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18 publications mentioning rno-mir-466b-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-466b-1. 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: 100
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-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, rno-mir-466d, 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
DEX treatment up-regulated the expression of miRNA-483, miRNA-181a-1, miRNA-490 and miRNA-181b-1, while it down-regulated the levels of miR-122, miR-466b, miR-200b, miR-877, miR-296, miRNA-27a and precursor of miR-504. [score:9]
ACTH up-regulated the expression of miRNA-212, miRNA-182, miRNA-183, miRNA-132, and miRNA-96 and down-regulated the levels of miRNA-466b, miRNA-214, miRNA-503, and miRNA-27a. [score:9]
The levels of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377, and miRNA-96 were up-regulated, whereas miR-125b, miRNA-200b, miR-122, miRNA-466b, miR-138, miRNA-214, miRNA-503 and miRNA27a were down-regulated in response to 17α-E2 treatment. [score:7]
Real-time PCR (qRT-PCR) measurements demonstrated that ACTH treatment upregulated the expression of miRNA-212, miRNA-183, miRNA-182, miRNA-132 and miRNA-96, while down -regulating the expression of miRNA-466b, miRNA-214, miRNA-503 and miRNA-27a. [score:7]
Real-time quantitative PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats. [score:7]
qRT-PCR measurements confirmed that the expression of miR-212, miRNA-183, miRNA-182, miRNA-132, miRNA-370, miRNA-377 and miRNA-96 was up-regulated and that of miRNA-122, miRNA-200b, miRNA-466b, miRNA-138, miRNA-214, miRNA-503 and miRNA-27a down-regulated in adrenals from 17α-E2 treated rats (Fig. 3 ). [score:7]
Using qRT-PCR, we confirmed the down-regulation of miRNA-200b, miR-122, miR-19a, miRNA-466b, and miRNA-27a expression (Fig. 3 ). [score:6]
In contrast, dexamethasone down-regulated the expression of several of the miRNAs by more than 1.5 fold, i. e., miR-122 (8.2-fold), miR-466b (2.31-fold), miR-200b (1.9-fold) miR-877 (1.61-fold), miR-296 (1.61-fold)and precursor of miR-504 (1.53-fold) (Fig. 2D ). [score:6]
Bt [2]cAMP stimulation of granulosa cells caused down-regulation of a majority of miRNAs, including miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, miRNA-138 and miRNA-19a, but expression levels of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 were significantly increased. [score:6]
NR5A1 was predicted to be the target gene of miR-342, while LDL-R was predicted to be the target gene of miR-182 and miR-466b. [score:5]
qRT-PCR measurements indicated that exposure of primary rat granulosa cells to Bt [2]cAMP for 24 h inhibited the expression of miRNA-200b, miRNA-466b, miRNA-27a, miRNA-214, and miRNA-138 and miRNA-19a while enhancing the expression of miRNA-212, miRNA-183, miRNA-182, and miRNA-132 (Fig. 4 ). [score:5]
Significant ACTH -induced down-regulation of miRNA-466b, miRNA-214, miRNA-503 and miRNA-27a was also observed (Fig. 3 ). [score:4]
ACTH and DEX down-regulated miR-466b more than 1.5-fold, but the effect of 17α-E2, although it showed a similar trend, was not statistically significant (p = 0.084). [score:4]
We next evaluated the effects of Bt [2]cAMP stimulation of rat ovarian granulosa cells and of mouse MLTC-1 Leydig tumor cells on the expression of twelve miRNAs (miRNA-212, miRNA-122, miRNA-183, miRNA-200b, miRNA-466b, miRNA-182, miRNA-96, miRNA-27a, miRNA-132, miRNA-214, miRNA-138 and miRNA-19a) whose adrenal expression was differentially altered in response to treatment of rats with ACTH, 17α-E2 or DEX. [score:3]
More specifically, we assessed the impact of Bt [2]cAMP treatment on the expression of miRNA-212, miRNA-122, miRNA-27a, miRNA-466b, miRNA-200b, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96 and miRNA-19a. [score:3]
