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33 publications mentioning hsa-mir-411

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-411. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 216
Among the potential miR-411 targets, we further selected transcripts that were down-regulated in FSHD myoblasts based on the current knowledge that miRNAs negatively regulate target gene expression. [score:11]
Over -expression of miR-411 leads to down-regulation of YAF2, MYOD and myogeninTo identify mRNA transcripts that can be potentially regulated by miR-411, mRNA profiles generated using the same total RNA samples used for miRNA profiling were analyzed to identify potential mRNA targets of miR-411. [score:9]
Based on the findings, we hypothesized that the over -expression of miR-411 affects the expression of myogenic factors through the inhibition of YAF2 expression. [score:9]
Over -expression of miR-411 down-regulated expression of Yaf2 (A), Myod (B), myogenin (C), and Myh1 (D) as analyzed by real-time qRT-PCR (n=4). [score:8]
The results showed that Yaf2 expression level was significantly down-regulated (−4.5 fold, p<0.05) by miR-411 over -expression (Figure  4A). [score:8]
Whether the up-regulation of miR-411 directly contributes to the disease pathogenesis, or is part of a compensatory response to suppress the prematurely activated MYOD program still needs to be further investigated. [score:7]
We then used mRNA profiling to identify potential regulatory targets of miR-411, which was significantly upregulated in the miRNA profiling. [score:7]
Starting with the up-regulation of miR-411, YAF2 is suppressed, which will then positively regulate YY1. [score:7]
We also identified YAF2 as a potential regulatory target of miR-411 by analyzing the miRNA and mRNA expression profiling data generated from primary myoblasts. [score:6]
Over -expressing miR-411 in C [2]C [12] cells leads to down-regulation of Myod, myogenin, and Myh1. [score:6]
To date, it is not known whether the down-regulation of miR-411 contributes to the disease phenotype or participates in the muscle regeneration process in the mdx mouse mo del. [score:6]
Interestingly, myogenic factors, Myod (−1.4 fold, p<0.05) and Myog (−2.1 fold, p<0.05) as well as a myotube differentiation marker, Myh1 (−1.7 fold, p<0.05), were also significantly down-regulated by miR-411 over -expression (Figure  4B-D). [score:6]
Over -expression of miR-411 leads to down-regulation of YAF2, MYOD and myogenin. [score:6]
In this research, we showed that YAF2 was down-regulated in FSHD myoblasts and is a potential target of miR-411. [score:6]
The miR-411 expression in the control myoblasts as well as the negative probes in both the disease and control cells was not visible (Figure  2). [score:5]
Figure 4Over -expression of miR-411 reduced the expression level of differentiation markers in C [2]C [12] murine myoblasts. [score:5]
In addition, expression of myogenic markers including Myod, myogenin, and myosin heavy chain 1 (Myh1) were suppressed by miR-411. [score:5]
The results showed that over -expression of miR-411 reduced YAF2 mRNA expression. [score:5]
Figure 1 The up-regulation of miR-411 was validated in primary and immortalized FSHD myoblasts using qRT-PCR. [score:4]
In this study, we demonstrated that miR-411 was up-regulated in both primary and immortalized FSHD myoblasts in comparison to control myoblasts. [score:4]
In this study, miR-411 was reported to be down-regulated (−1.8 fold) in the gastrocnimeous muscles of the mdx mice. [score:4]
The study demonstrated that miR-411 was differentially expressed in FSHD myoblasts and may play a role in regulating myogenesis. [score:4]
Based on previous findings as well as our own observations, we propose a potential mo del of how up-regulation of miR-411 can be involved in the myogenic defect observed in FSHD myoblasts. [score:4]
To identify mRNA transcripts that can be potentially regulated by miR-411, mRNA profiles generated using the same total RNA samples used for miRNA profiling were analyzed to identify potential mRNA targets of miR-411. [score:4]
