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9 publications mentioning rno-mir-466d

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-466d. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 204
Thus, the target site 2 seems to have better chance to be targeted with miR-466 than the target site 1. In the alkali burn corneal injury mo del, miR-466 decreased corneal opacity and inhibited both lymphangiogenesis and angiogenesis, possibly attributable to decreased Prox1 expression. [score:11]
Our results on human lymphatic endothelial cell and alkali burn corneal injury mo del demonstrated that miR-466 directly targeted the 3' UTR of Prox1 and suppressed the expression of Prox1, resulting in inhibition of lymphangiogenesis. [score:10]
Therefore, suppressed Prox1 expression by miR-466 may have inhibited the expression of angiogenic modulators such as VEGF-C and angiopoietin-2, resulting in reduced angiogenesis in the alkali burn corneal injury animal mo del. [score:9]
These results showed that target site 2, but not the target site 1, on the 3' UTR of the Prox1 was targeted by miR-466. [score:7]
The luciferase assay showed that miR-466 directly targeted the well conserved 7mer-1A site in the 3' UTR of Prox1 (target site 2), as the suppressive effect of the miR-466 mimic on luciferase activity was almost abolished when this site was mutated. [score:7]
The LNA™ microRNA Power Inhibitor for hsa-miR-466 and the negative control inhibitor (NC inhibitor) were purchased from Exiqon (Vedbaek, Denmark). [score:7]
In addition, over -expression of mmu-miR-466 inhibited Nfat5 expression and was associated with renal dysfunction [34]. [score:7]
The results of the current study demonstrated that hsa-miR-466 inhibited Prox1 expression and suppressed tube formation in human primary lymphatic endothelial cells. [score:7]
Furthermore, HDLEC transfected with a miR-466 inhibitor showed enhanced tube formation as compared to control inhibitor transfected cells, and this inhibitory effect was counteracted by Prox1 siRNA. [score:6]
The coordinates for miR-466 target sites 1 and 2, as well as the target site for miR-4305 and miR-4795-5p, are shown in parentheses (GenBank accession number NM_002763). [score:5]
We also tested whether the inhibition of miR-466 enhanced tube formation in HDLEC and whether Prox1 siRNA counteracted the effect of a miR-466 inhibitor. [score:5]
This notion is supported by previous findings demonstrating that miR-466 induced apoptosis by targeting a few anti-apoptotic genes [29], and that this induced apoptosis resulted in the inhibition of angiogenesis [30, 31]. [score:5]
To test whether both were directly targeted by miR-466, point mutations were introduced to psiC-Prox1 to produce psiC-Prox1-m1, psiC-Prox1-m2, and psiC-Prox1-m1m2 (Figure  4A and B). [score:5]
However, as miRNAs usually have multiple targets, our observations may be attributable to angiogenic modulators other than Prox1 targeted by miR-466. [score:5]
The inhibitory effects of miR-466 on Prox1 expression, tube formation, and lymphatic vessel formation were comparable to those of miR-181. [score:5]
In primary lymphatic endothelial cells (HDLEC), miR-466 mimic transfection suppressed Prox1 mRNA and protein expression, while miR-4305 mimic transfection did not. [score:5]
Thus, miR-466 is expected to have broader and greater inhibitory effects on lymphangiogenesis-related diseases than bevacizumab. [score:5]
The results of the current study showed that the expression of Prox1 was inhibited by miR-466 at both the mRNA and protein levels. [score:5]
The target site 2 contains five contiguous sequences that can be used for an effective 3' pairing with the nucleotides 14 ~ 18 of miR-466, while the target site 1 does not. [score:5]
The sequences are as follows: inhibitor for hsa-miR-466, 5′-GTGTTGCGTGTATGTGTA-3′; NC inhibitor, 5′-GTGTAACACGTCTATACGCCCA-3′. [score:5]
Experiments using mutated reporter constructs of the two possible seed match sites on the 3' UTR of Prox1 suggested that the target site 2 directly bound miR-466. [score:4]
Another possibility is that miR-181a may also target angiogenesis-related genes other than Prox1 more effectively than miR-466. [score:3]
Subsequently, a luciferase reporter assay was conducted to assess whether miR-466, miR-4305, and miR-4795-5p directly targeted the 3' UTR of Prox1. [score:3]
Figure 2 Effects of miR-466 and miR-4305 on Prox1 expression. [score:3]
However, the 7mer-m8 site complementary to the target site 1 of miR-466 and the 8mer site complementary to the seed region of miR-4795-5p were not well conserved. [score:3]
In the current study, miR-466, miR-4305, and miR-4795-5p were chosen as new miRNA candidates that could target the 3' UTR of Prox1 based on the results of a bioinformatics analysis. [score:3]
HDLEC were then transfected with a miR-466 inhibitor alone or together with Prox1 siRNA. [score:3]
HDLEC transfected with the miR-466 inhibitor alone showed significantly increased tube formation (Figure  5D and E). [score:3]
