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67 publications mentioning mmu-mir-193b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-193b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 263
Freshly sorted LT-HSCs (100 cells per well) were double transduced with four different combinations of either a vector coding for murine c-KIT (without 3′-untranslated region and miR-193b target site, Supplementary Fig. 3b) or a corresponding empty vector (both co -expressing VENUS), and a miR-193b expression vector or a corresponding empty vector (both co -expressing eBFP2). [score:11]
To consolidate that the observed phenotype in miR-193b -expressing LT-HSCs was at least partly due to the reduced c-KIT expression, we lentivirally expressed both c-Kit lacking the miR-193b target site (Supplementary Fig. 3b) and miR-193b in LT-HSCs (Fig. 6b). [score:9]
All significantly regulated genes (41 up-regulated and 117 down-regulated) in the absence of miR-193b were subjected to DAVID analysis. [score:8]
All significantly regulated genes (41 up-regulated and 117 down-regulated) in the absence of miR-193b were subjected to Ingenuity Pathway Analysis. [score:8]
Using a regulation threshold of 1.5-fold (P<0.05), we identified 41 upregulated and 117 downregulated genes in the absence of miR-193b (Supplementary Fig. 6 and ). [score:8]
The list of significantly differentially regulated genes (1.5-fold upregulated or downregulated in miR-193b [−/−] LSK, P<0.05) was submitted as a list with official gene symbols for DAVID analysis and aligned with murine genetic background. [score:8]
These results underline that the cytokine -induced activation of STAT5 leads to the rapid upregulation of the miR-193b as a STAT5 -dependent miR, and the time shift between maximum pSTAT5 (at 20 min) and maximum miR-193b expression (at 60 min) would be expected from a transcribed target gene of STAT5. [score:8]
Conversely, lentiviral expression of miR-193b in LT-HSCs led to a dramatic reduction of miR-193b -expressing progeny over time, whereas the percentages of control vector transduced cells or of cells lentivirally expressing the unrelated miRs-132/212 remained largely constant (Fig. 3b,c, and Supplementary Figs 3a and 4a). [score:7]
To quantify the ability of miR-193b to target c-Kit mRNA expression, FACS-sorted LT-HSCs and MPPs were lentivirally transduced for ectopic miR-193b expression or control at multiplicity of infection (MOI)=100 and cultured for 4 days. [score:7]
Re -expression of c-KIT lacking the 3′-untranslated region in miR-193b-transduced LT-HSCs via lentiviral co-infection and culture for several days. [score:5]
Indeed, there was a 30% reduction of c-Kit mRNA expression in LT-HSCs ectopically expressing miR-193b (Fig. 5c). [score:5]
As the c-Kit mRNA contains a predicted conserved miR-193b target sequence (Fig. 5b), and c-KIT activity was elevated in the absence of miR-193b, we predicted that miR-193b can modulate c-KIT expression in HSPCs. [score:5]
The expression of miR-193b was instantly induced by cytokine stimulation and showed the strongest expression at 60 min after stimulation before it already declined at 120 min. [score:5]
Although the induction of miR-193b expression was even more pronounced in lineage-committed progenitors and mature blood cells than in LT-HSCs caused by 5-FU treatment, the expression level in these committed cells was still 1,000 times lower than in LT-HSCs (Supplementary Fig. 1b). [score:5]
Next, we assessed the c-KIT protein expression in miR-193b [−/−] BM cells and showed via FACS that miR-193b -deficient cells expressed 30% more c-KIT protein in comparison to their respective miR-193b [+/+] counterparts (Fig. 6a), indicating that the absence of miR-193b leads to higher c-KIT protein levels. [score:5]
Although cells expressing miR-193b and a control vector nearly disappeared over the course 7 days, miR-193b -expressing cells co-transduced with c-KIT expanded in culture, thereby rescuing the miR-193b -mediated effect (Fig. 6c). [score:5]
Especially, the initiation of pre-cancerous (stem) cells at an early disease stage might be supported by enhanced self-renewal in the absence of the tumour-suppressing miR-193b, as STAT5 activation plays a key role in establishing pre-cancerous clonal dominance in stem cells 37 38. [score:5]
