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21 publications mentioning mmu-mir-744

Open access articles that are associated with the species Mus musculus and mention the gene name mir-744. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 271
In comparison with everolimus, MMP-9 expression was significantly reduced in miR-744-3p suppressed LSCC cell lines indicating that targeting miR-744-3p had a therapeutic impact in preventing MMP-9 upregulation in LSCC. [score:10]
As miR- 744- 3p could simultaneously target dual signaling channels responsible for MMP-9 activation, we hypothesized that suppressing miR-744-3p could have a therapeutic impact on inhibiting MMP-9 expression and should have a better efficacy than everolimus. [score:9]
Significant downregulation of MMP-9 mRNA expression level was observed in LSCC cell lines with miR-744-3p suppression. [score:8]
Figure 6Significant downregulation of MMP-9 mRNA expression level was observed in LSCC cell lines with miR-744-3p suppression. [score:8]
As miR-744-3p expression level in LSCC tissue was negatively correlated to the PDCD4 and PTEN transcript levels in the same tissue cohort, we proposed that miR-744-3p could possibly function as MMP-9 enhancer by inhibiting PDCD4 and PTEN expression in LSCC. [score:7]
As activated AKT and NF-κB (p65) could promote MMP-9 upregulation in head and neck cancers, we hypothesized that the miR-744-3p modulated MMP- 9 expression in LSCC. [score:6]
Genes consistently suggested as potential targets of miR-744-3p and downregulated transcripts in LSCC. [score:6]
Hence, suppression of miR-744-3p can powerfully prevent LSCC metastasis by inhibiting MMP-9 through inactivation of those 2 pathways above. [score:5]
By miR-744-3p suppression, MMP-9 mRNA expression level was significantly reduced in both of SNU899 and SNU1076. [score:5]
To explore the functional impact of miR-744-3p overexpression on LSCC migration and invasion, we monitored the dynamic changes of migration and invasion capacities of LSCC cell lines (SNU899 and SNU1076) expressing the miR-744-3p shRNA. [score:5]
G: SNU899 with mock control vector; (H) SNU899 stably expressing miR-744-3p shRNA; (I) SNU1076 with mock control vector; (J) SNU1076 stably expressing miR-744-3p shRNA. [score:5]
By miR-744-3p suppression, expression levels of PTEN and PDCD4 were significantly increased in both of SNU899 and SNU1076. [score:5]
Furthermore, the expression level of PTEN and PDCD4 were negatively correlated with miR-744-3p expression level. [score:5]
As shown in Figure 3B, suppressing miR-744-3p in the LSCC cell lines (SNU899 and SNU1076) resulted in significant increase in PTEN and PDCD4 transcript expression (P < 0.05). [score:5]
In the Ago2-IP/IgG-IP, PDCD4 and PTEN mRNA levels were reduced when the endogenous expression of miR-744-3p were suppressed by shRNA (Figure 3C). [score:5]
The suppression of miR-744-3p significantly enhanced luciferase expression from the reporter plasmid containing the wild- type PTEN 3′-UTR sequence or containing the wild- type PDCD4 3′-UTR sequence. [score:5]
In silico analysis showed that miR-744-3p targeted PDCD4 and PTEN simultaneouslyTo evaluate the functional target of miR-744- 3p, the target transcript was predicted using miRWalk. [score:5]
Here, our results suggested that miR-744-3p could possibly control the mTOR signaling cascade by inhibiting PTEN expression in LSCC. [score:5]
On one hand, miR-744-3p suppressed the mTOR upstream regulatory element PTEN in the PI3K/AKT/mTOR regulatory axis, which controlled MMP-9 transcription. [score:5]
Our data illustrated that the NF- κB (p65) inhibitory property of PDCD4 was effectively abolished by the high expression of miR-744-3p in LSCC. [score:5]
Expression alteration of PTEN, PDCD4, phosphorylated AKT, phosphorylated NF-κB and MMP-9 caused by miR-744-3p suppression in LSCC. [score:5]
