulated miRNAs in MRL- lpr mice, 11 miRNAs (miR-154, miR-127, miR-379, miR-382, miR-433, miR-300, miR-376b, miR-394, miR-299, miR-495, and miR-329) are located at a genomic imprinted DLK1-Dio3 region. [score:4]
Conceivably, upregulated DLK1-Dio3 miRNAs such as miR-154, miR-379, and miR-300 might accelerate lupus by promoting the production of lupus-related cytokines. [score:4]
We tested only miR-154, miR-127, miR-411, and miR-379 in cells from MRL- lpr mice since these four miRNAs were the most upregulated miRNAs in 5-aza-CdR treated splenocytes from MRL control mice. [score:4]
Further studies are needed to determine the target genes of miR-154, miR-379, and miR-300 in immune cells in a lupus setting, an aspect not yet known. [score:3]
We reported here that deliberate inhibition of selected DLK1-Dio3 miRNAs such as miR-154, miR-379, and miR-300 significantly reduced the production of lupus -associated cytokines IFNγ, IL-1β, IL-6, and/or IL-10 (Fig 6). [score:3]
While miR-154 showed a similar increase in splenocytes and in different splenic immune cell subsets, the other six DLK1-Dio3 miRNAs including miR-127 (Fig 5B), miR-411 (Fig 5C), miR-379 (Fig 5D), miR-382 (Fig 5E), miR-433 (Fig 5F), and miR-300 (Fig 5G) were upregulated more dramatically in CD4 [-]CD19 [-] cells when compared to that in purified CD4 [+] T and CD19 [+] B cells. [score:3]
The expression level of miR-379 was analyzed in antagomir-127 treated cells to show the specificity of antagomir (F). [score:3]
In this study, we performed Taqman miRNA assays to confirm the upregulation of selected DLK1-Dio3 miRNAs such as miR-154, miR-127, miR-379, miR-382, miR-300, and miR-433 in MRL- lpr splenocytes. [score:3]
The dysregulation of DLK1-Dio3 miRNAs was also evident in B6- lpr and NZB/W [F1] lupus mice (such as miR-127 and miR-379) [28, 44], and in human lupus patients (such as miR-134, miR-379, and miR-433)[21, 29]. [score:2]
The expression levels of miR-154 (A), miR-127 (B), miR-411 (C), miR-379 (D), miR-382 (E), miR-433 (F), and miR-300 (G) in vehicle and 5-aza-CdR treated splenocytes, purified CD4 [+] T cells, CD19 [+] B cells, and splenic CD4 [-]CD19 [-] cells were quantified by Taqman miRNA assays. [score:2]
Unlike that we observed in splenocytes, there was a slight but significant increase of several DLK1-Dio3 miRNAs such as miR-154, miR-127, miR-379, and miR-382 even in the unstimulated CD4 [+] T cells from MRL mice (medium). [score:1]
There was a greater than 10 fold increase for selected DLK1-Dio3 miRNAs such as miR-154, miR-127, miR-411, miR-379 in 5-aza-CdR plus Con A treated MRL splenocytes. [score:1]
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3
[+] score: 41
Before the onset of lupus, male and female NZB/W [F1] mice have comparable levels of lupus -associated miRNAsIn our previous study where we utilized only female NZB/W [F1] mice, we reported that a set of miRNAs including the miR-96-182-183 cluster, miR-155, miR-31, miR-127, and miR-379 were upregulated only in the splenocytes from diseased 36–40-wk-old (8–9 months) female NZB/W [F1] mice, but not in the splenocytes from the pre-diseased 16–18-wk-old (3–4 months) NZB/W [F1] mice when compared to those in the control NZW mice [34]. [score:7]
In our previous study where we utilized only female NZB/W [F1] mice, we reported that a set of miRNAs including the miR-96-182-183 cluster, miR-155, miR-31, miR-127, and miR-379 were upregulated only in the splenocytes from diseased 36–40-wk-old (8–9 months) female NZB/W [F1] mice, but not in the splenocytes from the pre-diseased 16–18-wk-old (3–4 months) NZB/W [F1] mice when compared to those in the control NZW mice [34]. [score:7]
We initially analyzed the expression of lupus -associated miRNAs including the miR-96-182-183 cluster, miR-155, miR-31, miR-127, miR-379, and miR-148a in splenocytes from male and female NZB/W [F1] mice at 17–18 wks old, an age before the onset of disease in NZB/W [F1] mice. [score:5]
