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19 publications mentioning mmu-mir-434

Open access articles that are associated with the species Mus musculus and mention the gene name mir-434. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 214
In the current study, we show that aging dysregulates many miRNAs in skeletal muscle, including the highly downregulated miRNA miR-434-3p that inhibits apoptosis by targeting eIF5A1 that promote apoptosis by the intrinsic mitochondrial pathway. [score:9]
We confirmed the above data by demonstrating that overexpression of miR-434-3p resulted in inhibition of caspase-3, −8 and −9 activations, and permeabilization of the outer mitochondrial membrane along with downregulation of eIF5A1. [score:8]
In agreement with our findings, a previous study demonstrates that overexpression of miR-434-3p in vivo rat skeletal muscle post-transcriptionally suppresses eIF5A1 expression and both miR-434-3p and eIR5A1 are regulated in muscle in an opposite manner after spinal cord injury [37]. [score:8]
Moreover, we for the first time demonstrate that aging muscle up-regulated eIF5A1 protein expression, suggesting a negative correlation in the expression levels between miR-434-3p and eIF5A1 in the aging muscle. [score:8]
Using extensive bioinformatics analysis, we identified the eukaryotic translation initiation factor 5A1 (eIF5A1) as one of the potential target genes of the most highly downregulated miRNA miR-434-3p. [score:8]
Interestingly, we found that skeletal muscle from aging mice downregulated of miR-434-3p expression that was negatively correlated with the levels of eIF5A1, suggesting that dysregulation of miR-434-3p in aging muscle may be responsible, in part, for the pathogenicity of sarcopenia. [score:7]
In this study, up-regulation of eIF5A1 protein and downregulation of miR-434-3p in aging skeletal muscle suggest that miR-434-3p/eIF5A1 pathway may induce apoptosis in skeletal muscle during aging and that may be one of the epigenetic causative mechanisms for the induction of sarcopenia. [score:7]
Because many miRNAs can target a single mRNA, other human miRNA(s) that target eIF5A1 may have a similar role of miR-434-3p and that specific miRNA(s) may reinstate the translational significance of miR-434-3p. [score:7]
In our study, we found that miR-434-3p was the highly downregulated mRNA (4.08 fold) in the aging muscle; this is also in agreement with the previous study in which aging mice downregulates this miRNA at 5.0 fold in skeletal muscle [20]. [score:7]
Overexpression or knockdown of miR-434-3p in myotubes validated eIF5A1 as a target mRNA of miR-434-3p that negatively regulated apoptosis through eIFA1. [score:7]
First, we tested whether miR-434-3p transcriptionally or post-transcriptionally suppresses endogenous eIF5A1 expression. [score:5]
To determine whether miR-434-3p-regulated apoptosis involves inhibition of activation of caspases, the effects of their over -expression on the activation of executioner caspase-3 as well as initiator caspases −8 and −9 were examined in myotubes over a period of 24 h. All three caspases were activated in response to TPEN or Stps treatment; however, caspase 3 activity was dramatically higher when compared to caspases 8 and 9, especially in Stps treated myotubes (Fig. 5A and B). [score:5]
The differentially expressed miRNAs in earlier studies appeared consistently in mouse skeletal muscle from our study; for example, the expression pattern of miR-146a-5p, miR-146b-5p, miR-434-3p, miR-127-3p, and miR-148a-3p are similar to previous studies. [score:5]
We demonstrate that knockdown of miR-434-3p in myotubes induced activation of caspase-3, −8 and −9, and permeabilization of the outer mitochondrial membrane along with up-regulation of eIF5A1, suggesting that loss of miR-434-3p promotes apoptosis by facilitating activation of the intrinsic mitochondrial pathway. [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]