MiR-744-3p shRNA showed higher efficacy than everolimus in suppressing MMP-9 expression in LSCC. [score:4]
On the other hand, miR-744-3p activated another MMP-9 regulatory axis by provoking the signaling cascade controlled by NF-κB p65 via PDCD4 suppression (Figure 7). [score:4]
In silico analysis showed that miR-744-3p could directly target the mRNA transcript of both programmed cell death 4 (PDCD4) and phosphatase and tensin homolog (PTEN), both of which had been reported to be correlated with LSCC metastasis [11– 13]. [score:4]
MiR-744-3p shRNA, however, showed higher efficacy than everolimus in suppressing MMP-9 expression in LSCC (Figure 6). [score:4]
Figure 2(A–D) Figures of LSCC cell lines with mock control vector or expressing miR-744-3p shRNA. [score:3]
To evaluate the functional target of miR-744- 3p, the target transcript was predicted using miRWalk. [score:3]
Target gene prediction analysis revealed that PDCD4 and PTEN 3′-UTR harbored the binding sites for miR-744-3p seed sequence. [score:3]
Mice injected with miR-744-3p suppressed LSCC cells group had lower number of metastatic cancer nodules in comparison with the control group (Figure 2G–2J). [score:3]
High miR-744-3p was crucial to activate MMP-9 expression in LSCC. [score:3]
In contrast, high miR-744-3p expression was significantly associated with the cervical lymph node metastasis in LSCC (P = 0.007). [score:3]
Correlation between PTEN, PDCD4 mRNA expression and clinical characteristics of LSCC patients as well as miR-744-3p expression. [score:3]
Interaction between miR-744-3p and its target genes was confirmed by microRNA:mRNA immunoprecipitation using anti-Ago2 monoclonal antibody-immobilized beads (Wako) and human Argonaute 2 miRNA isolation kit (Wako Pure Chemical Industries). [score:3]
The phosphorylated IKKα/β and IκB-α level remained unchanged in the miR-744-3p suppressed LSCC cell lines (Figure 4A). [score:3]
The miR-744-3p shRNA coding sequence was cloned into lentivector pGreenPuro (System Biosciences) to generate the miR-744-3p shRNA expressing vector (pGreenPuro-miR-744-shRNA vector). [score:3]
Expression of PTEN and PDCD4 transcripts and their interaction with miR-744-3p in LSCC. [score:3]
In silico analysis showed that miR-744-3p targeted PDCD4 and PTEN simultaneously. [score:3]
As shown in Figure 3D and 3E, there was a significant increase in the luciferase activity when miR-744-3p was suppressed endogenously. [score:3]
Our results revealed a novel pathway employed by LSCC in promoting LSCC migration and metastasis by overexpressing miR-744-3p. [score:3]
de/apps/zmf/mirwalk/) was used to predict the candidate transcripts which are targeted by miR-744-3p [52]. [score:3]
Our results confirmed that the expression level of miR-744-3p could have a functional impact on the migration and invasion propensity of LSCC cells. [score:3]
Clinical findings and expression of miR-196a, miR-196b and miR-744-3p in LSCC. [score:3]
Thus, we proposed that miR-744-3p overexpression could promote migration and invasion of the LSCC cells. [score:3]
MMP-9 expression was reduced in miR-744-3p silencing LSCC. [score:3]
Influence of miR-744-3p suppression on LSCC metastasis. [score:3]
Suppression of miR-744-3p reduced AKT and NF-κB (p65) activation through PTEN and PDCD4 enhancement in LSCC. [score:3]
Expression levels of miR-744-3p, PTEN mRNA and PDCD4 mRNA within the Ago2-IP complex were quantitated by Real-time PCR on LightCycler [®] 480. [score:3]
Generation of stable LSCC clone expressing miR-744-3p shRNA or PDCD4. [score:3]
The high miR-744-3p expression level could significantly increase the risk of lymph node metastasis in LSCC. [score:3]
As shown in Figure 4C and 4D, MMP- 9 mRNA and protein level were remarkably reduced in miR-744-3p suppressed SNU899 and SNU1076 (P < 0.05). [score:3]