Figure 4 Target site search for miR-466 in the Prox1 3' UTR. [score:3]
mmu-miR-466, which can be induced by apoptosis [29] and metabolic oxidative stress [32], was shown to enhance viral replication by inhibition of INF-α [33]. [score:3]
To test whether miR-466 and miR-4305 have the ability to modulate Prox1 expression, HDLEC were harvested 48 h after miRNA mimic transfection. [score:3]
The shaded boxes are putative miR-466, miR-4305, and miR-4795-5p target sites. [score:3]
The 7mer-1A site complementary to the target site 2 of miR-466 and the 8mer site complementary to the seed region of miR-4305 were well conserved among species (Figure  1B). [score:3]
However, co -transfected Prox1 siRNA counteracted the effect of the miR-466 inhibitor (Figure  5D and E). [score:3]
However, the inhibitory effect of miR-466 on blood vessel formation in the in vivo corneal injury mo del was slightly weaker than that of miR-181a. [score:3]
Confirming target sites for miR-466 in the Prox1 3' UTRs. [score:3]
The results of the current study demonstrated that miR-466 inhibited Prox1, which is known to be activated by various growth factors including VEGF-A, −C, and -D [11, 44]. [score:3]
HDLEC transfected with the miR-466 mimic suppressed tube formation as compared to the scrambled control. [score:2]
The miR-181a mimic exerted the highest level of inhibitory effects on tube formation (approximately 84%) followed by the miR-466 mimic (approximately 57%; Figure  5B) when compared to the scrambled control. [score:2]
Furthermore, miR-466 reduced angiogenesis and lymphangiogenesis, resulting in clearer corneas than those observed in the scrambled control -treated mice in an animal cornea injury mo del. [score:1]
The animals were then randomly allocated to three treatment groups: scrambled control, miR-181a, and miR-466. [score:1]
Additionally, miR-466 was also selected, as the 3' UTR of Prox1 contained two putative binding sites for this miRNA (7mer-m8 and 7mer-1A sites), unlike other miRNAs. [score:1]
The scrambled control and miR-466 m (mutant form) were used to confirm sequence-specific binding between miR-466 and the 3' UTRs. [score:1]
HDLEC were transfected with miR-181a, miR-466, miR-4305 mimics, or the scrambled control. [score:1]
To accomplish this, HEK293T cells were co -transfected with increasing concentrations of the miR-466 mimic and psiC-Prox1 reporter plasmid. [score:1]
The 3' UTR of Prox1 contains two putative binding sites for miR-466 (Figure  1A). [score:1]
Dose -dependent effect of the miR-466 mimic. [score:1]
As expected from the fact that both of the putative seed match sites were eliminated, luciferase activity was not affected when psiC-Prox1-m1m2 was co -transfected with miR-466 (Figure  4C). [score:1]
When the animals were injected with miR-466, blood vascular infiltration was 51% of the scrambled control group level (Figure  6J). [score:1]
Both the miR-466 and miR-4305 mimics, but not the miR-4795-5p mimic, significantly reduced the luciferase activity of the Prox-1 3' UTR reporter vector. [score:1]
MicroRNA Prox1 miR-466 miR-181 Tube Formation Lymphangiogenesis Cornea transplantation Alkali burn Approximately 10%–50% of cornea transplantation recipients experience graft rejection within one year [1]. [score:1]
Therefore, miR-466 may be useful for investigating the mechanisms of lymphangiogenesis and for developing treatments for lymphangiogenic eye diseases. [score:1]
When the animals were injected with miR-466, corneal thickness was between those observed for the scrambled control and the miR-181a -injected animals, while F-actin positive staining was 56% of the scrambled control group level (Figure  6K). [score:1]
Luciferase activity was not affected in the cells co -transfected with wild-type or mutant Prox1 3' UTR reporter vectors and miR-466 m (mutant form of miR-466) or the scrambled control (Figure  4C). [score:1]
Transfecting the cells with 10 nM or higher concentrations of the miR-466 mimic caused a dose -dependent reduction in the luciferase activity of psiC-Prox1 (Figure  3). [score:1]
Forty eight hours after transfection with miR-466 mimic, HDLEC were cultured on a Matrigel-coated 96 well plate for 4–6 h and the extent of tube formation was assessed. [score:1]
However, luciferase activity was unaffected in the cells transfected with the miR-466 mimic together with psiC-Prox1-m2 (Figure  4C). [score:1]
However, the functions of hsa-miR-466 in human cells have yet to be fully elucidated. [score:1]
HDLEC were transfected with the miR-181a, miR-466, miR-4305 mimics, or the scrambled control. [score:1]
Luciferase activity was partially reduced in the cells transfected with the miR-466 mimic together with either psiC-Prox1 or psiC-Prox1-m1 (Figure  4C). [score:1]
In contrast, miR-466- or miR-181a -injected animals showed reduced opacity (Figure  6B and 6C). [score:1]
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2
[+] score: 30