Interestingly, these cells also showed visible staining of miR-411 in their cytoplasm, suggesting the up-regulation of miR-411 may be involved at a later stage when the cells are further affected. [score:4]
Alternatively, the up-regulation of miR-411 may be a compensatory mechanism to the hypothesized premature activation of the MYOD program. [score:4]
The expression of miR-411 has been reported in brain, however the function and cellular localization of the miRNA is unknown. [score:3]
We further examined the effects of over -expressing miR-411 in C [2]C [12] myoblasts and its potential role in myogenesis. [score:3]
While not seen in control myoblasts (A), the expression of miR-411 was visible in the cytoplasm of some FSHD myoblasts (B: marked by asterisks). [score:3]
However, our data suggested that reduction of miR-411 may have a positive effect on muscle regeneration considering its potential to suppress factors that promote myoblast maturation. [score:3]
The expression levels of miR-411, Yaf2 and myogenic markers, Myod, myogenin (Myog), and Myh1 were examined by qRT-PCR. [score:3]
The cells which expressed higher level of miR-411 were larger in size. [score:3]
In addition, we over-expressed miR-411 in C [2]C [12] cells to determine the effect of miR-411 on myogenic markers. [score:3]
C [2]C [12] cells were transfected with miR-411 to determine whether miR-411 affects YAF2 expression in myoblasts. [score:3]
One of the 8 differentially expressed miRNAs, miR-411, was validated by quantitative RT-PCR in both primary (2.1 fold, p<0.01) and immortalized (2.7 fold, p<0.01) myoblasts. [score:3]
By analyzing both miRNA and mRNA data using Partek Genomics Suite, we identified 4 mRNAs potentially regulated by miR-411 including YY1 associated factor 2 (YAF2). [score:2]
To further determine whether miR-411 can regulate YAF2 and downstream pathways, C [2]C [12] myoblasts were transfected with miR-411 precursor oligos, followed by cell differentiation for 5 days. [score:2]
MiR-411 expression was significantly higher in the proliferating primary myoblasts (A) and immortalized myoblasts (B) of patients with FSHD (n=4). [score:2]
While each specific regulatory relationship needs to be further investigated, our findings demonstrated a potential role of miR-411 in regulating myogenesis, and provides a novel molecular regulatory mechanism that may be involved in FSHD pathogenesis. [score:2]
Expression levels of miR-411 were analyzed by qRT-PCR using TaqMan MicroRNA assays according to the manufacturer’s instructions. [score:2]
The miR-411 predicted targets were identified then compared to the mRNA transcript list using Partek Genomics Suite 6.5 to identify potential miRNA-mRNA interactions. [score:2]
MiRNA-411 was differentially expressed in FSHD primary myoblasts. [score:2]
Cells were transfected with 30 mM Ambion pre-miR-411 precursor oligos (Life Technologies) using Lipofectamine 2000 (Life Technologies) following the manufacture protocol. [score:1]
Only miR-411 was validated using the second set of samples (2.1 fold, p<0.01) (Figure  1A). [score:1]
showed cytoplasmic localization of miR-411 in FSHD myoblasts. [score:1]
The results showed that miR-411 was localized in the cytoplasm of the myoblasts. [score:1]
The cellular localization of miR-411 was determined by in situ hybridization using LNA probes. [score:1]
Putative miR-411 binding sites in the 3 [′] UTR of 5 splice variants of YAF2. [score:1]
Differentiation was induced 6 hours after the pre-miR-411 transfection. [score:1]
It is not clear whether a probe detecting miR-411 was on the array used in the previous profiling study therefore it is not known whether miR-411 was changed in patients’ muscle samples. [score:1]
White columns indicate the control scramble-miRNA oligos (Sc) and black columns indicate the miR-411 oligos (411). [score:1]
While no study was conducted to investigate the function of miR-411, differential expression of miR-411 was reported in a miRNA profiling study of a mouse mo del of Duchenne muscular dystrophy known as the mdx mouse mo del [54]. [score:1]