By miR-744-3p suppression, PTEN and PDCD4 protein levels were significantly increased, while phosphorylated AKT and phosphorylated NF-κB protein levels were significantly reduced. [score:3]
The association between high miR-744-3p expression and regional lymph node positive suggested that miR-744-3p could possibly play a part in controlling LSCC migration and invasion. [score:3]
The reduction of miR-744-3p could significantly inhibit the LSCC cell migration and invasion. [score:3]
In SNU899 and SNU1076 with miR-744-3p suppression, the levels of PTEN and PDCD4 proteins were significantly increased, while phosphorylated AKT and phosphorylated NF-κB (p65) protein levels were significantly reduced. [score:3]
By miR-744-3p suppression, MMP-9 protein level was significantly reduced. [score:3]
Suppressing miR-744-3p reduced the metastatic ability of LSCC. [score:3]
Similar enhancement of luminenscent signal intensity due to miR-744-3p suppression was not observed in the groups with mutant PTEN 3′-UTR sequence or mutant PDCD4 3′-UTR sequence. [score:3]
The two single strands of the 3′- UTR of PTEN harboring a mutation in the binding sites of hsa-miR-744-3p were also synthesized. [score:2]
The Luciferase vectors containing the binding sites for miR-744-3p in 3′-UTR of PDCD4 with or without mutation were constructed using the above methods. [score:2]
Compared with the mock control, the stable LSCC clone compromising miR-744-3p shRNA exhibited significant reduction of miR-744-3p expression level. [score:2]
MiR-196a, miR-196b and miR-744-3p were significantly overexpressed in LSCC compared with their paired normal counterparts (P < 0.05). [score:2]
Next, we validated the microarray results by analyzing the aberrant expressed microRNA level (miR-7-1-3p, miR- 196a, miR-196b, miR-744-3p, let-7a-3p, miR-34a- 3p, miR-338-5p and miR-365a-5p) in a cohort of 47 LSCC tissues using QPCR and compared with the paired normal tissues (Figure 1). [score:2]
MiR-744-3p targeted PDCD4 and PTEN transcript in LSCC. [score:2]
Figure 7 MiR-744-3p promotes LSCC metastasis by simultaneously inhibiting PTEN and PDCD4. [score:2]
MiR-744-3p promotes LSCC metastasis by simultaneously inhibiting PTEN and PDCD4. [score:2]
We found that deregulation of miR-744- 3p was a common event in LSCC. [score:2]
MiR-744-3p was overexpressed in LSCC tissues. [score:2]
Compared with the mock control, MMP-9 mRNA level significantly decreased to 40% and 15% in SNU899 and SNU1076 when miR-744-3p shRNA were expressed in the LSCC cell lines (P < 0.05). [score:2]
Compared with mock control group, the suppression of miR-744- 3p significantly reduced miR-744-3p, PTEN and PDCD4 binding to the Ago2 protein. [score:2]
Collectively, our data suggested that miR-744-3p was an oncogenic microRNA in LSCC. [score:1]
In the mutant construct of which miR-744-3p binding sequence on the PDCD4 or PTEN 3′-UTR were disrupted, the luciferase activity remained stable with no significant changes. [score:1]
MiR-7-1-3p, miR- 196a, miR-196b and miR-744-3p were detected in LSCC but not normal epithelial cultures. [score:1]
Six transcripts (PDCD4, PTEN, SCN2B, IGFBP5, GPR64, BOC) had mirSVR score < −0.01 suggesting that they could potentially form thermodynamically stable complexes with the mature miR-744-3p (Table 3). [score:1]
The pGreenPuro-miR-744-shRNA or pCDH-PDCD4 vector as well as their mock vectors was further packaged into lentiviral particles by 293-FT cells (Life technologies) using the Lenti Starter Kit (System Biosciences). [score:1]
Mature miR-744-3p sequence, MIMAT0004946 was used in the computational analysis. [score:1]
To confirm the in vitro data, the miR-744-3p suppressed LSCC cell line was injected into nude mice and the formation of lung metastatic foci were evaluated on day 60 after injection. [score:1]
The sense and antisense strands of the 3′-UTR of PTEN containing the binding sites of hsa-miR-744- 3p were synthesized. [score:1]
