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34 publications mentioning mmu-mir-423

Open access articles that are associated with the species Mus musculus and mention the gene name mir-423. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 205
Training-Induced Downregulation of HCN4 and I [f] and Resulting Sinus Bradycardia Is result of Upregulation of miR-423-5pWe hypothesized that the training -induced upregulation of miR-423-5p results in the downregulation of HCN4 and, consequently, a lower heart rate. [score:13]
In the exercise-trained mouse, we then identified an upregulation of miR-423-5p (regulatory microRNA) and Nkx2.5 (transcription factor)—further experiments showed that Nkx2.5 can upregulate miR-423-5p and miR-423-5p can downregulate HCN4. [score:11]
In addition, we show that HCN4 is a novel target for post-transcriptional repression by miR-423-5p and the training -induced downregulation of HCN4 and I [f], and consequently, the bradycardia is the result of an upregulation of Nkx2.5 and consequently miR-423-5p in the sinus node. [score:9]
We selected miR-423-5p for further study because it was predicted to target HCN4, it was significantly upregulated using both next-generation sequencing (2.8-fold increase above baseline) and qPCR (8.1-fold increase above baseline), and it produced the largest suppression of luciferase activity among the miRs tested. [score:8]
After applying a 5% Benjamini–Hochberg false discovery rate correction, miR-5099, miR-486-3p, miR-423-5p, Let-7d-3p, miR-676-3p, miR-181b-5p, and Let-7e-5p were significantly upregulated and miR-10b-5p downregulated (Figure 2E, hatched bars). [score:7]
We hypothesized that the training -induced upregulation of miR-423-5p results in the downregulation of HCN4 and, consequently, a lower heart rate. [score:7]
Training-Induced Downregulation of HCN4 and I [f] and Resulting Sinus Bradycardia Is result of Upregulation of miR-423-5p. [score:7]
Further experiments showed that in the sinus node of swim-trained mice, upregulation of miR-423-5p (intronic miR) and its host gene, NSRP1, is driven by an upregulation of the transcription factor Nkx2.5. [score:7]
We conclude from these data that the upregulation of miR-423-5p in the sinus node after training involves an upregulation of the transcription factor, Nkx2.5. [score:7]
In the mouse, evidence suggests that the downregulation of HCN4 and I [f] is the result of an upregulation of Nkx2.5 and, consequently, miR-423-5p. [score:7]
Upregulation of miR-423-5p appeared to be restricted to the trained sinus node—basal expression of miR-423-5p was lower in the atrium and ventricle and was unaltered by training (Figure 3F). [score:6]
2– 4 Inhibition of miR-423-5p (especially because upregulation of miR-423-5p could be restricted to the sinus node; Figure 3F) could be an alternative therapeutic strategy to electronic pacemaker implantation for pathological sinus node dysfunction seen in some veteran athletes. [score:6]
It is possible that miR-423-5p is one of 20% of intronic miRs that are predicted to inhibit expression of their host gene. [score:5]
Although Figure 3A through 3C shows that miR-423-5p targets HCN4, it is possible that it has other targets. [score:5]
Interaction between miR-423-5p and HCN4 was confirmed by a dose -dependent reduction in HCN4 3′-untranslated region luciferase reporter activity on cotransfection with precursor miR-423-5p (abolished by mutation of predicted recognition elements). [score:4]
Furthermore, mutation of predicted miR-423-5p binding sequences in the HCN4 3′- UTR (Figure 3B) abolished the effect of miR-423-5p on reporter expression (Figure 3C). [score:4]
[31] In this case, whether Nkx2.5 upregulates both NSRP1 and miR-423-5p may depend on the precise circumstances. [score:4]
B, Anti-miR abolishes training -induced upregulation of miR-423-5p in sinus node. [score:4]
F, Upregulation of miR-423-5p by Nkx2.5. [score:4]
HCN4 Is Target Gene for miR-423-5p. [score:3]