Click here for file Putative miR-411 binding sites in the 3 [′] UTR of 5 splice variants of YAF2. [score:1]
MiR-411 belongs to the miR-379 family and is located in the miR-379/miR-656 cluster within the DLK-DIO3 region on human chromosome 14 [56]. [score:1]
Each sample was transfected with miR-411 oligos (411) or negative oligo control (Sc). [score:1]
Figure 2 Cellular localization of miR-411 in FSHD myoblasts. [score:1]
was performed using 5 [′]-digoxigenin (DIG) labeled miRCURY locked nucleic acid (LNA) detection probes, including hsa-miR-411 (38398–01), U6 (99002–01) and Scramble-miR (99004–01) (Exiqon) following the protocol from Exiqon and Roche with few modifications. [score:1]
All five splice variants have one or two putative miR-411 binding site in their 3 [′] UTR (Additional file 4: Figure S1). [score:1]
The function of miR-411 in brain or other tissues is currently unknown. [score:1]
The seed region of miR-411 is underlined. [score:1]
To determine the cellular localization of the miR-411 in myoblasts, we visualized miR-411 by in situ hybridization. [score:1]
Thus, miR-411 may be a potential candidate as a biomarker in FSHD studies. [score:1]
In situ hybridization was performed using 5 [′]-digoxigenin (DIG) labeled miRCURY locked nucleic acid (LNA) detection probes, including hsa-miR-411 (38398–01), U6 (99002–01) and Scramble-miR (99004–01) (Exiqon) following the protocol from Exiqon and Roche with few modifications. [score:1]
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[+] score: 35
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-127, mmu-mir-132, mmu-mir-133a-1, mmu-mir-136, mmu-mir-144, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-10b, mmu-mir-185, mmu-mir-190a, mmu-mir-193a, mmu-mir-203, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-215, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-144, hsa-mir-152, hsa-mir-127, hsa-mir-136, hsa-mir-146a, hsa-mir-185, hsa-mir-190a, hsa-mir-193a, hsa-mir-206, mmu-mir-148a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-337, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-29b-2, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, hsa-mir-337, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-215, mmu-mir-411, mmu-mir-434, hsa-mir-486-1, hsa-mir-146b, hsa-mir-193b, mmu-mir-486a, mmu-mir-540, hsa-mir-92b, hsa-mir-378d-2, mmu-mir-146b, mmu-mir-193b, mmu-mir-92b, mmu-mir-872, mmu-mir-1b, mmu-mir-3071, mmu-mir-486b, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, hsa-mir-203b, mmu-mir-3544, hsa-mir-378j, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-let-7k, hsa-mir-486-2
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
Down-regulated miRNAs Up-regulated target genes mmu-mir-148a ARL6IP1, ARPP19, ATP2A2, CCNA2, CSF1, EGR2, ERLIN1, ERRFI1, FIGF, GADD45A, GMFB, ITGA5, KLF4, KLF6, LIMD2, MAFB, NFYA, PDIA3, PHIP, PPP1R10, PPP1R12A, PTPN14, RAI14, RSBN1L, SERPINE1, SIK1, SLC2A1, TMEM127, TMSB10, TMSB4X mmu-mir-411 APOLD1, SPRY4 mmu-mir-136 RYBP, ARL10, GLIPR2, UGGT1 Up-regulated miRNAs Down-regulated target genes mmu-mir-34a/c DAB2IP, DMWD, EVI5L, FAM107A, MAZ, SPEG, TFRC, TTC19 mmu-mir-92b COL1A2, DAB2IP, G3BP2, HOXC11, LBX1, NFIX, PKDCC, PRKAB2 mmu-mir-132 ACTR3B, AMD1, GPD2, HBEGF, KBTBD13, KCNJ12, PRRT2, SREBF1, TLN2 mmu-mir-146a IRAK1, TLN2 mmu-mir-152 EML2, GPCPD1, NFIX, RPH3AL, SH3KBP1, TFRC, TRAK1, UCP3 mmu-mir-155 DUSP7, G3BP2 mmu-mir-185 DAB2IP, FAM134C, SYNM, TMEM233 mmu-mir-203 APBB2, CACNG7, FKBP5, GDAP1, HBEGF, KCNC1, SIX5, TMEM182 mmu-mir-206 DMPK, G3BP2, GPD2, KCTD13, MKL1, SLC16A3, SPEG mmu-mir-215 KLHL23 Figure 5The network displays the predicted interactions between age-related miRNAs and mRNAs from the sequencing and was generated using Cytoscape (version 3.0, www. [score:17]
miRNA Fold Change P-value mmu-miR-337-5p −5.2 0.0149 mmu-miR-3544-3p −5.1 0.0147 mmu-miR-540-5p −4.9 0.0200mmu-miR-337-3p [a] −3.0 0.0324mmu-miR-3544-5p [a] −3.0 0.0308 mmu-miR-434-3p −2.1 0.0001 mmu-miR-3071-5p −2.0 0.0004mmu-miR-136-3p [a] −2.0 0.0004mmu-miR-3071-3p [a] −1.6 0.0000 mmu-miR-136-5p −1.6 0.0000 mmu-miR-143-5p −1.2 0.0004 mmu-miR-190a-5p −1.0 0.0139 mmu-miR-872-3p −0.9 0.0152 mmu-miR-193a-3p −0.9 0.0164 mmu-miR-144-3p −0.8 0.0298 mmu-miR-127-3p −0.7 0. 0002mmu-miR-434-5p [a] −0.6 0.0082 mmu-miR-148a-3p −0.6 0.0130 mmu-miR-411-5p −0.6 0.0091 a miRNA* (passenger) strand processed from opposite arm of the mature miRNA. [score:1]