MiR-7-1-3p, miR-196a, miR-196b and miR-744-3p were detected in LSCC but not normal epithelial cultures. [score:1]
Illustration of potential pathways for miR-744-3p mediating metastasis in LSCC. [score:1]
The association between miR-744-3p and PDCD4 or PTEN was further validated using luciferase activity reporter containing PDCD4 or PTEN 3′-UTR. [score:1]
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2
[+] score: 62
As shown in Figure 3, the expressions of miR-711, miR-714, miR-744, miR -2137, miR -5130, miR -346, and miR -328 was still upregulated in the I/R group, but the expression of miR-24 and miR-490 were downregulated, compared to the control group grafts. [score:10]
The expressions of miR-711, miR-714, miR-744, miR-2137, miR-5130, miR-1892, miR-328, miR-346, miR-5099, and miR-705 were significantly upregulated in I/R injured heart grafts, while miR-490, miR-491, miR-210, miR-362, miR-24, miR-423, miR-128, miR-328, miR -181, and miR-532 were downregulated. [score:9]
Recent studies have shown that miR-744 targets TGF-β and eukaryotic translation elongation factor 1 alpha 2(eEF1A2) which is able to promote cell growth and inhibit apoptosis [52], [53], [54]. [score:7]
The findings of our study demonstrate that miR-711, miR-2137 miR-705, miR-5130, miR-346, miR-714, and miR-744 were significantly upregulated (>2 fold change) in I/R injured hearts, while miR-210, miR-490, miR-491, miR-425, miR-423-3p, and miR-532-3p were downregulated. [score:7]
As compared with cells under normxia, miR-711, miR-714, miR-328, miR-346, miR-210, miR-744, miR-5130, miR-181a and miR-2137 were significantly over-expressed in hypoxia/reperfusion treated cardiomyocytes, while the expression of miR-491, miR-211, miR-532, miR-185, miR-425, miR-128, miR-24 was down-regulated (Figure 4B). [score:7]
Compared with grafts taken out on day 2 post-transplantation, the expression of miR-2137, miR-714, miR-744, miR -2137, miR -5130, miR -346, and miR -328 were slightly decreased, whilst the expression of miR-711 continued its upregulation in the I/R injured grafts. [score:7]
It has been reported that the expression of miR-714 and miR-744 are significantly higher in mice aorta with vascular calcification [48]. [score:3]
We extracted grafts with I/R and with non-I/R at day 7 after transplantation and detected the expression level of miRNAs (miR-711, miR -714, miR-744, miR -2137, miR -5130, miR -346, miR -490, miR -491, miR -24, and miR -328). [score:3]
miR-744 is known to be expressed in cardiac valves [49] and involved in cancer cell growth and proliferation [50], [51]. [score:3]
Additionally, miR-2137, miR-1893, miR-744, miR-705 and miR-714 are highly expressed in heart tissue and cardiomyocytes as well, suggesting that these miRNA are important for cardiomyocytes survival and growth. [score:3]
Taken together, the increased expression of miR-2137 may play a role in I/R injury in heart transplantation through regulating CAMTA 1. miR-705, miR-714 and miR-744 have not been extensively investigated yet. [score:2]
Our data showed that eEF1A2 was decreased in I/R injured hearts, implying that there may be a causative relationship between miR-744 and eEF1A2. [score:1]
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3
[+] score: 47
Ischemia for 2 h without reperfusion induced upregulation of miR-21 expression that could still be detected after reperfusion for 1 and 7 d. In addition, miR-493 expression could be observed after ischemia and reperfusion for 4 h and 1 d but did not last for 7 d. When miRNA expression was compared in the muscle samples of C57BL/6 and Tlr4 [−/−]/ NF- κB [−/−] mice subjected to 2 h of ischemia and 1 d of reperfusion, only 3 miRNAs (miR-15a, miR-744, and miR-1196) showed significantly increased expression in C57BL/6 mice and decreased expression in Tlr4 [−/−]/ NF- κB [−/−] mice (Table 2). [score:13]