Interestingly, our quantitative PCR assay in Figures 2A and 4F show that miR-434-3p was nearly 4-fold significantly downregulated in aging muscle when compared to that in the muscle of young mice, suggesting that aging significantly affected the expression of miR-434-3p. [score:4]
Overall, these data provide experimental evidence that eIF5A1 is a direct target gene of miR-434-3p. [score:4]
Subsequently, we tested that whether eIF5A1 3′UTR is directly targeted by miR-434-3p. [score:4]
Our luciferase assay experiments with mutations in the binding sites clearly confirmed eIF5a1 is a direct target mRNA of miR-434-3p (Fig. 3F). [score:4]
Because eIF5A1 is a direct downstream target of miR-434-3p, we sought to determine if modulation of miR-434-3p would control apoptosis through eIF5A1 in myotubes. [score:4]
The DIANA miRPath provided 8 predicted skeletal muscle pathways, including apoptosis for the highly downregulated miRNA-434-3p (Table 5). [score:4]
We confirmed that miR-434-3p indeed suppressed eIF5A1 mRNA expression by binding on the 3′UTR of eIF5A1, as evidenced by western blot analysis and luciferase assay. [score:4]
Therefore, we mutated the miR-434-3p binding site on eIF5A1-3′-UTR to determine whether eIF5A1 is a direct target of miR-434-3p. [score:4]
Myotubes transfected with miR-434-3p mimic significantly suppressed all three caspases activities, and the cotransfection of miR-434-antagomir restored the TPEN or Stps -induced caspases activities whereas myotubes transfected with NS-miR had no effect on all three caspases activities in response to TPEN or Stps treatment (Fig. 6A and B). [score:3]
Myotubes carrying miR-434-3p showed overexpression of miR-434-3p by approximately three-fold (Fig. 3B). [score:3]
These data confirm that miR-434-3p protects myocyte from apoptosis induced by different apoptotic stimuli via eIF5A1 and a negative correlation between the expression of miR-434-3p and eIF5A1 in aging muscle. [score:3]
Such altered expression of elF5A1 was reduced when those myotubes were transfected with miR-434-3p antagomir (Fig. 4D). [score:3]
In addition, the miR-434-3p is absence in human according to miRBase 21 that limits the translational significance. [score:3]
eIF5A1 is a target mRNA of miR-434-3p. [score:3]
These data provided a strong rationale to test the possibility that eIF5A1 may be a downstream target of miR-434-3p. [score:3]
Enforced expression of miR-434-3p significantly decreased eIF5A1 mRNA levels (Fig. 3C). [score:3]
Our data in Fig 5C and D showed suppression of caspases 3, 8 and 9 activities by miR-434-3p, suggesting the possibility that miR-434-3p may maintain Δψm. [score:3]
Interestingly, the database listed eIF5A1 as one of the potential targets of miR-434-3p. [score:3]
To further confirm the role of miR-434-3p in apoptosis, we used staurosporine (Stsp), a well-known transcription inhibitors, has been shown to induce apoptosis in several cell types including myocytes [33, 34]. [score:3]
Overexpression of miR-434-3p reduces activation of caspases 3, 8, and 9 in myotubes. [score:3]
Using extensive bioinformatics analysis, we identified eIF5A1 as one of the potential target genes of miR-434-3p. [score:3]
Figure 3(A) Sequence alignment of putative miR-434-3p targeting site in the 3′-UTR of eIF5A1 shows high levels of complementarity. [score:3]
These data suggest that the diminished depolarization of mitochondrial membrane potential of myotubes in response to TPEN and Stsp may be due to suppression of apoptosis by miR-434-3p through eIF5A1. [score:3]
Although miR-434-3p was the most highly downregulated miRNA in the skeletal muscle of aged mice, the signal intensity was relatively small (1767) when compare to other miRNAs such as miR-1 (59283) and miR-126-3p (42474) as evidenced by microarray that is not a quantitative assay and signal intensity more than 500 is biologically relevant. [score:3]
The miR-434-3p binding sites on eIF5A1 3′UTR were mutated as we described previously [58] using QuikChange II site-directed mutagenesis kit (Stratagene). [score:2]
Furthermore, we found that GA muscle from aging mice displayed lower expression levels of miR-434-3p when compared to that in the GA muscle of young mice (Fig. 4F). [score:2]