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[+] score: 25
For example, we found a significant downregulation of miR-27a, miR-411 and miR-497 in bladder cancer patient B09 and a significant upregulation of miR-379, miR-381 and miR-411 in kidney cancer patient K44 (Figure  5B). [score:7]
Combined effects of miRNA editing and alternative 5′ cleavage on miR-411 target specificity. [score:3]
One miRNA in our dataset, miR-411, exhibited both substantial miRNA editing and 5′ length variation, resulting in four miRNA variants with distinct seed sequences (Figure  2A) and, as a consequence, largely non-overlapping sets of predicted target genes (Figure  2B). [score:3]
The miR-411 variants were expressed in roughly similar proportions (Figure  2C) and at relatively high levels; miR-411 fell within the 100 most highly expressed miRNAs in all investigated tissues, except mouse kidney [3]. [score:3]
However, Chiang et al. noted a similar association between miR-411 editing and 5′ variation in independently generated mouse data [18], which makes this explanation unlikely. [score:1]
Importantly, however, we also observed high editing frequencies elsewhere, for example, in human kidney where miR-411 was edited at 59% (559 edited and 387 unedited reads) and miR-381 at 32% (199 edited and 428 unedited reads). [score:1]
The most highly edited miRNA in our dataset was miR-411, for which editing reached 83% (2,225 edited and 454 unedited reads) in mouse cerebellum (Table S2 in Additional file 2). [score:1]
In principle, this observation might be explained by biases during library preparation, which might lead to preferential amplification of some miR-411 variants over others [26]. [score:1]
Figure 2 Conserved editing and 5′ length variation of miR-411. [score:1]
Not all miRNA editing events are ancient: we found six cases of miRNA editing (miR-376a-1, miR-376b, miR-376c, miR-379, miR-381 and miR-411) that were limited to placental mammals and that therefore represent evolutionary novelties (Figure  1). [score:1]
Consistent with this, miR-376b, miR-381 and miR-411 are thought to be edited primarily by ADAR [12, 13]. [score:1]
Editing of miR-376b, miR-376c, miR-379, miR-381, miR-411 and miR-497 was significantly correlated with age in both species, demonstrating that the age-related increase of editing frequencies at specific sites is conserved between species (Figure  4B). [score:1]
Instead, the observed skew suggests that the base change introduced by the editing machinery influences subsequent processing steps of the miR-411 precursor, presumably by altering structural motifs within the hairpin [27]. [score:1]
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[+] score: 24
To test the hypothesis that such a gain in stability can positively influence pri-miRNA processing – we have selected miR-411 as a representative miRNA, based on its editing across all tissues studied, an A-C mismatch at the editing site, seed sequence editing and its being one of the miRNAs showing downregulation and hypoediting in GBM. [score:4]
Interestingly, in our study, miR-411 is a potential tumor suppressor miRNA [41] where an editing event leads to increased processing – indicating such possibilities in a larger scale. [score:3]
Figure 8Increased expression of mature edited form of hsa-miR-411. [score:3]
miRNAs [a]Presence in samples [b]Median editing (in %) Seed editing event Position in precursor Target Prediction [c]Overlap (%) Before/After editing hsa-mir-598-3p 6/5/0 0.49/0.34/0 Yes 62 11/9 0 (0) hsa-mir-376a-1-5p 6/6/0 11.24/8.43/0 Yes 9 131/166 4 (3.05) hsa-mir-337-3p* 4/1/0 4.21/−/0 Yes 66 146/197 11 (7.53) hsa-mir-376c-3p 6/5/2 3.72/1.9/− Yes 48 156/192 11 (7.05)hsa-mir-1301-3p [#,*] 6/6/2 7.59/3.94/− Yes 52 230/7 2 (0.87) hsa-mir-421 6/6/3 1.40/0.61/0.57 Yes 54 271/4 1 (0.37) hsa-mir-99b-3p* 6/6/2 3.61/1.65/− Yes 47 33/21 0 (0) hsa-mir-641-5p 6/6/3 5.62/7.08/3.35 Yes 18 355/128 11 (3.1) hsa-let-7e-3p* 4/0/0 2.09/0/0 Yes 57 5/3 0 (0)hsa-mir-1251-5p [#,*] 4/4/0 11.98/11.87/0 Yes 10 58/305 4 (6.9)hsa-mir-381-3p [#] 6/6/5 6.87/7.15/3.07 Yes 52 638/302 48 (7.52) hsa-mir-411-5p 6/6/5 27. [score:3]