Among the dysregulated miRNAs, 3 TLR4/NF- κB-responsive miRNAs, miR-15a, miR-744, and miR-1196, were significantly upregulated in the skeletal muscles of C57BL/6 mice following IRI, but their expression notably decreased in similarly treated Tlr4 [−/−]/ NF- κB [−/−] mice. [score:7]
Three genes were regulated by at least 2 of these 3 upregulated miRNAs; that is, zinc finger BED domain containing 4 (Zbed4) was regulated by miR-15a, miR-744, and miRR-1196; leucine-rich repeat and sterile alpha motif containing 1 (Lrsam1), by miR-15a and miR-744; and the DEAD (Asp-Glu-Ala-Asp) box polypeptide 21 (Ddx21), by miR-744 and miR-1196. [score:6]
Among these 3 upregulated miRNAs, miR-15a showed increased expression in response to myocardial IRI [40], but association of miR-744 and miR-1196 with IRI has not been previously reported. [score:6]
The combined approach showed 5, 4, and 20 potential target genes for miR-15a, miR-744, and miR-1196, respectively, in the IRI muscle samples (Table 3). [score:3]
miRNA array analysis showed that the expression of miR-1196, but not miR-15a or miR-744, persisted till 7 d of reperfusion (Table 1). [score:3]
This study has profiled TLR4/NF- κB-responsive miRNAs (miR-15a, miR-744, and miR-1196) in thigh skeletal muscle isolated following IRI and identified their potential target genes by using prediction algorithms and RNA -binding protein immunoprecipitation microarray profiling of Ago2 immunoprecipitated complexes. [score:3]
Microarray and qPCR results of five miRNA targets including miR-15a, miR-744, and miR-1196 in the experimental muscle of C57BL/6 mice after 2 h of ischemia and 1 d of reperfusion were in general agreement, with a Pearson correlation value of 0.912 (Supplementary File 2). [score:3]
Notably, miR-744-directed posttranscriptional regulation of TGF- β1 is of central importance in wound healing, inflammation, and progressive tissue fibrosis, in human proximal tubular epithelial cells HK-2 [41]. [score:3]
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4
[+] score: 38
A hypothetical mo del of age -dependent miRNAs regulating LCs development and function is shown in Figure 6. Table 1 miRNAs in aging putative targets function in LC reference miR709↑ RANK LC development and homeostasis↓ 49 IRF8 LC development and homeostasis↓ 29 AhR impair LC maturation 33 miR449↑ TGFβRII LC development and homeostasis↓ 32, 46 RunX3 LC development and homeostasis↓ 30 CSF1R LC development and survival↓ 35 miR9↑ TGFβRII LC development and turnover↓ 32, 46 RunX3 LC development and homeostasis↓ 30 RANK LC development and homeostasis↓ 49 miR10a↓ Gfi1 LC development and homeostasis↓ 28 miR200c↓ C/EBP LC differentiation↓ 31 Langerin LC antigen uptake ↑ 22, 23 Gfi1 LC development and homeostasis↓ 28 miR744↓ TGFβI inhibit LC maturation 32, 46 miR20b↓ RANKL inhibit LC maturation 34 miR205↓ C/EBP LC differentiation↓ 31 The density of LCs in the epidermis is known to decrease with age in mice [21]. [score:19]
A hypothetical mo del of age -dependent miRNAs regulating LCs development and function is shown in Figure 6. Table 1 miRNAs in aging putative targets function in LC reference miR709↑ RANK LC development and homeostasis↓ 49 IRF8 LC development and homeostasis↓ 29 AhR impair LC maturation 33 miR449↑ TGFβRII LC development and homeostasis↓ 32, 46 RunX3 LC development and homeostasis↓ 30 CSF1R LC development and survival↓ 35 miR9↑ TGFβRII LC development and turnover↓ 32, 46 RunX3 LC development and homeostasis↓ 30 RANK LC development and homeostasis↓ 49 miR10a↓ Gfi1 LC development and homeostasis↓ 28 miR200c↓ C/EBP LC differentiation↓ 31 Langerin LC antigen uptake ↑ 22, 23 Gfi1 LC development and homeostasis↓ 28 miR744↓ TGFβI inhibit LC maturation 32, 46 miR20b↓ RANKL inhibit LC maturation 34 miR205↓ C/EBP LC differentiation↓ 31 (A) LCs were isolated using AutoMACS with anti-MHCII-PE and anti-PE microbeadsfollowed by a cell sorter. [score:19]