Of the eight lupus -associated miRNAs analyzed in this study, only miR-127 and miR-379 displayed sexual differential expression before the onset of lupus in NZB/W [F1] (Figure  1). [score:3]
We recently reported that female NZB/W [F1] mice had increased expression of lupus -associated miRNAs such as the miR-182-96-183 cluster, miR-31, miR-155, miR-127, and miR-379 only at an age when lupus is manifested [34]. [score:3]
However, our data tends to support that estrogen treatment promoted the expression of selected lupus -associated miRNAs such as the miR-182 cluster, miR-379, and miR-148a in orchidectomized male NZB/W [F1] mice. [score:3]
We noticed that the expression of miR-96, miR-379, and miR-148a was significantly increased in 30-wk-old female mice, but not in 23-wk-old female mice when compared to that in age-matched male mice (Figure  2A). [score:2]
There is also limited knowledge with regard to the immune regulatory function of miR-127 and miR-379. [score:2]
So far, there is limited knowledge about Dlk1-Gtl2 imprinted miRNA clusters such as miR-127 and miR-379 with regard to their function, especially their immune regulatory function. [score:2]
The sex differences in the expression of lupus -associated miRNAs, including the miR-182-96-183 cluster, miR-155, miR-31, miR-148a, miR-127, and miR-379, were markedly evident after the onset of lupus, especially at 30 wks of age when female NZB/W [F1] mice manifested moderate to severe lupus when compared to their male counterparts. [score:2]
Impressively, we found that after the onset of lupus, the expressions of lupus -associated miRNAs (miR-182-96-183, miR-31, miR-127, miR-379, and miR-148a, miR-155) were significantly increased in female NZB/W [F1] mice when compared to those in age-matched male mice. [score:2]
The only exception is miR-379, which was increased in the splenocytes from 10-wk-old estrogen -treated mice. [score:1]
miR-127 and miR-379 are encoded by a large miRNA cluster embedded in the mouse maternal imprinted region Dlk1-Gtl2 and human homologues DLK1-DIO3. [score:1]
Impressively, our previous microarray data indicated that in addition to miR-127 and miR-379, several other miRNAs from the Dlk1-Gtl2 region, including miR-433, miR-300, and miR-382, were also increased in MRL-lpr and B6-lpr mice [34]. [score:1]
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4
[+] score: 28
To reveal the role of these miRNAs in the muscular phenotype of myostatin knockout mice, we quantified their expression by qRT-PCR, and observed a significant increase in the expression of miR-411, miR-434-3p, miR-379, and miR-193b in myostatin knockout mice (Figure 1A). [score:7]
Most recently, Gao et al. showed that deletion of the maternally expressed miR-379/miR-544 cluster located between the Rian and Mirg genes resulted in callipyge-like muscular hypertrophy with increased Dlk1 expression in mice [28]. [score:5]
Among these, the increased expressions of miR-411, miR-434-3p, and miR-379 were of interest because these miRNAs are expressed from the mouse chromosome 12qF1 (chr12qF1), called as the Dlk1-Dio3 locus (Figure 1B). [score:5]
108 ± 4.23, P = 0.091), whereas overexpression of the remaining 7 miRNAs (miR-127, miR-300, miR-329, miR-337-3p, miR-376a, miR-379, and miR-381) showed no significant effect on myotube diameter (Figure 2D). [score:3]
However, the expression of the remaining 9 miRNAs (miR-411, miR-434-3p, miR-299*, miR-193, miR-146b, miR-379, miR-193b, miR-22, and miR-223) has not been verified. [score:3]
Figure 1(A) A significant increase in miR-411, miR-434-3p, miR-379, and miR-193b expression in myostatin -deficient skeletal muscle at 13 weeks of age was determined by quantitative RT-PCR. [score:3]
In fact, a remarkable increase in skeletal muscle mass in myostatin knockout mice was observed after 5 weeks of age [12], whereas muscle hypertrophy was not observed in mice with the deletion of the miR-379/miR-544 cluster after 3 weeks of age [28]. [score:2]