A significant (two-tailed t-test, p = 0.001) increase in expression (3.5 fold, average of three replicates) was observed only for the mature form of miR-411. [score:3]
In cell based assays it was found that the expression level of mature miR-411 (edited) was 3.5 fold higher than the un-edited version (Fig.   8). [score:2]
We have also shown for miR-411 in cell based assays that the edited form was significantly more expressed than the unedited version (Fig.   8 and Supplemental Figure  S10). [score:2]
A genomic region encompassing mir-411 was cloned in a modified pRIP vector (673 base-pairs). [score:1]
qRT-PCR was done to quantify the levels of Pri-, Pre- and mature mir-411. [score:1]
For eight of these hypoedited miRNAs the editing level was below the level of detection in all GBM samples and amongst others we observed up to 5-fold reduction of the level of editing in GBM (e. g. for hsa-miR-411, Table  1). [score:1]
The arrow shows the position of editing found experimentally in mature miR-411–5p. [score:1]
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[+] score: 16
MiR-126, miR-411, miR-20b, miR-15a and miR-181c were down-regulated under diabetic conditions and over-expressed after calcitriol was added. [score:6]
In addition, miR-411 was reported to be down-regulated in an autosomal dominant muscle disorder (facioscapulohumeral muscular dystrophy) suggesting that reduction of miR-411 might have a positive effect on muscle regeneration and promote myoblast maturation [31]. [score:4]
Differential expression of miR-411 was reported in a miRNA profiling study of the hippocampus and the marginal division in a rat brain [30]. [score:3]
MiR-181c, miR-15a, miR-20b, miR-411, miR-659, miR-126 and miR-510 were selected for further analysis because they are known to be modified in DM and in other biological disorders. [score:1]
In addition, 10 [-10] mol/l calcitriol was given to the cells 1 h after stimulation for an additional 23 h. The miRNA set that included (A) miR-659, (B) miR-510, (C) miR-181C, (D) miR-411, (E) miR-126, (F) miR-15a, and (G) miR-20b was validated using real time PCR. [score:1]
miR-659 and miR-411 were validated because in the microarray analysis they were significantly changed after the addition of calcitriol. [score:1]
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[+] score: 12
Among the 7 miRNAs dynamically regulated over the course of normal lung development (Group A), 5 of these miRNAs (miR-411, miR-431, miR-699, miR-29a and miR-29c) were up-regulated by oxygen exposure, suggesting that prolonged hyperoxia alters the expression of miRNAs utilized during normal lung development. [score:9]
In Group A, the expression values of four miRNA were decreased (Pattern 1; miR-322*, miR-411, miR-431, miR-609) and three were increased (Pattern 2; miR-146b, miR-29a, miR-29c). [score:3]
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[+] score: 12
0 hsa-mir-98 dbDEMC;miR2Disease hsa-mir-411 dbDEMC;HMDD v2.0 hsa-mir-28 dbDEMC hsa-mir-22 dbDEMC;miR2Disease;HMDD v2.0 In this study, we implemented both global and local LOOCV validation methods based on 5430 known miRNA-disease associations between 383 diseases and 495 miRNAs from HMDD v2.0 to evaluate the prediction accuracy of. [score:7]
0 hsa-mir-98 dbDEMC;miR2Disease hsa-mir-411 dbDEMC;HMDD v2.0 hsa-mir-28 dbDEMC hsa-mir-22 dbDEMC;miR2Disease;HMDD v2.0 The first column records top 1–25 related miRNAs. [score:5]
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[+] score: 7
Indeed, concomitantly with weight loss and improved AT inflammation (Additional file 2: Table S2), current data pointed decreased AT expression of miRNAs which detection inside isolated cells (for example, miR-146b, miR-376c, miR-411) and/or in the SN (miR-221, miR-222, miR-155, miR-223, miR-19a/b) rose in differentiated adipocytes upon inflammatory stimuli (Table  2). [score:3]