[39] Previously, the plasma level of miR-423-5p has been reported to be elevated in heart failure, acute myocardial infarction, stable coronary artery disease, and patients undergoing cardiac surgery. [score:3]
Both HCN4 mRNA and intrinsic heart rate showed a significant inverse correlation with expression of miR-423-5p (Figure 3D and 3E). [score:3]
Linear regression analysis showed that the sinus node expression level of miR-423-5p explained 68% of the variation in HCN4 (Figure 3D; R [2] = 0.68) and 46% of the variation in spontaneous beating rate of the sinus node (Figure 3E; R [2] = 0.46). [score:3]
[17] Using the wi dely used algorithms RNA22, [18] PITA, [19] and TargetScan Mouse v7.1, [20] we identified putative recognition sites for miR-423-5p (Online Figure II) and miR-486-3p (data not shown) within the mouse HCN4 3′-UTR sequence. [score:3]
miR-423-5p contributes to training -induced bradycardia by targeting HCN4. [score:3]
A separate study demonstrated that the suppressive effect of the anti-miR on miR-423-5p persisted for up to 3 weeks after administration (Online Figure IV). [score:3]
Nabiałek E Wańha W Kula D Circulating microRNAs (miR-423-5p, miR-208a and miR-1) in acute myocardial infarction and stable coronary heart disease. [score:3]
miR-423-5p could be a therapeutic target for pathological sinus node dysfunction in veteran athletes. [score:3]
miR-423-5p expression is shown in H9c2 cells not transfected (control) or transfected with Nkx2.5. [score:3]
Miyamoto S Usami S Kuwabara Y Horie T Baba O Hakuno D Nakashima Y Nishiga M Izuhara M Nakao T Nishino T Ide Y Nakazeki F Wang J Ueyama K Kimura T Ono K Expression patterns of miRNA-423-5p in the serum and pericardial fluid in patients undergoing cardiac surgery. [score:3]
To verify these predicted binding sites and experimentally establish HCN4 as a genuine target, we fused the HCN4 3′-UTR to a luciferase reporter gene (pHCN4-3′ UTR) and determined luciferase activity in H9c2 cells cotransfected with pHCN4-3′ UTR and synthetic precursors to miR-423-5p and miR-486-3p. [score:3]
Figure 3F suggests that miR-423-5p is preferentially expressed by the sinus node, and this raises the question of whether the sinus node is the source of miR-423-5p in heart failure. [score:3]
Surprisingly, Nkx2.5 had little effect on expression of NSRP1 (Online Figure IX), but it resulted in a robust increase in miR-423-5p (Figure 5F). [score:3]
Figure 3. HCN4 (hyperpolarization-activated cyclic nucleotide gated channel 4) is a target gene for miR-423-5p. [score:3]
miR-423 is located in the first intron of its host gene, NSRP1, and both are transcribed in the same sense direction (Figure 5A). [score:2]
All miRs tested significantly supressed luciferase activity relative to a control (scrambled) miR, although suppression was modest on transfection with miR-1 and miR-486-3p (34%; data not shown) compared with miR-423-5p (Figure 3A). [score:2]
[46] While our data suggest a prominent role for miR-423-5p in regulating HCN4, we cannot rule out a role for other miRs. [score:2]
Luo P He T Jiang R Li G MicroRNA-423-5p targets O-GlcNAc transferase to induce apoptosis in cardiomyocytes. [score:2]
Intriguingly, the anti-miR did not alter the heart rate in vivo in sedentary animals, despite successful knockdown of miR-423-5p (Online Figure V); the effect of the anti-miR was, therefore, restricted to the trained mouse. [score:2]
To test this, miR-423-5p was knocked down in vivo via 3 daily intraperitoneal injections of cholesterol-conjugated anti-miR-423-5p (anti-miR) in sedentary mice and in trained mice at day 25 to 27 of the swimming protocol (Figure 4A). [score:2]
Figure 5. Nkx2.5 regulation of miR-423-5p. [score:2]
Knockdown of miR-423-5p with anti-miR-423-5p reversed training -induced bradycardia via rescue of HCN4 and I [f]. [score:2]
[42] In these studies, although the source of miR-423-5p may be the myocardium, it is not known from what part of the heart it originates. [score:1]
After 2 weeks of detraining (after 4 weeks of training), there was a partial restoration of miR-423-5p (Figure 3G). [score:1]