The levels of expression of miRNA-212, miRNA-122, miRNA-138, miRNA-214, miRNA-183, miRNA-182, miRNA-132, miRNA-96, miRNA-466b, miRNA-200b, and miRNA-19a are shown. [score:3]
A comparison of effects of ACTH and DEX shows that both hormones increased the expression miRNA-181b, miRNA-672, and miRNA-100, and significantly decreased the levels of miRNA-92a, and miRNA-466b. [score: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]
0078040.g003 Figure 3Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
Quantitative RT-PCR (qRT-PCR) validation of miRNA-212, miRNA-200b, miRNA-183, miRNA-122, miRNA-19a, miRNA-466b, miRNA-182, miRNA-132, miRNA-138, miRNA-370, miRNA-96, miRNA-503, miRNA-27a and miRNA-214 levels in control, ACTH-, 17α-E2 or DEX -treated adrenals in vivo. [score:1]
Dexamethasone treatment decreased miRNA-200b, miR-122, miR-19a, miRNA-466b and miRNA27a levels, but increased miRNA-183 levels. [score:1]
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3
[+] score: 26
Amongst these, miR-383 was differentially expressed in all three rats and up-regulated to the largest degree in rat one, and the ten other miRNAs, let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592 and miR-1224 were differentially expressed in at least two rats. [score:8]
In these 10 deregulated miRNAs, seven (let-7d*, miR-181b, miR-187, miR-214, miR-466b, miR-592, miR-1224) are up-regulated in two rats, and one (miR-195) is down-regulated. [score:8]
In dysregulated miRNAs, let-7d*, miR-181b, miR-187, miR-214, miR-383, miR-466b, miR-592, miR-1224 are significantly overexpressed in MrD compared to hippocampus, and miR-195 is downexpressed. [score:5]
Hence, miR-383 was differentially expressed in three rats, and let-7d*, miR-181b, miR-187, miR-195, miR-214, miR-382, miR-411, miR-466b, miR-592, miR-1224 were differentially expressed in two rats at least (Additional file 2: Table S4). [score:5]
[1 to 20 of 4 sentences]
4
[+] score: 23
Of the 123 miRNAs, 15 were differentially expressed in the AS and CS mo del groups, of these, four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p; Table IV) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b; Table V). [score:12]
Of these 15 miRNAs, rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p were significantly upregulated, particularly miR-296 (Table IV), and 11 were downregulated (miR-135a and miR-466b were significantly downregulated, particularly miR-135a; Table V). [score:10]
In conclusion, rno-miR-296, rno-miR-141, rno-miR-382, rno-miR-219-5p, miR-135a and miR-466b may be involved in stress at the molecular level, thus causing myocardial injury. [score:1]
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5
[+] score: 19
In the DRGs, 6 miRNAs (miR-9, miR-320, miR-324-3p, miR-672, miR-466b, and miR-144) were significantly downregulated in the entrapment group and 3 miRNAs (miR-9, miR-320, and miR-324-3p) were significantly downregulated in the decompression group. [score:7]
In contrast, 3 miRNAs (miR-499, miR-1, miR-133a, and miR-466b) were upregulated in the denervated muscle and 3 miRNAs (miR-329, miR-204, and miR-139-3p) were downregulated after 6 months. [score:7]
In the DRGs, 6 miRNAs in the entrapment group (miR-9, miR-320, miR-324-3p, miR-672, miR-466b, and miR-144) and 3 miRNAs in the decompression group (miR-9, miR-320, and miR-324-3p) were significantly downregulated. [score:4]
Although there also appeared to be a decrease of miR-672, miR-466b, and miR-144 in the decompression group, it was not statistically significant in all 3 specimens. [score:1]
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6
[+] score: 17
One of the predicted miRNA-mRNA interactions, which could be confirmed in vivo, concerns the insulin-like growth factor (IGF)-1. IGF-1 is a known target of the down-regulated miR-466b-1-3p and has been demonstrated to be up-regulated by carnitine in the present study but also in previous studies [11, 35]. [score:9]