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5
[+] score: 29
Finally, the fact that consistent expression of five genes in circulating miRNA expression profiles exists from multiple mouse strains, at different ages, and with different disease mo dels provides strong evidence that miR-146a, miR-16, miR-195, miR-30e, and miR-744 are useful as circulating miRNA endogenous references. [score:7]
As shown in Figure 2, miR-146a and miR-16 are highly expressed in serum, while miR-30e, miR-195, and miR-744 have lower expression levels. [score:5]
As shown in Figure 2, these five serum miRNAs, miR-146a, miR-16, miR-195, miR-30e, and miR-744 were stably expressed in mouse regardless of strain, age, and disease condition. [score:5]
Furthermore, miR-146a and miR-16 are highly expressed in serum, while miR-30e, miR-195, and miR-744 have relatively lower expression. [score:5]
We have found five miRNAs, miR-146a, miR-16, miR-195, miR-30e, and miR-744 to be stably expressed in all tested strains across different ages and conditions. [score:3]
Notably, these five miRNAs, miR-16, miR-744, miR-195, miR-146a, and miR-30e share a 100% identity between human and mouse [32], [33], [34], [35]. [score:1]
−ΔC [T] values of miR-146a, miR-16, miR-195, miR-30e, and miR-744 show stability across all samples (w = weeks). [score:1]
0031278.g002 Figure 2−ΔC [T] values of miR-146a, miR-16, miR-195, miR-30e, and miR-744 show stability across all samples (w = weeks). [score:1]
These 72 miRNAs were candidate endogenous controls, following a series of statistical analyses only five genes (miR-146a, miR-16, miR-195, miR-30e, and miR-744) passed the criteria of ANOVA p>0.3, SD<1, and pair-wise |ΔΔ C [T]|<0.5. [score:1]
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6
[+] score: 25
We detected 2.4-fold upregulation of miR-431, a twofold upregulation of miR-744, and a 2.5-fold upregulation of miR-21, respectively (Figure 1B). [score:10]
In agreement with the microarray data, miR-431, miR-744, and miR-21 were significantly upregulated in regenerating neuronal cells. [score:4]
The graph indicates a significant increase of miR-744, miR-431, and miR-21 in DRG after sciatic nerve crush, whereas the expression level of miR-124 and miR 29a did not change (* p < 0.05, ** p < 0.01, N = 3). [score:3]
miR-431, miR-714, miR-744, miR-877, miR-130b, miR-21, miR-323-3p, miR-325, miR-409-3p, miR-154*, and miR-681 were significantly increased 4 days post-sciatic nerve crush in pre-conditioned DRGs, while miR-190, miR-1, miR-33, miR-32, miR-153, miR-335-5p, miR-193, and miR-488 showed significantly decreased expression. [score:3]
We also included miR-744 and miR-21 as positive controls and miR-124 and miR-29a as non-regulated controls in our real-time PCR experiments. [score:2]
miR-21: 5′-TAGCTTATCAGACTGATGTTGA-3′ miR-431: 5′-CAGGCCGTCATGCAAA-3′ miR-744: 5′-GGGCTAGGGCTAACAGCA-3′ miR-124: 5′-GCGGTGAATGCCAAAAA-3′ miR-29a: 5′-TAGCACCATCTGAAATCGGTTA-3′ Kremen1: 5′-ACAGCCAACGGTGCAGATTAC-3′ and 5′-TGT TGTACGGATGCTGGAAAG-3′ GAP-43: 5′TGGTGTCAAGCCGGAAGATAA-3′ and 5′-GCTG GTGCATCACCCTTCT-3′ S-12: 5′-TGGCCCGGCCTTCTTTATG-3′ and 5′-CCTAAGCG GTGCATCTGGTT-3′ Data from multiple independent experiments were analyzed with GraphPad Prism version 5 for Windows (GraphPad Software, San Diego, CA, USA). [score:1]
miR-21: 5′-TAGCTTATCAGACTGATGTTGA-3′ miR-431: 5′-CAGGCCGTCATGCAAA-3′ miR-744: 5′-GGGCTAGGGCTAACAGCA-3′ miR-124: 5′-GCGGTGAATGCCAAAAA-3′ miR-29a: 5′-TAGCACCATCTGAAATCGGTTA-3′ Kremen1: 5′-ACAGCCAACGGTGCAGATTAC-3′ and 5′-TGT TGTACGGATGCTGGAAAG-3′ GAP-43: 5′TGGTGTCAAGCCGGAAGATAA-3′ and 5′-GCTG GTGCATCACCCTTCT-3′ S-12: 5′-TGGCCCGGCCTTCTTTATG-3′ and 5′-CCTAAGCG GTGCATCTGGTT-3′ Data from multiple independent experiments were analyzed with GraphPad Prism version 5 for Windows (GraphPad Software, San Diego, CA, USA). [score:1]