Figure 4. Anti-miR to miR-423-5p reverses training -induced bradycardia and blunts HCN4 (hyperpolarization-activated cyclic nucleotide gated channel 4) channel remo deling. [score:1]
Computational predictions highlighted a prominent role for miR-423-5p. [score:1]
Control of miR-423-5p in the Trained Sinus Node. [score:1]
B, Predicted miR-423-5p binding sites in HCN4 3′-UTR and corresponding sequence of mutant HCN4 3′-UTR tested. [score:1]
miR-423-5p (determined by quantitative real-time reverse transcription polymerase chain reaction [qPCR]) in sinus node of vehicle- or anti–miR -treated sedentary and trained mice shown (n=6/5/5/5). [score:1]
G, Expression of miR-423-5p (measured by qPCR) in sinus node is partially restored on detraining (right). [score:1]
We observed a dose -dependent effect of miR-423-5p on luciferase activity of pHCN4-3′ UTR (Figure 3C). [score:1]
F, Expression of miR-423-5p (measured by quantitative real-time reverse transcription polymerase chain reaction [qPCR]) in atrium and ventricle is low and unaltered by training. [score:1]
qPCR analysis confirmed the majority of these changes (including in miR-423-5p; Figure 2F). [score:1]
[6] At day 28, that is, 3 days after the first administration, qPCR analysis showed a dramatic reduction in the level of miR-423-5p (Figure 4B). [score:1]
These findings demonstrate a specific interaction between miR-423-5p and HCN4, and the predicted recognition elements identified in the HCN4 3′ -UTR contribute to this. [score:1]
Luciferase activity is shown 24 h after cotransfection with different amounts of wild-type or mutant miR-423-5p. [score:1]
C, Luciferase reporter assay showing dose -dependent repression of HCN4 by miR-423-5p and loss of repression by mutation of HCN4 3′-UTR. [score:1]
A, map of NSRP1 gene (solid blocks show exons with introns in between) showing location of Nkx2.5 binding sites and intronic location of the miR-423 gene. [score:1]
D, Relationship between HCN4 mRNA and log miR-423-5p in sedentary and trained mice (n=5/5). [score:1]
In the mouse, the training -induced bradycardia is reversed by blocking the action of miR-423-5p. [score:1]
Blocking miR-423-5p with an anti-miR reversed the training -induced sinus bradycardia. [score:1]
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[+] score: 63
The expression of these 3 miRNA targets (miR-320, miR-762, and miR-423-5p) was found to be significantly upregulated in the serum (Figure  2B). [score:8]
However, in this study, daily FK506 injection for 7 d in sham-operated mice revealed no significant increase of these 3 circulating miRNAs in the serum, which implies that the expression of circulating miR-320, miR-762, and miR-423-5p can only be induced under FK506 immunosuppression, but not under allogeneic condition, and therefore may potentially serve as biomarkers for sufficient immunosuppression. [score:7]
miR-320, miR-762, and miR-423-5p were significantly upregulated in the whole blood and serum, but not in the nerve graft, of the mice receiving an allograft with FK506 immunosuppression at 1, 3, 7, 10, and 14 d after nerve allotransplantation. [score:6]
In this study, we have demonstrated that none of the 3 circulating miRNAs (miR-320, miR-762, and miR-423-5p) was significantly expressed in nerve allografts; effective mo dels for identifying the origin of these expressed circulating miRNAs are still not available. [score:5]
With around 4- to 6-fold expression, miR-320, miR-762, and miR-423-5p were significantly upregulated in the whole blood of the mice receiving allograft with FK506 at 1, 3, 7, 10, and 14 d after nerve allotransplantation, when compared to those mice receiving allograft without FK506 (Figure  2A). [score:5]
miR-423 has been defined also as a new oncogenic miRNA in hepatocellular carcinoma through the suppression of the tumor suppressor p21Cip1/Waf1 [56]. [score:5]
