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25 publications mentioning mmu-mir-365-1

Open access articles that are associated with the species Mus musculus and mention the gene name mir-365-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 66
Furthermore, our study found that the expression of miR-365-3p was significantly upregulated from Day 15 of gestation to Days 26, 50, and 95 of gestation, which shows similar expression pattern with the PLET1-L transcript as shown in Figure 5. This is opposed to the observations that miR-365-3p could reduce the PLET1-L 3′ UTR luciferase reporter activity in vitro and that the PLET1-L 3′ UTR showed higher luciferase activity. [score:8]
The quantitative RT-PCR (qRT-PCR) was carried out to detect the expression levels of the two PLET1 transcripts and the miR-365-3p expressed in the conceptuses (Day 15 of gestation) and placentas (chorioallantoic tissue, Days 26, 50, and 95 of gestation) on the CFX384 real-time PCR detection System (Bio-Rad Laboratories, Inc. [score:5]
The value of 2−ΔΔ Ct represents the relative expression level of miR-365-3p. [score:3]
To detect the expression profile of the miR-365-3p, total RNA was reverse transcribed using Mir-X [TM] miRNA First-Strand Synthesis Kit (Takara Bio Inc. [score:3]
Moreover, the present data suggest that miR-365-3p has an impact on the expression of the PLET1 gene. [score:3]
2.6. miR-365-3p Was Differentially Expressed during Days 15, 26, 50, and 95 of Gestation in Pigs. [score:3]
In this study, the expression data of miR-365-3p and PLET1-L 3′ UTR were derived from porcine placenta samples. [score:3]
In addition, overexpression of the miR-365-3p mutant had no significant effect on the PLET1-S 3′ UTR luciferase reporter activity. [score:3]
The results suggest that a possible interaction may exist between PLET1-S 3′ UTR and miR-365-3p, although we did not find the perfect seed matches of miR-365-3p in the PLET1-S 3′ UTR by using the online miRNA target prediction tools described above. [score:3]
The qRT-PCR was used to detect the expression pattern of miR-365-3p in conceptus and placenta during the periods Days 15, 26, 50, and 95 of gestation. [score:3]
However, the cell location of miR-365-3p has yet to be assessed, so data shown in Figure 8 may not exactly be the expression pattern of miR-365-3p in trophoblast cells. [score:3]
This may explain the unexpected correlation of expression pattern between miR-365-3p and the PLET1-L transcript in porcine placenta. [score:3]
We found that overexpression of the miR-365-3p significantly decreased the luciferase activity of the wild-type plasmid compared to that of the NC control. [score:2]
As shown in Figure 8, the miR-365-3p expression levels were significantly increased in placentas from Days 26, 50, and 95 of gestation as compared to that in conceptuses from Day 15 of gestation. [score:2]
As expected, overexpression of the miR-365-3p mutant had no significant effect on luciferase activity of this reporter compared to that in cells transfected with NC-miRNA. [score:2]
Therefore, further studies using porcine trophoblast cells will be needed to elucidate the detailed molecular mechanisms underlying the miR-365-3p -mediated regulation on the porcine PLET1. [score:2]
It is worth noting that the 5′ end of the seed sequence of miR-365-3p matches the first 4 bp of the distal (second) core polyadenylation signal (AUUAAA) (Figure 4); Third, we validated the interaction between miR-365-3p and porcine PLET1 by transfection of three constructs (the PLET1-L 3′ UTR, PLET1-S 3′ UTR and mutant PLET1-L 3′ UTR where the putative miR-365-3p binding site was mutated) into PK15 cells, respectively. [score:1]
Together with data shown in Figure 7, our study demonstrated the interaction between the PLET1 and miR-365-3p in vitro, and indicates that in addition to the predicted canonical binding site in the PLET1-L 3′ UTR, a non-canonical miR-365-3p binding site might be within the PLET1-S 3′ UTR. [score:1]
Validation of the Interaction between miR-365-3p and PLET1. [score:1]
We then developed a second PLET1-L 3′ UTR luciferase reporter carrying a mutant miR-365-3p binding site. [score:1]
The miRNA mimics of miR-365-3p, the miR-365-3p mutant (mut-miR-365-3p), and NC-miRNA (a scrambled sequence) were each synthesized as duplexes. [score:1]
As showed in Figure 7B, neither miR-365-3p nor miR-365-3p mutants could result in significant decrease in the PLET1-L-mut luciferase reporter activity (Figure 7B). [score:1]
Finally, we constructed the truncated wild-type plasmid containing the predicted binding site of miR-365-3p and the corresponding mutant plasmid containing the mutated seed binding site. [score:1]