MiR-193b targets c-KIT expression and thereby modulates signalling in HSPCs. [score:4]
The differential miR pattern revealed five miRs that were >2-fold upregulated by TPO only in the presence of STAT5A/B: miR-193b, miR-132, miR-125a, miR-331-5p and miR-669a (Fig. 1a and ). [score:4]
These results show that STAT5-activated miR-193b regulates c-KIT expression, probably among other important factors, and thereby subsequently influences signalling networks to control the fate of LT-HSCs. [score:4]
We used IPA to identify canonical pathways that are affected by miR-193b and upstream regulators predicted to be responsible for the observed mRNA expression changes. [score:4]
To obtain information about the miR-193b- dependent biological processes from the RNAseq data, gene expression data were analysed using Ingenuity Pathways Analysis with default settings according to the manufacturer's instructions (IPA) v. 5.0 (Ingenuity Systems Inc). [score:3]
For the miR-193b overexpression transplantation, 350 FACS-sorted LT-HSCs from 3-month-old C57. [score:3]
For ectopic miR-193b expression experiments, FACS-sorted LT-HSCs (100 cells per well in 96-well format) were lentivirally transduced (MOI=100) and cultured for up to 9 days in SFEM supplemented with 100 ng ml [−1] SCF and TPO. [score:3]
As hypothesized, no donor cell reconstitution was detected in mice transplanted with LT-HSCs ectopically expressing miR-193b (Fig. 5e). [score:3]
Reduced cell expansion and lack of blood reconstitution following transplantation with LT-HSCs overexpressing miR-193b resembles the phenotype of LT-HSCs harbouring dysfunctional c-KIT 19 20. [score:3]
Comparing miR-193b [−/−] and miR-193b [+/+] samples revealed differentially expressed peptides using the linear mo dels proposed by Smyth 40, which are implemented in the R-package ‘limma'. [score:3]
Because LT-HSCs with diminished c-KIT function are severely impaired in recipient repopulation 19 20, we assessed the blood reconstitution of miR-193b -expressing LT-HSCs after transplantation. [score:3]
The miR-193b expression was normalized to snoRNA202. [score:3]
Ectopic c-Kit expression can rescue miR-193b -mediated effects in HSPCs. [score:3]
To determine the kinetics of miR-193b expression after cytokine stimulation, FACS-sorted LT-HSCs were starved for 1 h and stimulated for 0, 20, 60 and 120 min with 100 ng ml [−1] SCF, 100 ng ml [−1] TPO, 20 ng ml [−1] interleukin (IL) 3, 20 ng ml [−1] IL6, 5 U ml [−1] EPO in SFEM (Serum-free Expansion Medium, Stemcell Technologies) at 37 °C/5% CO [2]. [score:3]
Of note, ectopic expression of miR-193b in GMPs did not influence their expansion, and the percentage of transduced cells did not change over time (Supplementary Fig. 4b), indicating a distinct function of miR-193b in LT-HSCs. [score:3]
Therefore, as miR-193b expression is triggered by STAT5 signalling, this axis represents a classical negative feedback mechanism. [score:3]
Gene expression in LSK cells of miR-193b [−/−] and miR-193b [+/+] mice. [score:3]
We performed of LSKs from miR-193b [−/−] and miR-193b [+/+] mice to elucidate differences in the gene expression profile. [score:3]
Importantly, already 20 min after stimulation there was a twofold increase in miR-193b expression in comparison to unstimulated LT-HSCs (Fig. 4e). [score:3]
wPRE (Schambach 2006) was used to construct the miR-193b and the miR-132/212 expression vectors. [score:3]
More importantly, we determined a 40% reduction of c-KIT surface expression on HSPCs that expressed miR-193b in comparison to control vector transduced cells, measured by FACS (Fig. 5d). [score:3]
Furthermore, the activation of STAT5 and AKT persisted longer in the absence of miR-193b, which suggests a negative regulation of the signalling kinetics by the miR-193b. [score:2]
Again, both the WT and knockout group reconstituted the secondary recipients almost equally well, which clearly indicated that miR-193b -deficient LT-HSCs were fully functional (Fig. 1f). [score:2]
How to cite this article: Haetscher, N. et al. STAT5-regulated microRNA-193b controls haematopoietic stem and progenitor cell expansion by modulating cytokine receptor signalling. [score:2]