To clarify whether the expression of circulating miRNAs was induced by FK506 per se, that is, regardless of the nerve allotransplantation, we quantified the expression of miR-320, miR-762, and miR-423-5p in the serum drawn from sham-operated mice with or without daily FK506 injection for 7 d by using qRT-PCR. [score:5]
We only found 3 significantly expressed circulating miRNAs (miR-320, miR-762, and miR-423-5p) in the mice receiving allograft with FK506 against those without FK506 immunosuppression. [score:5]
In addition, no significant expression of these 3 circulating miRNAs (miR-320, miR-762, and miR-423-5p) was found in the nerve graft of the mice receiving allograft with FK506 (Figure  3). [score:3]
Three circulating miRNAs (miR-320, miR-762, and miR-423-5p) were identified in the whole blood and serum of the mice receiving an allograft with FK506 immunosuppression, within 2 weeks after nerve allotransplantation. [score:3]
We identified the circulating miR-320, miR-762, and miR-423-5p as potential biomarkers for monitoring the immunosuppression status of the nerve allograft. [score:3]
We identified the circulating miR-320, miR-762, and miR-423-5p as potential biomarkers for monitoring the immunosuppression status of nerve allografts. [score:3]
In addition, there was significant expression of 3 miRNAs (miR-320, miR-762, and miR-423-5p) in the mice receiving an allograft with FK506, when compared to those mice receiving allograft without FK506. [score:2]
Three miRNAs (miR-320, miR-762, and miR-423-5p) in the circulation and 3 miRNAs (miR-125b-3p, miR-672, and miR-467b*) in the nerve graft were subjected to further quantification and validation. [score:1]
No association of miR-423-5p with neurological illness or immunological condition has been reported in the literature. [score:1]
Elevated serum levels of miR-423-5p correlated with important clinical prognostic parameters in systolic heart failure patients [53] and served as a diagnostic biomarker for heart failure caused by dilated cardiomyopathy [54] or left ventricle remo deling after myocardial infarction [55]. [score:1]
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[+] score: 40
Seven of these miRNAs were found to be significantly downregulated (miR-449a-3p, miR-298-5p, miR-92a-1-5p, miR-423-5p, miR-423-3p, miR-128-3p, miR-340-3p), and 1 was found to be significantly upregulated (miR-21a-3p) at 6 hours after transient scrotal heat treatment. [score:7]
MiR-449a-3p, miR-298-5p, miR-92a-1-5p, miR-423-5p, miR-423-3p, miR-128-3p and miR-340-3p were found to be significantly downregulated (A-G, all p < 0.05), and miR-21a-3p was found to be significantly upregulated at 6 hours after heat treatment (J, p = 0.006). [score:7]
Altogether, our and previous findings have led us to hypothesize that miR-423-5p downregulation may contribute to heat stress -induced spermatogenic impairment, as increased germ cell apoptosis and suppressed germ cell proliferation were identified as the main mechanisms leading to heat-stress induced testicular damage [31, 32]. [score:6]
We further identified significant associations of miR-449a-3p, miR-92a-1-5p, miR-423-3p, and miR-21a-3p with the germ cell AI, suggesting that these miRNAs may directly or indirectly regulate apoptosis-related pathways. [score:4]
Furthermore, our report is the first to identify the downregulation of miR-423-5p in the testis in response to scrotal hyperthermia. [score:4]
Finally, we validated the differential expression levels of miR-449a-3p, miR-92a-1-5p, miR-423-3p, miR-340-3p, and miR-21a-3p, which were in agreement with our sequencing results. [score:3]
Other studies found that miR-423-5p regulates gastric cancer cell proliferation and invasion [29] and promotes hepatocarcinoma cell autophagy [30]. [score:2]
Previously, Wan et al. reported that miR-423-5p knockdown correlated with reduced proliferation and increased mitochondria -dependent apoptosis among glioma stem cells [28]. [score:2]