miR-434-3p overexpression was determined by qPCR assay (B). [score:2]
Overall our findings suggest that the dysregulation of the miR-434-3p/eIF5A1 pathway in aging muscle may play a role in the pathogenicity of sarcopenia. [score:2]
Surprisingly, miR-434-3p and eIF5a1 3′UTR binding is only by six base pair matching that may cause a weaker interaction. [score:1]
Myotubes were transfected with NS -mimetic, miR-434-3p mimetic with or without miR-434-3p antagomir or no transfection for 24 h followed by eight hours TPEN (100 μM) or Stps (1 μM) incubation. [score:1]
The transfection of miR-434-3p antagomir along with luc-eIF5A1-3′-UTR and miR-434-3p mimics restored the luciferase activity. [score:1]
Quantification of the fluorescent intensities indicated that myotubes treated with TPEN or Stsp significantly decreased the ∆ψm index while myotubes transfected with miR-434-3p mimic reversed the scenario; in contrast, the cotransfection of antagomir restored the effect of TPEN and Stsp in ∆ψm (Fig. 5C). [score:1]
Myotubes were transfected with miR-434-3p mimics or NS-miR for 36 h before treatment with TPEN for 24 h. Our data show that myotubes transfected with NS-miRNA before TPEN exposure had no protection against TPEN -induced apoptosis (Fig. 4A). [score:1]
miR-434-3p protects apoptosis through eIF5A1. [score:1]
The transfection of miR-434-3p antagomir along with miR-434-3p mimics restored the TPEN -induced myotubes death (Fig. 4A). [score:1]
This significance was confirmed by solution hybridization detection (miR-434-3p) and western blot (eIF5A1). [score:1]
Myotubes were transfected with NS -mimetic, miR-434-3p mimetic, miR-434-3p antagomir or no transfection for 24 h followed by eight hours TPEN (100 μM) or Stps (1 μM) incubation. [score:1]
Figure 5Myotubes were transfected with NS -mimetic, miR-434-3p mimetic, miR-434-3p antagomir or no transfection for 24 h followed by eight hours TPEN (100 μM) or Stps (1 μM) incubation. [score:1]
While myotubes treated with Stsp had a higher percentage of death, transfection of those myotubes with miR-434-3p mimic increased the proportion of myotubes survival and co-transfection of myotubes with miR-434-3p antagomir reversed the effect of miR-434 -mimic (Fig. 4C). [score:1]
Moreover, eIF5A1 has a conservative miR-434-3p seed sequence in its 3′-UTR (Fig. 3A). [score:1]
On the other hand, transfection of myotubes with miR-434-3p mimics strongly reduced eIF5A1 protein levels and the cotransfection of myotubes with miR-434-3p antagomir reinstated eIF5A1 protein levels (Fig. 4B). [score:1]
The next day, myoblast differentiation was induced for three days, and the myotubes were transfected with 30nM of miR-434-3p mimetic or the NS microRNA (miR-NS) control (miRvana; Life Technologies). [score:1]
A reporter construct containing the luciferase gene fused to the eIF5A1 3′-UTR (luc-eIF5A1-3′-UTR) or luciferase gene fused to the mutated eIF5A1 3′-UTR (luc-eIF5A1-3′-UTR-M) (Fig. 3E) was co -transfected with NS-miR or miR-434-3p mimics with or without miR-434-3p antagomir into myotubes. [score:1]
To test this possibility, we transfected myotubes with NS-miR (non-specific miRNA) or miR-434-3p mimic. [score:1]
U6 and GAPDH were served as loading controls for miR-434-3p and eIF5A1, respectively. [score:1]
miR-434-3p protects myocytes from apoptosis through eIF5A1. [score:1]
Predicted biological pathways controlled by miR-434-3p. [score:1]
As shown in Fig. 3F, while cells transfected with luc-eIF5A1-3′-UTR alone or co -transfected with NS-miR had luciferase activity, cells co -transfected with miR-434-3p mimics displayed a reduction in luciferase activity significantly. [score:1]
This suggesting that miR-434-3p may have a crucial role in the etiology of aging. [score:1]
miR-434-3p protects myotubes from caspase activation and loss of mitochondrial membrane potential. [score:1]
Figure 4Myotubes were transfected with NS -mimetic, miR-434-3p mimetic with or without miR-434-3p antagomir or no transfection for 24 h followed by eight hours TPEN (100 μM) or Stps (1 μM) incubation. [score:1]