This suggests that the elevated mRNA level of IGF-1 is a result of a decreased repressive activity of the down-regulated miR-466b-1-3p and that miRNA-mRNA interactions indeed play a significant role in mediating biological effects of carnitine. [score:4]
Among these 21 differentially expressed miRNAs, 17 (miR-10b-5p, miR-223-3p, miR-208a-5p, miR-434-3p, miR-190a-5p, miR-30d-5p, miR-347, miR-493-5p, miR-29a-5p, miR-451-5p, miR-190b-5p, miR-466c-5p, miR-883-5p, miR-466b-1-3p, miR-21-3p, miR-3596c, miR3584-3p) were proven significant (P < 0.05) by qRT-PCR, one (miR-487b-3p) had a tendency to be significant (P = 0.06), and three (miR-138-2-3p, miR-1188-3p, miR-665) were not confirmed to be significant (Table  2). [score:3]
To further investigate whether the carnitine -induced increase in the mRNA level of IGF-1, a putative target gene of miR-466b-1-3p but also miR-208a-5p, is also associated with an increase in the protein level of IGF-1, we determined protein levels of IGF-1 in skeletal muscle of the obese Zucker rats. [score:1]
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7
[+] score: 13
A comparison between these identified microRNAs and those showing expression changes in the present microarray analysis revealed similar expression changes for miR-21 24 hours after SCI as well as for 4 other microRNAs, namely, miR-184, miR-340-5p, miR-369-3p and miR-466b, at 7 dpo (Table 2). [score:5]
Expression changes respect to control/sham 1 dpo 7 dpo Name Liu Present Liu Present rno-miR-130b 1.42 NE rno-miR-146a 1.72 INC S rno-miR-15b 1.15 DEC NS rno-miR-17 1.74 INC NS rno-miR-18a 2.71 NE 3.41 NE rno-miR-200c 4.12 NE rno-miR-206 3.26 NE rno-miR-20a 1.69 NC rno-miR-20b-5p 1.83 NE rno-miR-21 1.37 INC S rno-miR-214 2.01 INC NS rno-miR-219-5p −1.82 DEC S rno-miR-221 1.1 NE rno-miR-223 3.58 INC S 3.4 INC S rno-miR-24-2* 2.41 DEC NS rno-miR-290 3.66 INC NS 2.96 DEC S rno-miR-378 1.31 INC NS rno-miR-410 −1.21 NE rno-miR-466b 3.05 DEC S rno-miR-541 1.11 INC S rno-miR-874 2,8 NEData restricted to microRNAs with significant changes in expression (2-fold or greater) according to Liu et al. [6]. [score:5]
These analyses identified four microRNAs with expression changes at 7 dpo; these included miR-340-5p and miR-369-3p, which are both involved in proliferation and adipogenic differentiation, as well as the proapoptotic miR-184 [109] and miR-466b. [score:3]
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8
[+] score: 13
In contrast, DOR activation significantly upregulated miR-466b expression in the hypoxic kidney. [score:6]
Relative miRNA expression levels of miR-466b and miR-511 in the kidney following 10 days of hypoxia as determined by quantitative RT-PCR. [score:3]
Interestingly, the combination of long-term hypoxia and UFP-512 treatment returned miR-466b expression to control levels (Figure 4a). [score:3]
The miRNA-466b levels were significantly repressed by either long-term hypoxia or UFP-512 treatment. [score:1]
[1 to 20 of 4 sentences]
9
[+] score: 12
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]
C: microRNAs miR-466b and miR-21 were up regulated; miR-146b was down regulated 26 weeks post-irradiation vs. [score:3]
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10
[+] 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-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-466d, 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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[+] score: 10
Specifically, upregulation of miR-466b (1.99-fold change, p = 0.017), miR-542-5p (3.09-fold change, p = 0.020), miR-568 (2.14-fold change, p = 0.020), miR-3580-3p (1.99-fold change, p = 0.017), miR-3581 (1.79-fold change, p = 0.019), and miR-3597-5p (1.9-fold change, p = 0.037), and downregulation of miR-345-5p (−1.56-fold change, p = 0.006) and miR-743b (−2.74-fold change, p = 0.031) were detected for aGvHD samples compared to controls (Figures 5A,B). [score:6]