The relative levels of miR-449a-3p (A), miR-92a-1-5p (C), miR-423-3p (E) and miR-128-3p (F) correlated significantly and negatively with the germ cell AI (r = -0.58, -0.58, -0.45, and -0.48, respectively; p = 0.007, 0.007, 0.045, and 0.033, respectively); the relative level of miR-21a-3p (H) correlated significantly and positively with the AI (r = 0.56, p = 0.01). [score:1]
We found that the relative levels of miR-449a-3p, miR-92a-1-5p, miR-423-3p and miR-128-3p correlated significantly and negatively with the germ cell AI (r = -0.58, -0.58, -0.45, and -0.48, respectively; p = 0.007, 0.007, 0.045, and 0.033, respectively). [score:1]
Finally, some of the identified miRNAs (e. g., miR-449a-3p, miR-92a-1-5p, miR-423-3p, and miR-128-3p) correlated closely with germ cell apoptosis. [score:1]
Figure 7The relative levels of miR-449a-3p (A), miR-92a-1-5p (C), miR-423-3p (E) and miR-128-3p (F) correlated significantly and negatively with the germ cell AI (r = -0.58, -0.58, -0.45, and -0.48, respectively; p = 0.007, 0.007, 0.045, and 0.033, respectively); the relative level of miR-21a-3p (H) correlated significantly and positively with the AI (r = 0.56, p = 0.01). [score:1]
The relative levels of miR-298-5p (B), miR-423-5p (D) and miR-340-3p (G) were not significantly correlated with germ cell AI. [score:1]
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[+] score: 23
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-99a, mmu-mir-140, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-192, hsa-mir-148a, hsa-mir-30d, mmu-mir-122, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-122, hsa-mir-140, hsa-mir-191, hsa-mir-320a, mmu-mir-30d, mmu-mir-148a, 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-21a, mmu-mir-22, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-92a-2, mmu-mir-25, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-92a-1, hsa-mir-26a-2, hsa-mir-423, hsa-mir-451a, mmu-mir-451a, hsa-mir-486-1, mmu-mir-486a, bta-mir-26a-2, bta-let-7f-2, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-320a-2, bta-mir-99a, bta-mir-181a-2, bta-mir-27b, bta-mir-140, bta-mir-92a-2, bta-let-7d, bta-mir-191, bta-mir-192, bta-mir-22, bta-mir-423, bta-let-7g, bta-mir-10b, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, hsa-mir-1246, bta-mir-24-1, bta-mir-26a-1, bta-mir-451, bta-mir-486, bta-mir-92a-1, bta-mir-181a-1, bta-mir-320a-1, mmu-mir-486b, hsa-mir-451b, bta-mir-1246, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2
It is possible that bta-miR-423-5p may be upregulated in dairy cattle affected with mastitis, whereas circulating bta-miR-423-5p may be down-regulated in beef cattle when exposed to a pathogen that produces respiratory disease. [score:9]
Several microRNAs had similar expression when comparing results from the present study with those of There were nine microRNAs (bta-miR-10b, bta-miR-423-3p, bta-miR-99a-5p, bta-miR-181a, bta-miR-423-5p, bta-miR-148a, bta-miR-26a, bta-miR-192, and bta-miR-486), that were upregulated in earlier stages of life in both studies. [score:6]
Jin et al. [22], using bovine mammary gland epithelial cells challenged with E. coli, found an upregulation of bta-miR-423-5p. [score:4]
Punga et al [31], in a study using lung samples affected with myasthenia gravis (a chronic autoimmune disorder caused by an antibody -mediated attack against neuromuscular junctions) in humans, indicate that hsa-miR-423-5p is over-expressed. [score:3]
Serum antibody to M. bovis microRNA Negative Positive SE P-value bta-let-7b 11,691 15,421 1,200 0.0336 bta-miR-24-3p 15,908 24,390 1,495 0.0002 bta-miR-92a 83,405 64,330 4,156 0.0023 bta-miR-423-5p 124,920 101,818 6,315 0.0133 A total of 21 microRNAs were associated with season (Table 3). [score:1]
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5
[+] score: 16
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]
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]
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6
[+] score: 12
On the contrary, altered expression of miR-423-5p was significantly decreased in the group of men (NGT vs IGT) only. [score:3]