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5
[+] score: 26
Figure 4. The ‘extended VCR’ of stratum 2 (shared by Homo and Pelodiscus sequences): (a) miR-16 target site (also shown in Fig. 2e) and nearby target sites for miR-376a, miR-335-3p, miR-493 and miR-379 (the Xenopus sequence contains a 44-bp insertion at the site of the asterisk that includes two target sites for miR-335-3p are shown in red); (b) conserved pair of target sites for miR-320a and miR-182; (c) conserved triplet of target sites for miR-378, miR-99a and miR-30a A notable feature of stratum 2 is a pair of complementary sequences, 800 nucleotides apart, that are predicted to form the stems of a strong double helix (18 bp, –32.3 kcal/mol). [score:11]
Figure 4. The ‘extended VCR’ of stratum 2 (shared by Homo and Pelodiscus sequences): (a) miR-16 target site (also shown in Fig. 2e) and nearby target sites for miR-376a, miR-335-3p, miR-493 and miR-379 (the Xenopus sequence contains a 44-bp insertion at the site of the asterisk that includes two target sites for miR-335-3p are shown in red); (b) conserved pair of target sites for miR-320a and miR-182; (c) conserved triplet of target sites for miR-378, miR-99a and miR-30aA notable feature of stratum 2 is a pair of complementary sequences, 800 nucleotides apart, that are predicted to form the stems of a strong double helix (18 bp, –32.3 kcal/mol). [score:11]
miR-376a, miR-379 and miR-493 are encoded in a large cluster of maternally expressed imprinted microRNAs found only in eutherian mammals [27]. [score:3]
The Mono delphis and Xenopus sequences also have a predicted binding site for miR-379-5p adjacent to the miR-493 binding site (Fig.  4a). [score:1]
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6
[+] score: 24
Analysis of global profiles of miRNA expression in skeletal muscle with microarray shows that expression of 4 miRNAs (miR-29a, miR-29b, miR-29c and miR-150) are up-regulated [23], whereas expression of 11 miRNAs (miR-379, miR-127, miR299-5p, miR-434-3p, miR-335, miR130a, miR-19b, miR-451, miR-148a, miR-199a and miR-152) are down-regulated in skeletal muscle of type 2 diabetic rats [23]. [score:13]
For example, it has been shown that expression of 4 miRNAs (miR-29a, miR-29b, miR-29c and miR-150) is up-regulated [23], whereas expression of 11 miRNAs (miR-379, miR-127, miR299-5p, miR-434-3p, miR-335, miR130a, miR-19b, miR-451, miR-148a, miR-199a and miR-152) is down-regulated in skeletal muscle of type 2 diabetic rats [23]. [score:11]
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7
[+] score: 24
Cyclophosphamide treatment led to significantly lower miR-96-5p, miR-182-5p, and miR-379-5p expression and significantly higher miR-150-5p expression relative to the saline -treated C3. [score:5]
In the results of the splenocytes from the MRL/lpr mice, ASC treatment did not change the miR expression significantly, but cyclophosphamide treatment decreased the expression of miR-31-5p, miR-96-5p, miR-127-3p, miR-182-5p, miR-183-5p, and miR-379-5p significantly compared with the saline-treatment. [score:4]
In splenocytes from the MRL-lpr mice (the samples in our previous study), the expression levels of miR-18a-5p, miR-31-5p, miR-96-5p, miR-127-3p, miR-182-5p, miR-183-5p, and miR-379-5p were significantly higher, while those of miR-101a-3p and miR150-5p were significantly lower in the C group than in the N group. [score:3]
The expression levels of miR-31-5p, miR-96-5p, miR-182-5p, miR-183-5p, and miR-379-5p were significantly higher, while those of miR150-5p were significantly lower in C3. [score:3]
The expression levels of miR-31-5p, miR-96-5p, miR-127-3p, miR-182-5p, miR-183-5p, and miR-379-5p 5p in the Y group were significantly lower than in the C group (Supplementary Fig. 3). [score:3]