These findings indicate the existence of the interaction between miR-365-3p and the predicted binding site in the porcine PLET1-L 3′ UTR. [score:1]
Random 4 base substitutions in the seed sequence of miR-365-3p were introduced to create the miR-365-3p mutant (mut-miR-365-3p) when synthesized, and NC-miRNA was used as the negative control. [score:1]
We found the following: (1) The PLET1-S 3′ UTR luciferase reporter activity decreased ~2.0-fold in cells transfected with miR-365-3p compared to NC-miRNA, and overexpression of miR-365-3p mutant did not result in the decrease of PLET1-S 3′ UTR luciferase activity (Figure 7A); (2) The PLET1-L 3′ UTR luciferase reporter activity decreased ~3.0-fold in cells transfected with miR-365-3p compared to NC-miRNA. [score:1]
Therefore, our observation may suggest a non-canonical binding mechanism involved in the interaction between miR-365-3p and the PLET1-S 3′ UTR. [score:1]
Our study predicted a putative binding site of miR-365-3p in pig PLET1-L 3′ UTR. [score:1]
Of the four miRNAs, only the miR-365-3p mimic could result in decrease in luciferase activity. [score:1]
The two plasmids (PLET1-S and PLET1-L) that mentioned above and PLET1-L 3′ UTR plasmid where the putative miR-365-3p binding site was mutated (designed as PLET1-L-mut) were used to validate the interaction of miR-365-3p and PLET1-L 3′ UTR. [score:1]
In summary, these results demonstrated the interaction between the PLET1 and miR-365-3p in vitro. [score:1]
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2
[+] score: 52
In our data set, miR-365-3p was well expressed and highly up-regulated (Cluster 4), whereas miR-99b-5p was less well expressed, but one of the most prominently up-regulated miRNAs during osteoclast differentiation (Cluster 7). [score:11]
To determine whether the strongly up-regulated miRNAs had a positive role in osteoclastogenesis, bone marrow-derived monocytes (BMMs) were transiently transfected with inhibitors for miR-99b-5p or miR-365-3p. [score:6]
In this study, we identified a profile of miRNAs differentially expressed in the early, middle and late stages of osteoclastogenesis in primary cultures and validated the function of 2 highly up-regulated miRNAs, miR-365 and −99b, during osteoclastogenesis. [score:6]
Overall, identifying other mRNA targets of miR-365 and −99b will be critical for understanding the signaling cascades regulated by these miRNAs in osteoclasts. [score:4]
We next verified changes in the expression of several miRNAs using quantitative RT-PCR (qRT-PCR), focusing on 3 miRNAs that had not been previously identified, to our knowledge, in cells of the osteoclast lineage: miR-99b-5p, miR-365-3p and miR-451. [score:3]
Inhibition of miR-365 activity could lead to increased cell number, a potential explanation for the increased osteoclast number observed in our studies (Figure 2). [score:3]
In other cell types, miR-365 has been shown to target Cyclin D1 and CDC25A, as well as pro-apoptotic BAX [30], [31]. [score:3]
Expression of miR-99b-5p and miR-365-3p increased 12 fold between days 1 and 5 of culture (Figure 2A). [score:3]
In contrast, miR-365 is transcribed from two independent genetic loci (on mouse chromosomes 11 and 16), and the expression of miR-365 from the chromosome 16 locus is activated by Sp1 and NFκB, two transcription factors that promote osteoclastogenesis [33], [34]. [score:3]
The expression of miR-365, miR-99b, and miR-451 was detected by qPCR in a MiQ qPCR cycler (Bio-Rad) and normalized to U6 small nuclear RNA (RNU6b) levels, using the absolute quantification method. [score:3]
In contrast to miR-99b, inhibition of miR-365 increased osteoclast number, while decreasing osteoclast size. [score:3]
These data suggest that miR-365 may fine tune osteoclastogenesis, regulating osteoclast size and number in an opposing manner. [score:2]
The increased levels of miR-365 during osteoclast differentiation could slow proliferation and increase survival. [score:1]
It may be of interest to determine if only one miR-365 locus or both loci contribute to the miR-365 signal detected during osteoclast differentiation. [score:1]
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3
[+] score: 31
Among the 14 miRNAs, miR-30b/c, -133a/b, -195, -200a, -320 and −365 emerged as chief candidates of pathogenesis based on the inverse relationship with the increased expression level of their target genes in EHBD, high miRNA expression in EHBDs relative to livers (with the exception of miR-30b/c), expression in cholangiocytes of the biliary epithelium, and a decreased expression of miR-365, -195, -30 and -200a in a cholangiocyte line infected with RRV. [score:11]