miR-21: 5′-TAGCTTATCAGACTGATGTTGA-3′ miR-431: 5′-CAGGCCGTCATGCAAA-3′ miR-744: 5′-GGGCTAGGGCTAACAGCA-3′ miR-124: 5′-GCGGTGAATGCCAAAAA-3′ miR-29a: 5′-TAGCACCATCTGAAATCGGTTA-3′ Kremen1: 5′-ACAGCCAACGGTGCAGATTAC-3′ and 5′-TGT TGTACGGATGCTGGAAAG-3′ GAP-43: 5′TGGTGTCAAGCCGGAAGATAA-3′ and 5′-GCTG GTGCATCACCCTTCT-3′ S-12: 5′-TGGCCCGGCCTTCTTTATG-3′ and 5′-CCTAAGCG GTGCATCTGGTT-3′Data from multiple independent experiments were analyzed with GraphPad Prism version 5 for Windows (GraphPad Software, San Diego, CA, USA). [score:1]
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7
[+] score: 21
For example, miR-652 is upregulated, whereas miR-744 is downregulated in older hearts. [score:7]
Short-term overexpression of miR-744 results in enhanced cell proliferation, while long-term expression causes chromosomal instability and tumor suppression in vivo [84]. [score:7]
These miRNAs include miR-652, miR-711, miR-744, and miR-762, all of which are downregulated during aging. [score:4]
miR-744 is also found differentially expressed in senescent cell lines and mesenchymal stem cells. [score:3]
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8
[+] score: 12
Out of these, eight miRNAs were affected after both low- and high-dose irradiation: five miRNAs (mmu-miR-33-3p, mmu-miR-200c-5p, mmu-miR-140-3p, mmu-miR-744-3p, and mmu-miR-669o-5p) were downregulated and three miRNAs (mmu-miR-152-3p, mmu-miR-199a-5p, and mmu-miR-375-3p) were upregulated. [score:7]
Several miRNAs were connected to DNA damage repair as well such as miR-33 and miR-375, which were shown to regulate DNA damage checkpoint through the p53 (82, 84) and miR-744-3p, which significantly delayed IR -induced DNA damage repair by directly targeting RAD23B in prostate cancer cells (85). [score:5]
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9
[+] score: 11
AMPK is a known inhibitor of TGF 40, which was targeted by three miRNAs (miR-26a, miR-26b, and miR-744) that were upregulated by metformin in mouse lung. [score:8]
01 Stress response, cell proliferation miR-542 ↓2.60 NA miR-574 ↑2.09 Inflammation (Tlr9 activation), cell proliferation, apoptosis miR-669j ↑3.12 NA miR-672 ↑2.40 NA miR-674 ↑2.19 NA miR-744 ↑4.35Oncogene (Tgf) suppression miR-873 ↑2.53 ↑3.22 NA miR-1930 ↑3.31 NA miR-1934 ↑2.17 ↑3.27 NA miR-1942 ↑2.49 NA miR-3064 ↑2.50 NA miR-3065 ↑3.20 NA miR-3069 ↑2.98 NA miR-3071 ↑3.51 NA miR-3073 ↓2.78 NA miR-3092 ↑3.48 NA miR-3093 ↑3.28 NA miR-3109 ↓2.07 NAAll reported variations were statistically significant (P < 0.05). [score:3]
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10
[+] score: 8
Finally, the remaining 24 miRNA exhibited differential expression between tumor and parenchyma in both the absence and presence of cigarette smoke exposure, including 2 miRNA (mmu-miR-135b-5p, mmu-miR-1198-5p), whose expression levels increased in parenchyma but remained stable in tumor tissue following MS exposure, 5 miRNA (mmu-miR-21-5p, mmu-miR-31-5p, mmu-miR-146b-5p, mmu-miR-665-3p, mmu-miR-744-5p) that remained more highly expressed in tumors compared to parenchyma, and 17 miRNA with lower expression levels in tumors than in parenchyma, even upon cigarette smoke exposure (Figure 8). [score:8]
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11
[+] score: 7
The most significantly downregulated (mmu-miR-31, mmu-miR-455, mmu-miR-744, mmu-miR-695, mmu-miR-181a, mmu-miR-181d, mmu-miR-182, mmu-miR-190, mmu-miR-194) and upregulated miRNAs (mmu-miR-34c, mmu-miR-124, mmu-miR-142–3p, mmu-miR-706, mmu-miR-29c) were analyzed. [score:7]
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12
[+] score: 6