Our prediction pathway analysis for miR-434-3p identified apoptosis as one of the skeletal muscle-specific pathways. [score:1]
Briefly, the eIF5A1 3′UTR at the miR-434-3p canonical binding sites, were obtained by replacing the 5′-GCCTGUGGTTTAGG-3 consensus sequence by 5′-GCCTGTGAATTAGG-3. The eIF5A1-3′ UTR was mutagenized by site-directed mutagenesis by using the following primers: −5′-TGCTTGTGGTTTAGGTTCCC-3′ and 5′-ATCGGGGATGAGTAGGATAA −3′ for eIF5A1-3′UTR-M. Apoptosis was induced in myotubes by treated with TPEN or staurosporine (Stsp) (Santa Cruz Biotechnology, Inc. [score:1]
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2
[+] score: 27
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]
We randomly picked 9 miRNAs (miR-337, miR-540-3p, miR-127, miR-434-5p, miR-329, miR-543-3p, miR-376a, miR-300, and miR-381) expressed from the Dlk1-Dio3 locus and validated their expression by qRT-PCR. [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]
Overexpression of miR-434-5p tended to increase the myotube diameter (100 ± 4.89 vs. [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]
Myotubes were transfected with miR-411, miR-434-5p, and miR-540-3p mimics and immunostained with an anti-myosin heavy chain antibody and DAPI. [score:1]
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3
[+] score: 25
In agreement with this, we previously observed in this same set of samples that ovarian Foxo3a mRNA expression was higher in old df/df than N mice, although not different between young df/df and N mice [42] miR-434-3p was one the most expressed miRNAs in ovarian samples from the current study and was observed to be down-regulated with age in df/df mice. [score:8]
In fact, this same pattern of regulation was observed for other seven miRNAs (mmu-miR-29c, mmu-miR-296, mmu-miR-130b, mmu-miR-17, mmu-miR-434, mmu-miR-181c, mmu-miR-132), which further confirms the validity of our analysis and suggests miRNA regulation at the gene expression level [48]. [score:5]
In addition, miR-434-3p expression was also up-regulated in young df/df compared to young N mice. [score:5]
A previous study has shown that miR-434 up-regulation in the skeletal muscle tissue of aged mice is prevented by calorie restriction [58]. [score:4]
There is very little published data on the mRNAs targeted by miR-434, but it is known for targeting a retrotransposon-like gene (RTL1) which has a role in genomic imprinting of parental origin [59], although not changed between ages or genotypes in the RNASeq evaluation [20]. [score:3]
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4
[+] 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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5
[+] score: 21
In this study, there were 8 upregulated miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133a-1-5p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p) and 1 downregulated miRNA (mir-215-5p) present as potential targets for differentiation between gram -negative and gram -positive bacterial infection. [score:9]
Following exposure to gram -positive bacteria in the injection and skin graft mo dels, 7 upregulated miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p) and 1 downregulated miRNA (mir-215-5p) were found. [score:7]
Upon gram -positive bacterial infection, 9 miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133a-1-5p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p, mir-215-5p) showed upregulation greater than 4-fold with a p-value < 0.01. [score:4]
It was revealed that a total of 9 miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133a-1-5p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p, mir-215-5p) showed differences greater than 4-fold with p-value < 0.01 between the 2 libraries (Table  1). [score:1]
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6
[+] score: 17