Expression of miR-365, miR-195, miR-30c and miR-200a were significantly downregulated in RRV infected cholangiocytes. [score:6]
After 24 hours of RRV infection (100 multiplicity of infection [MOI]), the expression levels were downregulated by 1.30 to 1.53-fold for miR-365, miR-195, miR-30c and miR-200a (Figure  6) below levels of the vehicle control. [score:6]
In contrast, the developmental expression in EHBDs of miR-133b, -195 and -200a was lowest at 3 days of age and increased progressively to adult levels, while miR-365, -320 and -30c was highest during the suckling period (Figure  4, brown lines). [score:4]
Among these, miR-30b/c, -195 and −365 had 1 [st] tier links to biological processes of hematology and inflammation by influencing the expression of Pim1, Il10ra, Il7r (miR-195), Arrb2 (miR-365), Pik3cd, Cmpk2, Socs3, Cysltr1, Serpine1 and Ceacam1 (miR-30b/c). [score:3]
05mmu-miR-365−4.620.015−4.450.034mmu-miR-133a−3.650.015−2.670.032mmu-miR-200b−3.960.015−2.840.046mmu-miR-133b−4.410.009−4.350.032mmu-miR-200a−5.560.009−3.110.034 mmu-miR-195 −4.93 0.014 −8.71 0.05 * Minus sign implies fold change below controls. [score:1]
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4
[+] score: 29
Eight miRNAs (miR-101, miR-107, miR-122, miR-29, miR-365, miR-375, miR-378, and miR-802), whose expression was found to be downregulated in c-Myc and/or AKT/Ras liver tumors, were selected and their tumor suppressor activity was assessed in c-Myc and AKT/Ras mice. [score:8]
miRNA Oncogene Growth Inhibition miR-101 c-Myc +++ AKT/Ras +++ miR-107 c-Myc + AKT/Ras ++ miR-122 c-Myc ++ AKT/Ras ++ miR-29 c-Myc ++ AKT/Ras + miR-365 c-Myc ++ AKT/Ras ++ miR-375 c-Myc + AKT/Ras +++ miR-378 c-Myc − AKT/Ras − miR-802 c-Myc ++ AKT/Ras − Taken together, the present results indicate that miR-378 does not possess tumor suppressor activity on c-Myc and AKT/Ras induced hepatocarcinogenesis in mice. [score:5]
miRNA Oncogene Growth Inhibition miR-101 c-Myc +++ AKT/Ras +++ miR-107 c-Myc + AKT/Ras ++ miR-122 c-Myc ++ AKT/Ras ++ miR-29 c-Myc ++ AKT/Ras + miR-365 c-Myc ++ AKT/Ras ++ miR-375 c-Myc + AKT/Ras +++ miR-378 c-Myc − AKT/Ras − miR-802 c-Myc ++ AKT/Ras − Taken together, the present results indicate that miR-378 does not possess tumor suppressor activity on c-Myc and AKT/Ras induced hepatocarcinogenesis in mice. [score:5]
In summary, the present results indicate that miR-107, miR-122, miR-29, miR-365, and miR-802 possess weak to moderate tumor suppressive properties, as none of them is able to completely prevent oncogene driven liver tumor development in mice. [score:4]
Weak to moderate tumor suppressor potential of miR-107, miR-122, miR-29, miR-365, and miR-802 in c-Myc and AKT/Ras driven liver tumor development. [score:4]
Similar results were obtained when co -expressing miR-365 with c-Myc or AKT/Ras (Supplementary Figure 7A–7D). [score:3]
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5
[+] score: 27
In the present investigation, the majority of differentially regulated miRNAs were primarily up-regulated with only one miRNA down-regulated at 0.13 Gy (miR-365) and five down-regulated at 13 Gy (miR-709, miR-6239, miR-690, let-7k, and miR-1902); no down-regulated miRNAs were found at the intermediate dose levels (0.34–4.3 Gy). [score:12]
No down-regulated miRNAs were found at 0.34, 1.3, or 4.3 Gy, while only one miRNA (miR-365) was down-regulated at 0.13 Gy, and five miRNAs (let-7k, miR-690, miR-709, miR-1902, and miR-6239) were down-regulated at 13 Gy. [score:10]
In the present study, the number of differentially regulated miRNAs was relatively constant among the highest absorbed doses (0.34–13 Gy), ranging from 17 to 28, whereas only miR-365 was differentially regulated at the lowest absorbed dose (0.13 Gy). [score:3]
Interestingly, only miRNA (miR-365) was significantly regulated at 0.13 Gy, which was not found at the other dose levels. [score:2]
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6
[+] score: 15
For example, miR-29b specifically targets HDAC4 to epigenetically regulate multiple myeloma cell growth and survival [1], miR-22 targets and inhibits HDAC4 in antigen-presenting cells and plays a critical role in emphysema and TH17 responses [7], miR-125a-5p targets HDAC4 to suppress breast tumorigenesis [3], and miR-140 and miR-365 target HDAC4 and participate in cartilage and bone development [20, 21]. [score:15]
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7
[+] score: 15