The expression levels of miR-96-5p, miR-182-5p, and miR-379-5p were significantly lower, while those of miR150-5p were significantly higher in the Y group than in the C group. [score:3]
The expression levels of miR-31-5p, miR-96-5p, miR-182-5p, miR-183-5p, and miR-379-5p were significantly higher, while those of miR150-5p were significantly lower in the C group than in the N group. [score:3]
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8
[+] score: 21
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Among the downregulated miRNAs; miR-29 was found to target DNMT1, DNMT3A, DNMT3B and HDAC4),while miR-30 targets DNMT3A, HDAC2, HDAC3, HDAC6 and HDAC10, miR-379 targets DNMT1 and HDAC3 and miR-491 (miR-491 targets DNMT3B and HDAC7. [score:12]
Out of these 25 miRNAs, 18 miRNAs were differentially expressed in a consistent manner between the 2 groups (Figure 4A, highlighted); 8 miRNAs were downregulated in both groups (miR-16, miR-200, miR-205, miR-3064, miR-379, miR-431, miR-485 and miR-491) and 10 miRNAs were upregulated in both groups (miR-194, miR-1894, miR-211, miR-3072, miR- 3077, miR-4436, miR-5128, miR-669a, miR-669c and miR-6967). [score:9]
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9
[+] score: 18
These include on the one hand the up-regulated miRNAs: mmu-miR-342-3p, mmu-miR-142-3p, mmu-miR-142-5p, mmu-miR-21, mmu-miR-335-5p, mmu-miR-146a, mmu-miR-146b, mmu-miR-674 and mmu-miR-379; and on the other hand the down-regulated ones after HFD -induced obesity: mmu-miR-122, mmu-miR-133p, mmu-miR-1, mmu-miR-30a, mmu-miR-192 and mmu-miR-203. [score:7]
Mmu-miR-342-3p and mmu-miR-379 were both found to be up-regulated after HFD -induced obesity in the present study. [score:4]
The following miRNAs were found to be up-regulated in WAT after HFD feeding: mmu-miR-342-3p, mmu-miR-222, mmu-miR-221, mmu-miR-142-3p, mmu-miR-142-5p, mmu-miR-21, mmu-miR-335-5p, mmu-miR-146a, mmu-miR-146b, mmu-miR-647* and mmu-miR-379. [score:4]
The following 22 murine microRNAs were selected for qPCR validation of their expression: mmu-miR-1, mmu-miR-21, mmu-miR-30a*, mmu-miR-30e*, mmu-miR-122, mmu-miR-130a, mmu-miR-133b, mmu-miR-141, mmu-miR-142-3p, mmu-miR-142-5p, mmu-miR-146a, mmu-miR-146b, mmu-miR-192, mmu-miR-193a-3p, mmu-miR-200b, mmu-miR-200c, mmu-miR-203, mmu-miR-204, mmu-miR-222, mmu-miR-342-3p, mmu-miR-378 and mmu-miR-379. [score:3]
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10
[+] score: 17
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
In rats, miR-379 is specifically expressed in the brain where it is thought to regulate the transcription of miRNA genes [31]. [score:4]
We found that it was highly expressed in the skin of goat, indicating that the miR-379 family may play an important role in the transcriptional regulation of skin hair follicle genes. [score:4]
The largest number of sequences (14,461) in our goat dataset belonged to the miR-379 family which was one of the 21 co-expressed miRNAs families. [score:3]
Most reads (highest expression) were from the miR-379 family; next was miR-127 family with 5,235 reads. [score:3]
By comparing with sheep miRNA sequences, we found that 5 miRNA families containing miR-127, miR-136, miR-154, miR-229 and miR-379, were conserved in all these species It is, therefore, tempting to speculated that these 5 miRNA families are critical in mammal development. [score:2]
The largest miRNA family was the miR-154 family with 18 family members, next was the miR-379 family with six family members, then the miR-368 family with five family members, and finally the miR-329 family with four family members; other families had only one family member). [score:1]
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[+] score: 17
miR-127 and miR-379, which were greatly upregulated in splenocytes from lpr mice, were moderately increased in diseased NZB/W mice. [score:6]