Statistical data analysis revealed that the mean expression level of 9 miRNAs (i. e. ; miR-128, miR-99b-5p, miR-130b-3p, miR-142-3p, miR-374a-5p, miR-423-5p, miR-484, miR-629-5p, let-7d-3p) was significantly different (student t-test p<0.05) across the studied groups (Table 2). [score:3]
As shown on Fig 1, altered expressions of miR-128 and miR-423-5p in pre-diabetic patients compared to controls were confirmed with high significance (p<0.05). [score:2]
Considering the whole population, this analysis revealed 4 differentially expressed miRNAs (miR-128, miR-130b-3p, miR-374a-5p, miR-423-5p) in subjects with prediabetes and T2DM patients compared to control subjects with normal glucose tolerance. [score:2]
Our study also highlighted that some miRNAs (miR-128 and miR-374a, miR-142-3p, let-7d-3p, miR-423-5p) had sex-specific associations with prediabetes or diabetes. [score:1]
On the contrary, miR-423-5p decreased in the serum of prediabetic patients (Fig 1) was negatively correlated to HDL-cholesterol. [score:1]
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[+] score: 9
We used miRNA Targets and Expression to examine the predicted targets for the five differentially expressed miRNAs that appeared across all 3 analysis tools using EdgeR (mmu-mir-31-5p, mmu-mir1249-3p, mmu-mir-423-5p, mmu-mir-3102-3p, mmu-mir-1247-5p; Enright et al., 2003; John et al., 2005; Betel et al., 2008, 2010). [score:9]
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[+] score: 8
Similarly, in our study (data not shown), miR-21 was upregulated 2-fold in both the ischemic kidneys and plasma at 24 hrs, and miR-423-3p was upregulated 4-fold in the plasma of animals that had undergone ischemia. [score:7]
Ramachandran et al reported miR-21, miR-200c, miR-423, and miR-4640 being present in the urine of patients with AKI [29]. [score:1]
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9
[+] score: 7
Other miRNAs from this paper: hsa-mir-423, hsa-mir-3184
Eighty five of them were upregulated, and two microRNAs (mir-423 and mir-3184) were downregulated (Fig. 4a and Supplementary File S1). [score:7]
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10
[+] score: 7
Besides the identification of differential expression of miRNAs, our initial studies identified three reference endogenous miRNAs (miR-103, miR-191, and miR-423-3p). [score:3]
Through pilot large-scale comprehensive profiling studies, we identified three reference miRNAs, miR-109, miR-191, and miR-423-3p with GeNorm and Normfinder that were invariant in the mouse samples and were used as reference miRNAs for those studies. [score:1]
Three reference miRNAs, in addition to the spiked in UniSp2 were used for normalization in the validation experiments (ΔCq = NF − Cq [miRNA]) were NF is the normalization factor and NF = (Cq [miR-103] + Cq [miR-191] + Cq [miR-423-3p] + Cq [UniSp2])/4. [score:1]
Additionally, GeNorm and NormFinder algorithms were run and identified miR-103, miR-191, and miR-423-3p as appropriate reference miRNAs 11. [score:1]
M values and stability factors for GeNorm and NormFinder identify miR-423-3p, miR-191, and miR-103 as endogenous reference miRNAs for mouse experiments. [score:1]
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11
[+] score: 7
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30b, mmu-mir-99a, mmu-mir-126a, mmu-mir-132, mmu-mir-141, mmu-mir-181a-2, mmu-mir-185, mmu-mir-193a, mmu-mir-199a-1, mmu-mir-200b, mmu-mir-34c, mmu-let-7d, mmu-mir-196a-1, mmu-mir-196a-2, 