Mybl2, downregulated during colon epithelial cell maturation, is suppressed by miR-365. [score:6]
During colonic epithelium maturation, miR365 has been reported to regulate Myb-related protein B (MYBL2) expression, which is important in both cell cycle regulation and differentiation in various biological processes [31]. [score:5]
Therefore, the Mybl2 expression level controlled by miR365 may not involve in M-cell maturation. [score:3]
Among them, two miRNAs, miR34a and miR365, might be involved in M-cell maturation. [score:1]
[1 to 20 of 4 sentences]
8
[+] score: 15
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-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, 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-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Figure 8The Prdm1 targeting miRNAs miR-23b, miR-125a, miR-351, miR-30a/c/d, miR-182, miR-96, miR-98, miR-200b/c, and miR-365 are upregulated by HDI. [score:6]
In addition to miR-23b, miR-30a, and miR-125b, which, as we showed by qRT-PCR and miRNA-Seq, are upregulated by HDI, several other putative Prdm1 targeting miRNAs, including miR-125a, miR-96, miR-351, miR-30c, miR-182, miR-23a, miR-200b, miR-200c, miR-365, let-7, miR-98, and miR-133, were also significantly increased by HDI. [score:6]
org), we identified miR-125a, miR-125b, miR-96, miR-351, miR-30, miR-182, miR-23a, miR-23b, miR-200b, miR-200c, miR-33a, miR-365, let-7, miR-98, miR-24, miR-9, miR-223, and miR-133 as PRDM1/Prdm1 targeting miRNAs in both the human and the mouse. [score:3]
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9
[+] score: 9
Hierarchical clustering analysis revealed several groups of microRNAs that exhibit similar expression patterns, including a 9-microRNA group (mmu-miR-152, mmu-miR-365, mmu-let-7d*, mmu-miR-125a-5p, mmu-miR-181d, mmu-miR-99a, mmu-miR-100, mmu-miR-30c, mmu-miR-125b-5p, named as cluster X in Figure 1A ) which was down-regulated during the early phase of wound healing (day 1) as compared to unwounded skin (day 0), and returned to basal level during the later phase of wound healing (day 5) (Table 1 ). [score:5]
A 9-microRNA cluster (mmu-miR-152, mmu-miR-365, mmu-let-7d*, mmu-miR-125a-5p, mmu-miR-181d, mmu-miR-99a, mmu-miR-100, mmu-miR-30c, mmu-miR-125b-5p, which exhibited statistical significant down-regulation on day 1 and returned to basal level on day 5) was named as cluster X (marked by solid bar on the right). [score:4]
[1 to 20 of 2 sentences]
10
[+] score: 7
For example, miR-877-5p and miR-5114 were up-regulated, whereas miR-3963, miR-378a-3p, miR-193b-3p, miR-125a-5p, miR-378b, miR-365-3p, let-7e-5p, and miR-712-5p were down-regulated in the 0.01 Gy-irradiated mouse spleens compared with the sham spleens. [score:6]
In our qRT-PCR analysis (Fig. 1A), only 5 miRNAs (miR-378a-3p, miR-193b-3p, miR-125a-5p, miR-712-5p, and miR-3963) generated acceptable Ct values, whereas the other 5 miRNAs (miR-877-5p, miR-5114, miR-378b, miR-365-3p, and let-7e-5p) fell below the minimum threshold because of their lower abundance. [score:1]
[1 to 20 of 2 sentences]
11
[+] score: 7
As proof of the integrity of our miR expression assay data, the expression levels of three putative adipogenesis-relevant miRs (miR-103, miR-146 and miR-221) and five highly regulated miRs (miR-29a, miR29b, miR-365, miR93 and miR96) were analysed by RT-qPCR (S1 and S2 Figures; the corresponding expression values are summarised in the Supporting information S3 and S4 Tables). [score:7]
[1 to 20 of 1 sentences]
12
[+] score: 6
By contrast, the expression of miR-193b and miR-365, previously shown to be direct downstream targets of Prdm16 and required for BAT differentiation [8], were increased in mG [+] compared to mT [+] cells (Fig. 2D). [score:5]
In addition, the cluster of miR-193b and miR-365, downstream signals of Prdm16, are required for brown adipocyte differentiation [8]. [score:1]
[1 to 20 of 2 sentences]
13
[+] score: 5
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-16-1, hsa-mir-21, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-9-2, mmu-mir-151, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-122, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-214, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-194-1, mmu-mir-192, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-10a, mmu-mir-210, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-151a, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-16-1, gga-mir-194, gga-mir-10b, gga-mir-199-2, gga-mir-16-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-199-1, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-122-1, gga-mir-122-2, gga-mir-9-2, mmu-mir-365-2, gga-mir-9-1, gga-mir-365-1, gga-mir-365-2, hsa-mir-151b, mmu-mir-744, gga-mir-21, hsa-mir-744, gga-mir-199b, gga-mir-122b, gga-mir-10a, gga-mir-16c, gga-mir-214, sma-let-7, sma-mir-71a, sma-bantam, sma-mir-10, sma-mir-2a, sma-mir-3479, sma-mir-71b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, gga-mir-365b, sma-mir-8437, sma-mir-2162, gga-mir-9-3, gga-mir-210a, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-mir-10c, gga-mir-210b, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-9b-2, gga-mir-122b-2