miR-127 and miR-379 were also significantly upregulated in 9-month old NZB/W mice when compared to 3-4-month old NZB/W. [score:3]
Overall, our data revealed that the expression changes in lupus -associated miRNAs such as miR-182-96-183, miR-31, miR-127, miR-379, miR-155, and miR-150 that were observed in splenocytes were also evident in purified splenic B and T cells. [score:3]
However, the upregulation of miR-127 and miR-379 in 9-month old NZB/W is not significant when compared to 9-month old NZW mice (Fig. 4B). [score:3]
Consistent with the data observed in whole splenocytes, the expression of miR-182-96-183, miR-31, miR-127 and miR-379 was also significantly increased in purified splenic B cells and T cells from MRL-lpr mice when compared to MRL mice (Fig. 2B). [score:2]
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[+] 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-mir-298, 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-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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13
[+] score: 15
Among the list, members of the miR-29 family, miR-203, miR-762, and miR-1224, showed upregulation, whereas members of the miR-107 family, miR-127 and miR-130a/b, miR-342-3p, miR-351, miR-379, miR-455, and miR-467a, were downregulated in both strains. [score:7]
miR-379 is expressed in breast cancer, regulating interleukin-11 and Cyclin B1 [49]. [score:4]
miRNAs that were differentially expressed only in the LW during aging include miR-29c, miR-705, miR-99a, miR-127, miR-130a, miR-145, miR-151-5p, miR-379, miR-467a, and miR-574-3p. [score:3]
These miRNAs include miR-107, miR-127, miR-130a/b, miR-145, miR-342, miR-351, miR-379, miR-455, and miR-467. [score:1]
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[+] score: 14
The box plot shows the most differentially expressed miRNAs miR-223 and miR-379 for the disease phenotype EBA. [score:5]
Comparing the two groups, only two miRNAs were differentially expressed: miR-379 (adj. [score:3]
Specifically, we provide evidence that miRNA such as miR-223 and miR-379 may play critical role in disease progression and severity. [score:3]
A cluster analysis identified miR-379 and miR-223 to be associated with EBA severity/onset, where miR-379 was observed to be associated to loci on chromosome 6. The murine advanced intercross line allowed us to identify the genetic loci regulating multiple miRNA in skin. [score:2]
Additionally, an eQTL for miR-379 (−log P = 4.7, 98–116 Mb) was also mapped on chromosome 6, with its peak at ~104 Mb (rs6208251, nearest gene: Cntn6). [score:1]
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15
[+] score: 13
For example, we found a significant downregulation of miR-27a, miR-411 and miR-497 in bladder cancer patient B09 and a significant upregulation of miR-379, miR-381 and miR-411 in kidney cancer patient K44 (Figure  5B). [score:7]
However, the editing sites in miR-379 and miR-497 appear to be targets of ADARB1 [12, 13]. [score:3]
Editing of miR-376b, miR-376c, miR-379, miR-381, miR-411 and miR-497 was significantly correlated with age in both species, demonstrating that the age-related increase of editing frequencies at specific sites is conserved between species (Figure  4B). [score:1]
In addition, our remapping method proved to be more sensitive and was able to detect editing in additional species, for example, of miR-379 in human, and of miR-497* in mouse and opossum (Figure  3; Table S2 in Additional file 2). [score:1]
Not all miRNA editing events are ancient: we found six cases of miRNA editing (miR-376a-1, miR-376b, miR-376c, miR-379, miR-381 and miR-411) that were limited to placental mammals and that therefore represent evolutionary novelties (Figure  1). [score:1]
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16
[+] score: 12