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-20a, mmu-mir-22, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-34a, mmu-mir-200c, mmu-mir-212, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-378a, mmu-mir-451a, mmu-mir-674, mmu-mir-146b, bta-mir-26a-2, bta-let-7f-2, bta-mir-16b, bta-mir-20a, bta-mir-26b, bta-mir-99a, bta-mir-126, bta-mir-181a-2, bta-mir-199a-1, bta-mir-30b, bta-mir-193a, bta-let-7d, bta-mir-132, bta-mir-199b, bta-mir-200a, bta-mir-200c, bta-mir-22, bta-mir-23a, bta-mir-29b-2, bta-mir-423, bta-let-7g, bta-mir-200b, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-23b, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-34a, bta-mir-141, bta-mir-146b, bta-mir-16a, bta-mir-185, bta-mir-196a-2, bta-mir-196a-1, bta-mir-199a-2, bta-mir-212, bta-mir-26a-1, bta-mir-29b-1, bta-mir-181a-1, bta-mir-2284i, bta-mir-2284s, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, bta-mir-2284w, bta-mir-2284x, bta-mir-2284y-1, mmu-let-7j, bta-mir-2284y-2, bta-mir-2284y-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2284y-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2284z-4, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285t, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2284ab, bta-mir-2284ac
For example, miR-146b-5p and miR-378a-3p were highly expressed in mouse but they were present at a low level of expression in bovine; inversely, miR-199b-5p, miR-423-5p and miR-193a-5p were weakly expressed in mouse but highly in bovine (Table S2). [score:7]
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12
[+] score: 6
hsa-let-7c, hsa-miR-370, and hsa-miR-423-5p were strongly expressed in OFSCs (transcripts per million > 2,000) but each of them targeted only one gene, making them less possible as the key regulator in this study. [score:6]
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13
[+] score: 6
Compared to ALK(−) ALCLs, miR-203, miR-135b, miR-886-5p/3p, miR-20b, miR-106a and miR-183 were significantly upregulated in ALK(+) ALCLs while others (miR-155, miR-181a, miR-210, miR-29a/b, miR-342-5p/3p, miR-369-3p miR-374a/b, miR-423-5p, miR-625, miR-205, miR-146a and miR-26a) were down-regulated (Table 1). [score:6]
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14
[+] score: 5
Expression levels were normalized against three stably expressed reference miRNAs (hsa-miR-125a, hsa-miR-423 and hsa-miR-92) validated with GeNorm [46] and analyzed using qbase+ software version 2.6 (http://www. [score:5]
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15
[+] score: 5
In man, high expression of miR-423, miR-199a-3p, miR-93*, and miR-377 in plasma[17] and low expression of miR-146a-5p and miR-155in whole blood can predict acute GvHD[18]. [score:5]
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16
[+] score: 5
Venn analyses revealed sixteen differentially expressed miRNAs in wildtype primary mesenchymal cells that were treated with dexamethasone (Fig. 1A), of which eleven were up regulated (let-7 family, miR-125b, miR-146a, miR-148a + b, miR-152, miR-423) (Table S1) and five were down regulated (miR-1724a, miR-23a+b, miR-24-1,-2, miR-29a) (Table S1). [score:5]
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17
[+] score: 5
In our prior report that profiles the circulating miRNAs expression in a mouse mo del of nerve allotransplantation, we used BALB/c mice as recipient animals and C57BL/6 mice as donor animals for full major histocompatibility complex (MHC) disparity [30, 31] and identified the circulating miR-320, miR-762, and miR-423-5p as potential biomarkers for monitoring the immunosuppression status of the nerve allograft [18]. [score:5]
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18
[+] score: 4
044hsa-miR-18b2.20.014hsa-miR-423-5p1.70.048hsa-miR-932.10.014hsa-miR-1911.50.049hsa-miR-548b-5p2.30.015Downregulated miRNAs  hsa-miR-252.10.015hsa-miR-885-5p-4.20.00011hsa-miR-324-3p2.30.017hsa-miR-874-5.80.00018hsa-miR-3262.60.017hsa-miR-486-3p-4.60.00040hsa-miR-18a3.10.017hsa-miR-299-5p-4.20.0020hsa-miR-20b2.00.017hsa-miR-488-3.90.0063hsa-miR-1942.80. [score:4]
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19
[+] score: 4
Mmu-miR-423-5p, -455, -466f-3p, -466g, -467a* and -467b* were consistently upregulated at IT and LT. [score:4]
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20
[+] score: 3
Three miRNAs (miR-762, miR-423-5p, and miR-185) had expression levels significantly decreased in both brain and liver (p < 0.01). [score:3]
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21