In contrast, 5 miRNAs were downregulated in infected BV-2 cells: miR-let7b (4.0x), miR-207 (3.9x), miR-146a and miR-744 (both 2.1x), and miR-17 which was highly expressed in uninfected cells and decreased to below the level of detection with infection, representing the greatest change in BV-2s (Figure 1B). [score:6]
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13
[+] score: 4
By performing microarray screening on exosomes, we found nine inflammatory miRNAs which were deregulated in sera of chronic alcohol-fed mice compared to controls including upregulated miRNAs: miRNA-192, miRNA-122, miRNA-30a, miRNA-744, miRNA-1246, miRNA 30b and miRNA-130a. [score:4]
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[+] score: 3
MiR-744 and miR-1186 induce Ccnb1 expression and manipulate mouse cell proliferation with putative binding site in the gene promoter [11]. [score:3]
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Out of these, miR-208b-3p, miR-467b-5p, miR-345-3p, and miR-744-3p were differentially expressed during infection in both mouse strains. [score:3]
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[+] score: 3
Some microRNAs have been shown to target the promoters of genes and cause either gene activation (miR-373, miR-744, miR-1186) or gene repression (miR-320, miR-373). [score:3]
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[+] score: 2
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, mmu-mir-365-1, 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, 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
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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[+] score: 1
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-mir-208a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-328, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, mmu-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, mmu-mir-208b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, mmu-mir-299b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
The four novel miRNAs identified by miRdentify partially overlapped with known miRNAs: the ecaub_novel-miR-1175 was only two nucleotides shorter than eca-mir-744, ecaub_novel-mir-1176 overlapped the position of an Ensembl predicted ENSECAG00000025869, whereas the ecaub_novel-mir-1177 was identified on the opposite strand of the eca-mir-486, and ecaub_novel-mir-1778 was located in the region of another Ensembl predicted ENSECAG00000026103. [score:1]
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For the invariant method, we chose “mmu-miR-146a-5p”, “mmu-miR-16-5p”, “mmu-miR-30e-5p” and “mmu-miR-744-5p” as invariant serum miRNAs, as indicated in a previous study [40]. [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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-98, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-150, mmu-mir-155, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-217, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-150, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-34a, mmu-mir-98, mmu-mir-322, mmu-mir-338, hsa-mir-155, mmu-mir-17, mmu-mir-19a, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-217, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-338, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-18b, hsa-mir-503, mmu-mir-541, mmu-mir-503, mmu-mir-18b, hsa-mir-541, hsa-mir-744, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
miR-30d and miR150 as well as other miRNAs were induced by long-term culture for 2 weeks in the absence of differentiation stimulus, while miR-503 and miR-744 were reduced by the long-term culture (Fig. 4C, F). [score:1]
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We also noticed that a significant number of miRNAs (such as miR-516-3p, miR-744 and miR-506) that had not been previously annotated in male infertility studies were enriched in these gene sets. [score:1]
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