Of the multiple miRNAs which had terminal uridines that required Zcchc11 in our deep sequencing datasets and were predicted to target the 3′ UTR of IGF-1 (Figure 3B), we examined the ability of 4 (miR-126-5p, miR-194-2-3p, miR-379 and Let-7d) to suppress IGF-1 expression. [score:7]
Cross-method validation using qRT-PCR analyses of representative miRNAs of interest confirmed that levels of let-7a, let-7b, let-7c, miR-122, miR-139, and miR-379 were equivalent (Figure 2B). [score:1]
Interestingly, varying the length of the terminal uridine tail, to reflect the different forms observed for each of these miRNAs in our deep sequencing datasets, had minimal impact for both miR-126-5p and miR-379 (Figure 5C–5D), demonstrating that even a single uridine is sufficient to mitigate silencing by these miRNAs. [score:1]
The uridylation of miR-126-5p or miR-379 significantly diminished IGF-1 silencing by these miRNAs, while uridylation of miR-194-2-3p had no effect (Figure 5B). [score:1]
MiR-126-5p, miR-194-2-3p, and miR-379, but not Let-7d, significantly silenced the IGF-1 reporter (Figure 5A). [score:1]
mature by two-way ANOVA by student's t-test, N = 4. (C–D) miR-126-5p or miR-379 mimetics bearing 0, 1, 2, or 4 terminal uridines show a maximal effect on miRNA silencing by a single uridine addition. [score:1]
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[+] score: 9
Figure 2 A. is showing the real time expression pattern of miR-31-5p, miR-127-3p, miR-411-5p, miR-322-5p, miR-709, and miR-379 in WT, WT + UVR, TNFα KO and TNFα KO + UVR mice. [score:3]
The expression patterns of miR-31-5p, miR-127-3p, miR-411-5p, miR-322-5p, miR-709, and miR-379-5p were similar to the microarray results in our profiling study among four mice groups namely WT, WT + UVR, TNFα KO, and TNFα KO+UVR following acute UVR treatment (Figure 2A). [score:3]
A. is showing the real time expression pattern of miR-31-5p, miR-127-3p, miR-411-5p, miR-322-5p, miR-709, and miR-379 in WT, WT + UVR, TNFα KO and TNFα KO + UVR mice. [score:3]
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[+] score: 9
For example, over expression of miR-127, a Dlk1-Dio3 mat NAFLD candidate, in pancreas islet cells suppresses insulin secretion and causes glucose intolerance [51]; additionally, miR-342 and miR-379 are upregulated in white adipose tissue of obese mice [52]. [score:8]
For example, Labialle et al. reports that part of Dlk1-Dio3 mat region (the miR-379 / miR-410 cluster), which included five of the candidate NAFLD miRNAs (miR-376c, -379, -409, -411, and -495), affects energy metabolism including gluconeogenesis in neonatal mouse [35]; selective ablation of the miR-379 / miR-410 cluster causes lethal blood hypoglycemia. [score:1]
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[+] score: 8
Whereas, the expression of miR -148b was significantly inhibited in the VA of obese-diabetic NZ10 mice and the levels of miR-379 previously reported to be up-regulated in the adipose of high fat fed DIO mice was also significantly induced in the VA of obese-diabetic NZ10 mice (Table 1). [score:8]
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[+] score: 6
We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-882
Given that mir379 was an imprinted miRNA [93], LncRNA_1, which was selectively expressed in embryonic E18.5 brain and was comparable in expression with transcripts in the Rian locus [16], [17], was a candidate imprinted lncRNA. [score:5]
We also identified a putative intergenic lncRNA LncRNA_1 (Table S3) located in an imprinted cluster between Rian and Mirg flanked by mir882 and mir379. [score:1]
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[+] score: 5
We reported that chemically -modified antisense oligonucleotides (GapmeRs) targeting a long noncoding RNA, lncMGC, which is the host RNA of the miR-379 cluster, ameliorated fibrosis and hypertrophy in early stage of DN through inhibition of ER stress [13]. [score:5]
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[+] score: 5