On the other hand, the expression of ‘miRNokines’ such as miR-146b, miR-376c, miR-411, and miR-19a by inflamed adipocytes/obese AT may hint into functional activities beyond adiposity, such as recruitment of immune cells [25], or modulation of insulin-secreting cells [26]. [score:3]
Indeed, some miRNAs became undetectable (miR-1274B, miR-572, and miR-766), while others appeared de novo in cells (miR-140-5p, miR-222*, miR-376c, miR-411, and miR-146a) and their SNs (miR-146a, miR-146b, miR-19a, miR-223*, miR-425, and miR-9*) upon MCM -induced inflammation (Figure  2). [score:1]
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[+] score: 7
The miR-143 was significantly upregulated in HMCs in both conditions, while miR-146a and miR-411 were significantly downregulated in both conditions. [score:7]
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[+] score: 6
31 miR-411 –3.3 1.30E-07 14q32.31miR-494 [†] –2.0 1.90E-12 14q32.31 miR-503 –4.0 1.50E-15 Xq26.3 miR-532-5p –4.1 4.80E-19 Xp11.23miR-598 [†] –1.9 5.80E-10 8p23.1 miR-660 –2.4 1.60E-07 Xp11.23 Of the UV-regulated miRNAs 10 were found to be regulated by both UVA and UVB. [score:3]
31 miR-411 –3.3 1.30E-07 14q32.31miR-494 [†] –2.0 1.90E-12 14q32.31 miR-503 –4.0 1.50E-15 Xq26.3 miR-532-5p –4.1 4.80E-19 Xp11.23miR-598 [†] –1.9 5.80E-10 8p23.1 miR-660 –2.4 1.60E-07 Xp11.23Of the UV-regulated miRNAs 10 were found to be regulated by both UVA and UVB. [score:3]
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[+] score: 6
The majority of the miRNAs had alterations in expression that were consistent between the two species, except for miR-323-3p, miR-369-5p, miR-410, miR-411, miR-433, miR-494 and miR-130a, which were expressed discordantly in the tumors from the two different species (Table 1). [score:5]
Consistent with the interspecies shift based on PC2, 3 out of the first 5 implicated miRNAs (miR-411, miR-410, miR-382, miR-495 and miR-494) were differentially modulated in human and mouse samples (Table 1). [score:1]
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[+] score: 6
The overexpression of microRNA-411 in FSHD myoblasts has been implicated as a potential mechanism for the blocking of myogenic differentiation via directly suppressing YAF2 and YY1 transcriptional function [62]. [score:6]
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13
[+] score: 5
miR-324, together with four other miRNAs that show isoform differences in tumor versus non-tumor samples (miR-106b, miR-335, and miR-411), also exhibited variations in the major arm of the pre-miRNA expressed as a miRNA (Table S2, S3, S4, S6). [score:3]
We also noted A to G substitutions at nucleotide position four for miR-381 and position five for miR-411, miR-200b, and miR-379 (Table 1, Fig. S3A). [score:1]
Furthermore, several of these miRNA variants (miR-376 family members, miR-411, miR-379, and miR-320a) have previously been described in deep sequencing studies performed on human brain [36], [37], and therefore, are not specific to glioblastoma. [score:1]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-376c, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-342, hsa-mir-151a, hsa-mir-324, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-576, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-671, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-885, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
In a longitudinal study using plasma samples from non-HCV-infected injection drug users who eventually acquired the infection, miR-122 and miR-885-5p were increased in abundance during acute infection, whereas miR-494 and miR-411 were decreased in expression. [score:3]
Also, in an independent cohort of individuals, all but miR-411 were validated (200). [score:1]
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[+] score: 4
For miR-432, miR-411, miR 376-a, miR-381 and miR-487b, higher expression was associated with a lower relapse free probability. [score:3]