Other miRNAs from this paper: rno-mir-15b, rno-mir-32, rno-mir-378a, rno-mir-423, rno-mir-378b
Of special interest are three of the listed up-regulated miRNAs (miR-466d-3p, miR-466d-5p, and miR-466f-3p), which are highly expressed (> 2-fold) as well as promiscuous, with over 25 predicted mRNA targets each. [score:8]
We chose miR-466d-5p and miR-466f-3p because of their relative high expression (> 2-fold) and their promiscuity (> 25 predicted target mRNAs each). [score:5]
To validate the functional significance of identified miRNAs, we chose two representative miRNAs up-regulated with stretch (miR-466d-5p and miR-466f-3p). [score:4]
Specific inhibition of miR-466d-5p and miR-466f-3p resulted in a preservation of barrier permeability close to baseline unstretched conditions, suggesting a role for these miRNAs in regulating the RAEC response to cyclic stretch. [score:4]
Cells were transfected with specific inhibitors to miR-466d-5p and miR-466f-3p, or a scrambled negative control, and subjected to stretch or served as unstretched controls. [score:3]
On the fourth day of culture, we transfected custom-designed, specific inhibitors of miR-466d-5p, miR-466f-3p, or a scrambled negative control (Exiquon). [score:3]
We are encouraged, however, by the clear effect on permeability seen after the specific inhibition of miR-466d-5p and miR-466f-3p. [score:3]
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3
[+] score: 11
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, 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-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Of these miRNAs, 12 were upregulated (miR-34b, miR-138, miR-297a, miR-301, miR-449, miR-466, miR-493, miR-579, miR-582, miR. [score:4]
MiR-466 was the only miRNA that was upregulated both in lung and blood of mice bearing >10 microadenomas. [score:4]
The identity, fold-change variation, direction of alteration, and biological function of these miRNAs are reported in Table 2. In mice bearing adenomas, 5 miRNAs (miR-34b, miR-106a, miR-499, miR-466, and miR-493) were altered in the blood serum but not in lung. [score:2]
One miRNA only (miR-466) was altered in both body compartments of mice bearing >10 microadenomas in the lung fragment. [score:1]
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4
[+] score: 9
We performed network analyses using top 10 identified miRNAs (up-regulated: let-7i, let-7c, let-7a, miR-124, miR -145, miR-143, miR-34a, miR-466; down-regulated: miR-21, miR-146b) to predict their potential target transcripts. [score:9]
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5
[+] score: 4
The next point we addressed was the paradox that, although intron 10 of the rat and mouse genes contain mainly copies of SHORT1 including self-complementary microsatellites, the mouse has 65 miRNA-producing genes in this region, while the rat only has one gene that expresses Mir-466d. [score:3]
An exception might be the sequence containing has-mir-466 with (TATG)n and (CA)n microsatellites (Additional File 2 Table S4A). [score:1]
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6
[+] score: 4
revealed that four miRNAs (miR-29b-3p, miR-145-5p, miR-24-2-5p, miR-665) were significantly regulated (P<0.05), three miRNAs (miR-21-3p, miR-466b-2-3p, miR-466d) tended to be significantly regulated (P<0.15), and one miRNA (miR-34a-5p) was not confirmed to be significantly regulated by qRT-PCR (Table 2 ). [score:4]
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7
[+] score: 4
We found that 14 of the DEmiRNAs identified in our screen can regulate 2927 common putative target genes (Figure 5A), while 9 miRNAs, including miR-1249, miR-1306-3p, miR-32-3p, miR-327, miR-328b-3p, miR-3562, miR-3588, miR-423-5p, and miR-466d, had no common predicted genes. [score:4]
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8
[+] score: 3
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Furthermore, such DEX alteration of adrenal miRNA levels demonstrates that DEX suppression of endogenous ACTH secretion modulates a set of adrenal miRNAs, with the exception of miRNA-96, miRNA-466, and miRNA-27a, that are distinct from those modulated by treatment with exogenous ACTH. [score:3]
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9
[+] score: 1
5 mmu-miR-214 -1.7 -6.1 -10.9 mmu-miR-137 -31.7 -6.8 -144.8 mmu-miR-29c -1.8 -10.5 -10.7 rno-miR-532–5p -2.0 -59.1 -126.9 mmu-miR-466d-3p -2.7 -4.2 -9.9 mmu-miR-466d-5p -23.2 -64.7 -105.7 mmu-miR-22 -1.6 -4.6 -9.9 mmu-miR-582–5p -21.3 -59.4 -97.1 mmu-miR-690 -1.9 -2.1 -9.7 rno-miR-421 -21.3 -59.3 -97.0 mmu-miR-193 -4.9 -3. 5 -8.1 mmu-miR-369–5p -20.9 -58.3 -95.3 mmu-miR-27b* -2.1 -2.9 -8.0 mmu-miR-684 -20.8 -58.1 -94.9 mmu-miR-378 -1.6 -4.6 -7.7 mmu-miR-375 -20.6 -57.6 -94.2 mmu-miR-9* -1.9 -18.4 -7.7 mmu-miR-337–5p -20.5 -57.4 -93.8 mmu-miR-204 -2.5 -5.3 -7.5 mmu-miR-15a* -20.3 -56.8 -92.8 mmu-miR-28* -1.9 -3.2 -6.5 mmu-miR-532–5p -19. [score:1]
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