The array uncovered the induction of 117 miRNAs with the signal intensity ≥500 (the fluorescence amount of each miRNA probe is measured by a photo multiplier tube or charge-coupled device and signal scaled across the range of detection for the platform) in GA muscle (Table 1, Fig. 1A and 1B), including the highly downregulated miRNAs (≥1.5-fold) miR-194-5p, miR-101b-3p, miR-148a-3p, miR-199b-5p, miR-335-5p, miR-127-3p, miR-379-5p, miR-541-5p, miR-382-5p, miR-329-3p, miR-299-5p and miR-434-3p, and the highly up-regulated miRNAs (≥1.5 fold), miR-146b-5p and miR-146a-5p (Fig. 1C). [score:5]
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[+] score: 4
Such included some of the most upregulated miRNA in the array data, such as miR-379, miR-671-5p and miR-708 (Figure S4). [score:4]
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[+] score: 4
Particularly, among the down-regulated miRNAs the set of miR-124a, miR-189, miR-299-5p and miR-379, was previously reported associated with autoimmune disorders [17]. [score:4]
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26
[+] score: 3
Similar activity -dependent induction of miRNA expression were recently described for the mir-379∼mir-410 locus [11]. [score:3]
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[+] score: 3
Thus, p73, by increasing the expression of Ago-1/2, it could increase the processing of miRNAs, such as let-7 (HMGA2; lin-28; EGFR; Kras; c-myc; Bcl-xL), miR-134 (Nanog; LRH1; Oct-4; Collagenase-3; Stromelysin), miR-130b (ERK2; Fosl1; TGFβR1; ERα; Tcf-4; Collagenase-3; Ago4; Dicer; p63), miR-214 (EZH2; CTNNB1), miR-449a (CDK6; SirT1; HDAC1; E2F-1), miR-503 (CCND1; Fosl1), miR-181d (ERK2; TGFβR1; Tcl-1; ERα; AID; Bcl-2) and miR-379 (lin-28) [Figure 2] [31], [32]. [score:3]
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[+] score: 3
Mmu-miR-125b-5p, mmu-miR-34c-5p, mmu-miR-199b-5p, mmu-miR-379-5p, and mmu-miR-127-3p were increased in expression in Sca1 [+]CD31 [−] cells compared to Sca1 [+]CD31 [+] cells. [score:2]
The miRNAs were mmu-miR-125b-5p, mmu-miR-34c-5p, mmu-miR-199b-5p, mmu-miR-379-5p, mmu-miR-127-3p, mmu-miR-322-5p, mmu-miR-20a-5p, mmu-miR-15a-5p, mmu-miR-503-3p, and mmu-miR-204-5p. [score:1]
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[+] score: 2
Using the ViTa Database, the human homologs of miR-135b-5p, miR-147-3p, miR-31-5p, miR-379-5p, miR-7a-5p, as well as the miR-449 (-5p) and miR-34 (-5p) families, were predicted to bind to viral RNA segments of influenza A/Puerto Rico/8/34/Mount Sinai (H1N1). [score:1]
Of note, miR-31-5p, miR-379-5p, miR-7a-5p, as well as some members of the miR-449 (-5p) and miR-34 (-5p) families were moderately to highly abundant (>10 CPM), making it more likely that they would bind to a biologically relevant number of viral RNAs. [score:1]
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[+] score: 2
Each clusters had at least 2 genes, with mir-466∼467∼669 cluster (cluster # 2) having 71 genes and mir-379∼410 cluster (cluster #7) having 38 genes. [score:1]
In the present study, we found that the miR-379∼329∼667∼410 cluster has 38 mir genes, while the miR-466∼467∼669 cluster, being one of the largest miRNA clusters in mouse genome, has 71 miRNA genes. [score:1]
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[+] 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-17, hsa-mir-25, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-105-1, hsa-mir-105-2, dme-mir-1, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-124-3, mmu-mir-134, mmu-mir-10b, hsa-mir-10a, hsa-mir-10b, dme-mir-92a, dme-mir-124, dme-mir-92b, mmu-let-7d, dme-let-7, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-134, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-92a-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-25, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-92a-1, hsa-mir-379, mmu-mir-412, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-92-1, gga-mir-17, gga-mir-1a-2, gga-mir-124a, gga-mir-10b, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-1a-1, gga-mir-124b, gga-mir-1b, gga-let-7a-2, gga-let-7j, gga-let-7k, dre-mir-10a, dre-mir-10b-1, dre-mir-430b-1, hsa-mir-449a, mmu-mir-449a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-17a-1, dre-mir-17a-2, dre-mir-25, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, hsa-mir-412, hsa-mir-511, dre-let-7j, hsa-mir-92b, hsa-mir-449b, gga-mir-449a, hsa-mir-758, hsa-mir-767, hsa-mir-449c, hsa-mir-802, mmu-mir-758, mmu-mir-802, mmu-mir-449c, mmu-mir-105, mmu-mir-92b, mmu-mir-449b, mmu-mir-511, mmu-mir-1b, gga-mir-1c, gga-mir-449c, gga-mir-10a, gga-mir-449b, gga-mir-124a-2, mmu-mir-767, mmu-let-7j, mmu-let-7k, gga-mir-124c, gga-mir-92-2, gga-mir-449d, mmu-mir-124b, gga-mir-10c, gga-let-7l-1, gga-let-7l-2
The results showed that hsa-mir-758 can be assigned to the hsa-mir-379,380, 411 family; hsa-mir-767 can be assigned to the hsa-mir-105 family; and hsa-mir-802 can be assigned to the hsa-mir-511 family. [score:1]
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[+] 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-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-33a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-99a, mmu-mir-126a, mmu-mir-128-1, mmu-mir-130a, mmu-mir-140, mmu-mir-154, mmu-mir-204, mmu-mir-143, hsa-mir-204, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-222, hsa-mir-223, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-140, hsa-mir-143, hsa-mir-126, hsa-mir-129-2, hsa-mir-154, 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-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-340, mmu-mir-107, mmu-mir-32, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-223, mmu-mir-26a-2, mmu-mir-211, mmu-mir-222, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-26a-2, hsa-mir-379, hsa-mir-340, mmu-mir-409, hsa-mir-409, hsa-mir-499a, hsa-mir-455, hsa-mir-670, mmu-mir-1249, mmu-mir-670, mmu-mir-499, mmu-mir-455, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-101-2, bta-mir-103-1, bta-mir-16b, bta-mir-222, bta-mir-26b, bta-mir-27a, bta-mir-499, bta-mir-99a, bta-mir-126, bta-mir-128-1, bta-mir-34b, bta-mir-107, bta-mir-140, bta-mir-15b, bta-mir-218-2, bta-let-7d, bta-mir-29c, bta-mir-455, bta-let-7g, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-204, hsa-mir-1249, hsa-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-129-2, bta-mir-130a, bta-mir-143, bta-mir-154a, bta-mir-211, bta-mir-218-1, bta-mir-223, bta-mir-26a-1, bta-mir-301a, bta-mir-32, bta-mir-33a, bta-mir-340, bta-mir-379, bta-mir-409a, bta-mir-670, mmu-mir-1306, bta-mir-1306, bta-mir-1249, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-1260b, bta-mir-2284w, bta-mir-2284x, bta-mir-409b, hsa-mir-499b, bta-mir-1260b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, mmu-let-7j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-154c, bta-mir-154b, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, chi-let-7a, chi-let-7b, chi-let-7c, chi-let-7d, chi-let-7e, chi-let-7f, chi-let-7g, chi-let-7i, chi-mir-103, chi-mir-107, chi-mir-1249, chi-mir-126, chi-mir-1306, chi-mir-130a, chi-mir-140, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-15b, chi-mir-16b, chi-mir-204, chi-mir-211, chi-mir-222, chi-mir-223, chi-mir-2284a, chi-mir-2284b, chi-mir-2284c, chi-mir-2284d, chi-mir-2284e, chi-mir-26a, chi-mir-26b, chi-mir-27a, chi-mir-29a, chi-mir-29c, chi-mir-301a, chi-mir-33a, chi-mir-340, chi-mir-34b, chi-mir-34c, chi-mir-379, chi-mir-409, chi-mir-455, chi-mir-499, chi-mir-99a, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Indeed, the larger cluster containing 42 precursors (mir-379/656 cluster) in the bovine genome was found within a QTL region for milk fat percentage and content on BTA 21. [score:1]
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