MiR-193b targets c-KIT and thereby modulates signalling. [score:2]
The ectopic expression level of mature miR-193b and miR-132 was confirmed via qPCR using an ABI TaqMan microRNA Assay ID002467 and ID000457 (Life Technologies). [score:2]
Supplementary Data 1. Supplementary Data 2. Supplementary Data 3. Supplementary Data 4. Supplementary Data 5. In vivo expansion of functional LT-HSCs in the absence of STAT5-regulated miR-193b. [score:2]
In this study, we found that miR-193b is an important negative regulator of basal and cytokine-stimulated signalling and hyperactivation in LT-HSCs. [score:2]
To unravel the function of miR-193b in haematopoiesis, we generated miR-193b knock-out mice, which were viable without visible abnormalities 15. [score:2]
Further evaluation is warranted to determine whether miR-193b downregulation is an early event in tumourigenesis. [score:2]
The tolerated expansion of LT-HSCs over time might also be supported by our findings that the absence of miR-193b does not change the cell-cycle length in proliferating HSPCs, but rather regulates the decision of active cell-cycle entry versus quiescence. [score:2]
This aspect distinguishes miR-193b function from other haematopoietic negative regulators, such as PTEN, thereby suggesting that miR-193b is able to fine-tune HSC numbers. [score:2]
Assessing the donor-derived HSPC distribution in primary and secondary recipient BM, we observed a consistent increase in miR-193b [−/−] LT-HSCs and subsequent increase in LSK cell numbers (Fig. 1h,i). [score:1]
We further challenged the self-renewal ability of miR-193b -deficient LT-HSCs by transplanting unfractionated BM cells from primary recipients into secondary recipient mice. [score:1]
MiR-193b [−/−] LT-HSCs showed a higher induction of pAKT at 20 min, which remained above the pAKT levels of miR-193b [+/+] LT-HSCs until 120 min (Fig. 4e). [score:1]
To assess the endogenous miR-193b levels under steady-state and under stress, LT-HSCs, MPPs, KL and Lin [+] cells were FACS-sorted 10 days after injection of 150 mg kg [−1] 5-FU in four individual 12-week-old miR-193b [+/+] mice. [score:1]
Although donor cell engraftment in the BM was only slightly enhanced in the absence of miR-193b (Supplementary Fig. 2f), overall BM donor cellularity was markedly increased, thereby suggesting that miR-193b [−/−] LT-HSCs self-renew extensively after transplantation stress to repopulate the recipient (Supplementary Fig. 2h). [score:1]
To dissect these various cell fates at a single-cell resolution, we monitored the individual LT-HSCs and their progeny of miR-193b -deficient and WT mice using video-microscopy -based cell tracking (Fig. 3d and Supplementary Fig. 5). [score:1]
These results show at the phenotypic, molecular and functional level that the absence of miR-193b leads to an intrinsically controlled expansion of fully functional LT-HSCs, as they exhibit reduced quiescence and increased self-renewal. [score:1]
We asked whether miR-193b [−/−] LT-HSCs show a delayed differentiation that causes an accumulation of highly proliferative progenitors. [score:1]
Although no difference was found in the primary recipients of either miR-193b [−/−] or miR-193b [+/+] LT-HSCs (Fig. 1h), secondary recipient BM accumulated miR-193b [−/−] LT-HSCs and LSK cells (Fig. 1i). [score:1]
Therefore, we applied PamGene array technology to quantitatively compare the activity of hundreds of tyrosine and serine/threonine kinases in the BM cells of miR-193b [−/−] and miR-193b [+/+] mice in an unbiased way. [score:1]
5-FU (Medac) was intraperitoneally injected into miR-193b [−/−] and miR-193b [+/+] mice (150 mg kg [−1]) once a week. [score:1]
Next, we aimed to assess the molecular mechanism by which miR-193b restrains HSPC expansion and LT-HSC self-renewal. [score:1]
We injected 5-FU into miR-193b [−/−] and miR-193b [+/+] mice once a week, until the mice suffered from fatal haematopoietic failure (Fig. 2c). [score:1]
Indeed, there were a significant higher proportion of LT-HSCs and MPPs in cell-cycle (Ki67 [+]) in miR-193b [−/−] mice (Fig. 2a). [score:1]
Overall, we did not observe global changes in tyrosine or serine/threonine phosphorylation patterns in miR-193b -deficient cells. [score:1]