The upregulation of miR-542-5p or miR-466b was not confirmed in the validation samples (Figure 5C and data not shown). [score:4]
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[+] score: 7
Rno-miR-466b-2-3p and rno-miR-466b-5p are significantly up-regulated while other 20 miRNAs are significantly down-regulated Fig. 18 Venn diagrams for identified miRNAs. [score:7]
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[+] score: 6
Other miRNAs from this paper: 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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
First, a subgroup of miRNAs (miR-15b-5p, miR-17-5p, miR-18a-5p, miR-19a-3p, miR19b-3p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23b-5p, miR-24-3p, miR-27a-3p, miR-92a-3p, miR-93-5p, miR-142-3p, miR-344b-2-3p, miR-431, miR-466b-5p and miR-674-3p) displayed increased expression levels during latency (4 and 8 days after SE), decreased their expression levels at the time of the first spontaneous seizure and returned to control levels in the chronic phase (Fig. 2, Supplementary Fig. S1). [score:5]
A second pattern was about the opposite: miR-466b-1-3p, miR-494-3p and miR-598-5p displayed significantly decreased plasma levels during latency, and a tendency to return to the control levels in the chronic stage (Supplementary Fig. S7B). [score:1]
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[+] score: 4
In addition, compared to F0-N rats, stress in F0-S dams induced one miRNA (rno-miR-466b-1-3p) and suppressed the expression of three miRNAs (rno-miR-145-3p, rno-miR-24-1-5p and rno-miR-375) (all Ps <0.10). [score:4]
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[+] 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-298, 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-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
Family Members 1 mir-466b-1 mir-466b-2 2 mir-664-1 mir-664-2 There are 154 singleton human miRNAs with no defined homologs. [score:1]
Family Members 1 mir-466b-1 mir-466b-2 2 mir-664-1 mir-664-2There are 154 singleton human miRNAs with no defined homologs. [score:1]
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[+] score: 1
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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[+] 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-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, 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-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, 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-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
Type of site Context+ Context Structure Energy Is experimental validated rno-miR-326-5p MIMAT0017028 3 8mer 7mer-m8 imperfect −0.442 −0.242 431 −65.97 TRUE rno-miR-485-5p MIMAT0003203 2 7mer-m8 −0.343 −0.372 290 −34.96 TRUE rno-miR-300-5p MIMAT0004743 1 8mer −0.338 −0.421 156 −15.16 TRUE rno-miR-702-5p MIMAT0017884 1 8mer −0.317 −0.274 142 −13.86 TRUE rno-miR-203b-3p MIMAT0017800 2 7mer-m8 −0.298 −0.421 295 −29.93 TRUE rno-miR-33-3p MIMAT0017104 2 8mer 7mer-m8 −0.297 −0.813 305 −22.7 TRUE rno-miR-466b-3p MIMAT0017285 1 8mer −0.295 −0.47 159 −15.26 TRUE rno-miR-532-5p MIMAT0005322 1 7mer-m8 −0.268 −0.302 151 −10.71 TRUE rno-miR-511-5p MIMAT0012829 1 7mer-m8 −0.268 −0.302 152 −10.37 TRUE rno-miR-343 MIMAT0000591 1 7mer-m8 −0.262 −0.24 140 −13.75 TRUE rno-miR-203a-3p MIMAT0000876 1 8mer −0.245 −0. [score:1]
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[+] score: 1
Individually, hypoxia -induced and DOR -mediated effects on miRNAs miR-298 and miR-466b resolve at the same rate. [score:1]
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