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-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-127, mmu-mir-132, mmu-mir-133a-1, mmu-mir-136, mmu-mir-144, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-10b, mmu-mir-185, mmu-mir-190a, mmu-mir-193a, mmu-mir-203, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-215, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-144, hsa-mir-152, hsa-mir-127, hsa-mir-136, hsa-mir-146a, hsa-mir-185, hsa-mir-190a, hsa-mir-193a, hsa-mir-206, mmu-mir-148a, 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-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-337, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-29b-2, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, hsa-mir-337, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-215, mmu-mir-411, hsa-mir-486-1, hsa-mir-146b, hsa-mir-193b, mmu-mir-486a, mmu-mir-540, hsa-mir-92b, hsa-mir-411, hsa-mir-378d-2, mmu-mir-146b, mmu-mir-193b, mmu-mir-92b, mmu-mir-872, mmu-mir-1b, mmu-mir-3071, mmu-mir-486b, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, hsa-mir-203b, mmu-mir-3544, hsa-mir-378j, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-let-7k, hsa-mir-486-2
The differentially expressed miRNAs in previous studies appeared consistently in mouse skeletal muscle from our study; for example, up-regulated miRNAs such as miR-29b, -34a, -206, -215, and -223 in aged muscle were also elevated, and the down-regulated miRNA miR-434 was decreased in aged mouse muscle; thus, our data reproduce previous findings. [score:9]
For example, miR-206 was up-regulated in aged human skeletal muscle, while miR-434 was down-regulated in aged mouse skeletal muscle [10, 12]. [score:7]
miRNA Fold Change P-value mmu-miR-337-5p −5.2 0.0149 mmu-miR-3544-3p −5.1 0.0147 mmu-miR-540-5p −4.9 0.0200mmu-miR-337-3p [a] −3.0 0.0324mmu-miR-3544-5p [a] −3.0 0.0308 mmu-miR-434-3p −2.1 0.0001 mmu-miR-3071-5p −2.0 0.0004mmu-miR-136-3p [a] −2.0 0.0004mmu-miR-3071-3p [a] −1.6 0.0000 mmu-miR-136-5p −1.6 0.0000 mmu-miR-143-5p −1.2 0.0004 mmu-miR-190a-5p −1.0 0.0139 mmu-miR-872-3p −0.9 0.0152 mmu-miR-193a-3p −0.9 0.0164 mmu-miR-144-3p −0.8 0.0298 mmu-miR-127-3p −0.7 0. 0002mmu-miR-434-5p [a] −0.6 0.0082 mmu-miR-148a-3p −0.6 0.0130 mmu-miR-411-5p −0.6 0.0091 a miRNA* (passenger) strand processed from opposite arm of the mature miRNA. [score:1]
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7
[+] score: 15
Similarly, the expression miR-129 and miR-434 was increased and their targets (i. e., Sox4 and Ccnl1, respectively) were down-regulated [26] (Figures 2G and 2H). [score:8]
By contrast, some miRNAs that are significantly up-regulated were also observed, including miR-290 cluster members, miR-291a and miR-291b, miR-129-1-3p, miR-129-2-3p, miR-23a-3p, miR-434-3p, miR-145-5p, and miR-203-3p. [score:4]
Mir-434 is one of the highly expressed miRNA clusters in undifferentiated ES cells. [score:3]
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8
[+] score: 13
The miR-21 and miR-434 were observed twofold up-regulated and let-7a-1 0.5 fold down-regulated. [score:7]
Among other miRs, of considerable interest are miR-21a and miR-434: both of them were up-regulated in all treated mice, mostly by LPS, and the antibody prevented this effect more or less efficiently. [score:4]
The effects of nicotine and LPS were of similar direction for six miRs (miR-26, let-7f, let-7c, miR-30, miR-21a and miR-434) and showed an opposite impact for other four miRs (miR-9, let-7j, miR-218 and miR-125). [score:2]
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9
[+] score: 9
Unlike miR-434 and miR-136 (PAM class C), miR-127 expression gradually decreases during the differentiation process (PAM class A), a pattern inversely correlated to that of Rtl1 expression in ES cells, as assayed by Quantitative Reverse-transcriptase PCR (Q-RT-PCR; Figure 2D). [score:4]
Among these, a short cluster of maternally expressed miRNAs genes (miR-431, miR-433, miR-127, miR-434 and miR-136) is transcribed and processed from an antisense gene to the paternally expressed Retrotransposon-like 1 (Rtl1) gene, the recently characterized protein product of which appears to be indispensable for mouse foetal development [37]. [score:4]