Five of these (miR- 376a, miR-381, miR-411, miR-432 and miR-487) map to human chromosome 14q32.31. [score:1]
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[+] 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-17, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-148a, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-206, hsa-mir-1-1, hsa-mir-128-2, hsa-mir-29c, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-133b, hsa-mir-424, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-128-1, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-503, hsa-mir-378d-2, hsa-mir-208b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-17, ssc-mir-221, ssc-mir-133a-1, ssc-mir-1, ssc-mir-503, ssc-mir-181a-1, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-29a, ssc-mir-199a-2, ssc-mir-128-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-486-1, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-23b, ssc-mir-148b, ssc-mir-208b, ssc-mir-424, ssc-mir-127, ssc-mir-125b-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-411, ssc-mir-133a-2, ssc-mir-126, ssc-mir-199a-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-378j, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, hsa-mir-486-2, ssc-mir-378b
miR-128 was reported to participate in the regulation of adipogenesis, osteogenesis and myogenesis [36] and herein, together with ssc-miR-411, up regulated at 35 to 77 dpc and fluctuated at 77 dpc to 180 dpn (Figure 5C), might behave in a similar manner as ssc-miR-133b during porcine muscle development. [score:4]
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[+] score: 4
Stather et al. reported reduced expression of let-7e, miR-15a, and -196b in the peripheral blood of AAA patients and increased expression of miR-411 as compared to controls [165]. [score:4]
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18
[+] score: 3
Mir-23a/b, let-7, miR-145, miR-197, miR-411 and miR-412 are overexpressed in black women ULM patients than white women ULM patients. [score:3]
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[+] score: 3
A signature of 5 miRNAs (miR-376a, miR-381, miR-411, miR-432, and miR-487) along with miR-203 that can be mapped to both chromosome 14q32.1 and 14q32.33 is shown in ependymoma and other tumours to be regulated by DNA methylation, proving the global dysregulation of this chromosome in carcinomas [143, 149, 150]. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Four bovine miRNAs (miR-411, -423-5p, -574-3p and -652) were expressed at low levels in all tissue (Figure 4). [score:3]
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[+] 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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22
[+] score: 3
A previous study from our institution had predicted eleven of these fourteen (79%) miRNAs (hsa-miR-454, has-miR-582-5p, has-miR-181d, has-miR-500, has-miR-181c, has-miR-411, has-miR-363, has-miR-381, has-miR-302c*, has-miR-652 and has-miR-452), to target CYP3A4/5/7 3’-UTR using in silico approach [29]. [score:3]
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23
[+] score: 2
Other miRNAs from this paper: hsa-mir-1304
Only the position chr14:101,489,681 (hg19 human genome assembly) falling in mir-411 was edited in all tissues and showed differential RNA editing levels between brain and liver, heart and muscle (P < 0.05), suggesting that mir-411 may have different functions in human tissues and that RNA editing may contribute to a further layer of regulation. [score:2]
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[+] score: 2
For example, some highly modified miRNAs observed at 6 hpi were still present at high levels at 24 hpi (e. g. miR-125b-5p, miR-99b-5p, miR-29a-3p) and some miRNAs that appeared unmodified at 6 hpi were massively reduced by 24 hpi (e. g. miR-16-5p and miR-411-5p). [score:1]
Some miRNAs showed very high levels of modification (e. g. miR-125b-5p, miR-99b-5p, miR-29a-3p, miR-92a-3p, miR-148b-3p) whilst others showed very low levels of modification (e. g. miR-16-5p, miR-411-5p, miR-410-5p, miR-30e-5p and miR-125b-3p). [score:1]