Of the 10 miRNAs examined, all except miR-365 and miR-151 were differentially expressed between naïve and infected mice by 6–8 weeks post infection (Fig. 1, Table S2). [score:3]
Consistent with the array results, there was an increase in miR-199-5p, miR-199-3p, miR-214, miR-21, miR-210, and a reduction of miR-192, miR-194, miR-365, miR-122 and miR-151 in the liver tissue of S. mansoni infected mice as compared to naïve mice; miR-9 and miR-744 did not display differential expression and were not analysed further (Table 1). [score:2]
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14
[+] score: 5
The target gene of miR-365 was predicted by TargetScan, using the context++ score system, as has been instructed before [21]. [score:5]
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15
[+] score: 5
Guan et al. showed that miR-365 regulated chondrocyte differentiation by directly targeting HDAC4 [41]. [score:5]
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16
[+] score: 5
The top 10 differentially expressed miRNAs included miR-193b-5p, miR-365-1-5p, miR-129-5p, miR-122-5p, miR-6240 and miR-5130 which had lower expression in both SAT and VAT (WAT) than in BAT. [score:5]
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17
[+] score: 5
Inhibition of miR-193a/b and/or miR-365 in mouse primary brown pre-adipocytes impairs brown adipogenesis in vitro [14]. [score:3]
However, miR-193b null mice, that are also deficient in miR-365, have normal BAT development, differentiation and function [24]. [score:2]
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18
[+] score: 4
miR-365 is clustered with miR-193b which shows similar expression patterns to miR-365 in our system (Tables 2 and 3 ), thus suggesting that these miRNAs may be co-regulated. [score:4]
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19
[+] 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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, 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-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, 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-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-145 and miR-365 were specifically expressed in DRG (Fig. 3a). [score:3]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
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[+] score: 4
Luciferase reporter analysis revealed that the activity of reporter containing wild type 3’UTR of KLF4 was significantly suppressed (about 40% reduction) by miR-29, but not by miR-365 (Fig 7C). [score:3]
Luciferase reporters were co -transfected with miR-29 mimic or miR-365 mimic, an unrelated miRNA as negative control. [score:1]
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[+] score: 3
TaqMan miRNA probes (Applied Biosystems, Foster City, CA, USA) were used to quantify the reported miRNA expressions levels, including miR-133a, the miR-365/193b cluster, and U6 snRNA, which was used as an internal control. [score:3]
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[+] score: 1
Several microRNAs including miR-29, miR-365, and miR-17-92 [14, 19] control tumor cell proliferation, invasion and survival. [score:1]
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[+] score: 1
It was found that miR-494, miR-365 and miR-451 were present in liver, miR-206, miR-468 and miR-691 in spleen, and miR-223, miR-98 and miR-206 in lung. [score:1]
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[+] score: 1
Interestingly, we found among them several previously OA -associated miRs such as miR-27b, miR-199, miR-29a, miR-26, and miR-365 [16, 17]. [score:1]
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[+] score: 1
Accumulating evidence has shown a strong connection between miRNA (e. g., miRNA-103 [38], let-7b [39], miRNA-7a [40], miRNA-203 [41], miRNA-219 [24], miRNA-365-3p [27], and miRNA-183 cluster [42]) modulation and pain pathways from primary afferent nociceptors, the DRG, the spinal cord, and brain areas in different pain mo dels. [score:1]
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