[+] score: 3
Furthermore, using IPA, we found that some of them (e. g., IL1b, CSF2, and CCL3) are under the control of genes targeted by miRNAs present in EVs (e. g., ZFP36/miR-27b-3p and miR-423-5p, ABCA1/ miR-27b-3p) (Figure 6C). [score:3]
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22
[+] score: 3
miR-411 - ND miR-423-5p + +miR-423-5p was involved in muscle development and growth and showed greatest in the neonate development stage [57]. [score:3]
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23
[+] score: 3
After normalizing the expression levels with the corresponding geometric mean value of the reference genes U6 snRNA, mmu-miR-191, mmu-miR-423-5p, mmu-miR-361 and mmu-miR-103, the samples were checked for outliers to be excluded. [score:3]
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24
[+] score: 3
Two miRNAs, mmu-mir-324 and mmu-mir-423, lie within genes in which mutations were found, dishevelled 2 (Dvl2) and coiled-coil domain containing 55 (Ccdc55), respectively, though neither mutation identified in these genes is within the miRNA sequence itself. [score:3]
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25
[+] score: 2
In general, the rank order of the expression levels of the measured miRNAs was comparable in mice and rats, with the highest miRNA levels of miR-16-5p and miR-223-3p and the lowest levels of miR-199a-3p, miR-652-3p, miR-423-3p and miR-26b-5p (S1– S3 Figs). [score:1]
In rats we found one significant correlation between the normalized -Ct values of miR-423-3p and the dP/dt [max] values (R = -0.53, P-value = 0.036). [score:1]
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[+] score: 2
In eQTL hot spots as on chromosome 2 (28–51 Mb), miR-423-3p and miR-23b are clustered in the ‘yellow’ module. [score:1]
On chromosome 2, five miRNAs (miR-26a, mir-291a, miR-423, miR-671 and miR-23b) were mapped between 28–51 Mb (Fig.   2). [score:1]
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[+] score: 2
MiR-423-5p causes transcriptional silencing of progesterone receptor (PR) by targeting a highly conserved region in the promoter [8]. [score:2]
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28
[+] score: 1
U6 snRNA and miR-423-3p and miR-23a-3p were used for normalization. [score:1]
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29
[+] score: 1
MiR-122 was the most abundant miRNA in the FBS, followed by miR-1246, miR-423-5p, miR-148a-3p, and let-7 family (Fig. 1f). [score:1]
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30
[+] score: 1
A study published in Blood has shown that a mo del that includes 4 miRs (miR-423, miR-199a-3p, miR-93, and miR-377) could predict the probability of aGVHD with an AUC of 0.80 [28]. [score:1]
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31
[+] score: 1
miRNA levels were normalized against the average of five reference miRNAs (miR-423-5p, miR-103a-3p, miR-191-5p, miR-425-5p, and miR-93), which were used as internal controls in plasma samples. [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-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, 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-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Sharbati-Tehrani et al., [67] have reported 4 new miRNAs (miR-326, miR-423-3p, miR-484 and miR-451,) that could not be identified in our study, which could be attributed to the use of very specialized tissues (Jejunium, spleen, ileum and kidney) for their study. [score:1]
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[+] score: 1
Only one miRNA, miR-423-5p, was found to respond to the Dox treatment, as its fold abundance in the control J1 cells was greater than 1.25 in the qPCR (Table 1). [score:1]
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34
[+] score: 1
Briefly, results were normalized using the ΔΔCp method with multiple reference genes (U6, RNU1A1, miR-191-5p and miR-423-5p) [65]. [score:1]
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