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[+] score: 1
2 −2.40(52) hsa-miR-127-5p 14q32.2 −2.35(12, 29) hsa-miR-127-3p 14q32.2 −2.35(52, 59) hsa-miR-411* 14q32.2 −2.30 hsa-miR-125b-1* 11q24.1/21q21.1 −2.27 hsa-miR-411 14q32.2 −2.23(29) hsa-miR-379 14q32.2 −2.22(29, 52) hsa-miR-431* 14q32.2 −2.22 hsa-miR-767-5p Xq28 −2.20 hsa-miR-139-3p 11q13.4 −2.17 hsa-miR-154 14q32.2 −2.16(12) hsa-miR-1224-5p 3q27.2 −2.15 hsa-miR-187 18q12.1 −2.14(12) hsa-miR-95 4p16.1 −2.10(14) hsa-miR-369-5p 14q32.2 −2.05 hsa-miR-665 14q32.2 −2.05 hsa-miR-494 14q32. [score:1]
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[+] score: 1
Only the mature miR-411 sequences differ substantially from each other, due to a different annotation of their hairpin sequences. [score:1]
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27
[+] score: 1
However, we identified a large number of novel miRNAs (miR-411-5p, miR-375, miR-410, and miR-758) and genes (HYDIN, WDR65, PAQR5, MGARP, and FLJ45983) that have not previously been detected and may have roles during the steps of spermatogenesis. [score:1]
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[+] score: 1
Initially, we screened 2 different batches of CB ECFC-derived cells transfected with 23 mimics/inhibitors based on those identified in Fig. 1C but excluding hsa-miR411* and hsa-miR-31*, then rescreened 8 of these mimics on CB ECFC-derived cells from 5 different donors and measured their proliferation rate 72 hr post-transfection (data not shown). [score:1]
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[+] score: 1
Also noteworthy were hsa-miR-411 with a 7.5 fold increase, hsa-miR-182 with a 5.1 fold increase, and hsa- let-7 miRNAs with 4.3 to 5.1 fold increases (Figure 1). [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-27a, hsa-mir-29a, hsa-mir-101-1, dme-mir-1, dme-mir-2a-1, dme-mir-2a-2, dme-mir-2b-1, dme-mir-2b-2, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-101a, mmu-mir-124-3, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-137, mmu-mir-140, mmu-mir-142a, mmu-mir-155, mmu-mir-10b, mmu-mir-183, mmu-mir-193a, mmu-mir-203, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-183, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-222, hsa-mir-223, dme-mir-133, dme-mir-34, dme-mir-124, dme-mir-79, dme-mir-210, dme-mir-87, mmu-mir-295, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, dme-let-7, dme-mir-307a, dme-mir-2c, 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-137, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-193a, 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-29a, mmu-mir-27a, mmu-mir-34a, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-210, mmu-mir-223, mmu-mir-222, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-411, hsa-mir-193b, mmu-mir-193b, hsa-mir-944, dme-mir-193, dme-mir-137, dme-mir-994, mmu-mir-1b, mmu-mir-101c, hsa-mir-203b, mmu-mir-133c, mmu-let-7j, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, mmu-mir-124b
For example, miR-411 in human and mouse had more than 40% 5′-isomiRs on the 5p arm versus <1% on the 3p arm. [score:1]
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[+] score: 1
The miR-381-3p, miR-548u, miR-411-5p, miR-148a-5p, and miR-96-5p which were filtered in HFD comparison but not in intact comparison and no-T2D comparison might involve the progress of T2D fed with HFD only. [score:1]
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[+] score: 1
However, I have a few points for the authors to consider: Comment: The examined genomic locus covers many miRNA, and several of these belong to the same miRNA family (e. g. miR-379, miR-380, miR-411, miR-758, and miR-1197 all belong to the same family according to miRBase). [score:1]
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[+] score: 1
Sequences 200 nucleotides upstream to the transcription start site of miR-654, miR-431, miR-127, miR-432, miR-411, miR-544, miR-369-3p, miR-382 and miR-134 were then amplified using qPCR from DNA present in the immune complexes. [score:1]
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