Our time-course analysis revealed that of these five miRNAs, only miR-127, miR-434 and miR-136, are likely to contribute to Rtl1 silencing in ES cells (Figure 2D) because their cloning frequencies largely exceeds that of the other members of the cluster, which accumulate at background level (Figure 2C, Dataset S1). [score:1]
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10
[+] score: 7
The comparison between control- and MPA -treated cells revealed that 16 miRNAs were significantly modulated by more than two-fold (P < 0.05, Figure 1A), nine miRNAs were upregulated (miR-191*, miR-17*, miR- 470*, miR-451, miR-702, miR-434-3p, miR-493, miR-23a* and miR-485*) and seven were downregulated (miR-378*, miR-376a, miR-224, miR-190b, miR-16, miR-410 and miR-197) (Figure 1B). [score:7]
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11
[+] score: 6
Within the miR-127 cluster, no miRNA targets were identified by miRNA/mRNA pairing (Figure 4C), while all had direct mRNA targets when miRNA/protein pairs were analyzed, such as miR-380-5p, miR-370, and miR-434. [score:6]
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12
[+] score: 6
miR-434-5p - ND miR-451 +miR-451 expression was up-regulated in multidrug resistant cancer cell lines [58]. [score:6]
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13
[+] score: 5
Among these miRNAs, the expression of 10 miRNAs (miR337, miR714, miR346, miR500, miR101b, miR434, miR501, miR410, miR672 and miR425) was significantly decreased, and we therefore did not further examine the expression levels of these molecules by using quantitative RT-PCR (qRT-PCR). [score:5]
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14
[+] score: 4
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-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, 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-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The miRNA families that change expression in both mice and rats were: mir-7, mir-9, mir-10, mir-15, mir-17, mir-26, mir-29, mir-30, mir-101, mir-130, mir-181, mir-204, mir-339, mir-340, mir-368, mir-434, mir-467. [score:3]
50E-0367mmu-miR-339-5pmir-3390.206.807.92E-037.53E-028mmu-miR-34c-5pmir-340.246.689.54E-066.88E-0477mmu-miR-34a-5pmir-340.179.541.17E-029.66E-0245mmu-miR-340-5pmir-3400.178.511.71E-032.45E-0217mmu-miR-361-5pmir-3610.247.887.74E-052.90E-0319mmu-miR-376b-3pmir-3680.268.451.05E-043.50E-0356mmu-miR-376a-3pmir-3680.1910.215.63E-036.40E-0223mmu-miR-434-3pmir-4340.2210.461.76E-044. [score:1]
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15
[+] score: 4
The other 5 miRNAs all showed significant alterations in expression levels at 9 months of age, but these alterations became either not significant (miR-331-3p, miR-7a-5p, miR-501-3p and miR-434-3p) or reversed (miR-7b-5p) at 12 months of age. [score:3]
Among them, nine miRNAs (miR-99b-5p, miR-7b-5p, miR-7a-5p, miR-501-3p, miR-434-3p, miR-409-5p, miR-331-3p, miR-138-5p and miR-100-5p) showed consistent changes in both groups. [score:1]
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16
[+] score: 4
miR-434-5p was discovered to inhibit TYR to turn mouse skin white [35]. [score:3]
Wu D. T. Chen J. S. Chang D. C. Lin S. L. miR-434-5p mediates skin whitening and lightening Clin. [score:1]
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17
[+] score: 3
Eight of the significantly modulated miRNAs, miR-106b, miR-199a-3p, miR-214, miR-218, miR-31, miR-434-3p, miR-671-3p, and miR-574-3p were predicted to significantly modulate several nervous system function and disease related pathways. [score:3]
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18
[+] score: 3
The differentially expressed miRNAs include four pairs of mature miRNAs derived from the same pre-miRNA hairpin (miR-467a and miR-467a*, miR-434-5p and miR-434-3p, miR-199a and miR-199a*, miR-126-3p and miR-126-5p). [score:3]
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19
[+] score: 1
The four rodent-specific miRNAs—mmu-miR-351, mmu-miR-434, mmu-miR-467a, and mmu-miR-682—were excluded from further studies. [score:1]
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