Intriguingly, miR-193b [−/−] LT-HSCs showed an overshooting activation of pSTAT5 at 20 min, that did not decline as much as the pSTAT5 levels in miR-193b [+/+] LT-HSCs at 120 min (Fig. 4e). [score:1]
Transduction efficiencies were 94% and 90% for control and miR-193b, respectively. [score:1]
After digestion with BsrGI/ Acc65I, the genomic region including the miR-193b sequence was cloned into the BsrGI site of pRRL. [score:1]
Increased cytokine signalling in miR-193b −/− LT-HSCs. [score:1]
Recently, we demonstrated that STAT5A/B binds to the miR-193b promoter in the murine mammary gland 14. [score:1]
To verify that the absence of miR-193b does not influence the cell-cycle duration of HSPCs, we determined HSPC proliferation in vivo by pulsing miR-193b [−/−] and miR-193b [+/+] mice with 5-bromodeoxyuridine (BrdU) for 4 h. Accordingly, there was no difference in the cell-cycle distribution in LT-HSCs, MPPs, GMPs or MEPs, which further confirmed that the absence of miR-193b does not shorten the cell cycle of HSPCs (Fig. 3g). [score:1]
An increased number of miR-193b -deficient LT-HSCs are in active cell cycle. [score:1]
In vivo 5-FU treatment5-FU (Medac) was intraperitoneally injected into miR-193b [−/−] and miR-193b [+/+] mice (150 mg kg [−1]) once a week. [score:1]
Overall, the increased expansion of cells from miR-193b [−/−] LT-HSCs was due to a delay in differentiation and not a change in proliferation or survival. [score:1]
QPCR of miR-193b basal, stress and cytokine stimulation. [score:1]
N=7 miR-193b [−/−] mice, N=6 miR-193b [+/+] mice. [score:1]
In vivo expansion of LT-HSCs in the absence of miR-193b. [score:1]
To corroborate that miR-193b [−/−] LT-HSCs were fully functional, we performed a competitive transplantation of LT-HSCs from 1-year-old miR-193b -deficient or WT mice into recipients and then monitored donor blood reconstitution (Fig. 1c). [score:1]
However, in the absence of miR-193b there is an overshooting pSTAT5 and pAKT activation signal, which would have been dampened in the presence of the already increased miR-193b levels at 20 min. [score:1]
Interestingly, PI3K/AKT signalling was enhanced in miR-193b [−/−] HSPCs at basal levels and after cytokine stimulation. [score:1]
Although most of the WT mice died after the third round of 5-FU injections, all miR-193b -deficient mice died already after two subsequent injections, most likely because the hyperproliferative LT-HSCs were quickly extinguished (Fig. 2c). [score:1]
However, miR-193b [−/−] mice over 6 months of age displayed an unexpected increase in LT-HSCs in the LSK (Lineage [−]Sca1 [+]c-KIT [+]) compartment (Fig. 1b), whereas total LSK cell numbers were not altered (Supplementary Fig. 2e). [score:1]
More miR-193b -deficient LT-HSCs are in active cell cycle. [score:1]
We then assessed the immediate consequences of the absence of miR-193b on the function and fate of LT-HSCs. [score:1]
Interestingly, the absence of miR-193b had no influence on cell-cycle duration in dividing LT-HSCs and their progeny for many generations (Fig. 3e). [score:1]
Briefly, 2 × 10 [6] total BM cells isolated from four individual male mice of each genotype (miR-193b [−/−] and miR-193b [+/+]) were lysed in M-PER Mammalian Extraction Buffer (Pierce). [score:1]
Basal tyrosine and serine/threonine phosphorylation in miR-193b [−/−] and miR-193b [+/+] bone marrow cells. [score:1]
Male miR-193b -deficient (referred to as miR-193b [−/−]) and corresponding WT littermate control mice (referred to as miR-193b [+/+]) 15 were used in this study. [score:1]
Strikingly, when we analysed the distribution of LT-HSC and progenitor cells in primary recipient BM, we determined a more than twofold increase in phenotypic LT-HSC numbers in the absence of miR-193b in comparison to the WT controls (Fig. 1e). [score:1]
Strikingly, although miR-193b [−/−] LT-HSCs were more actively cycling and expanding, they did not exhaust and remained fully functional. [score:1]
The absence of miR-193b increases basal and cytokine-stimulated signalling in LT-HSCs. [score:1]
FACS-sorted LT-HSCs from 12-month-old miR-193b [−/−] or miR-193b [+/+] mice (CD45.2) were transplanted intravenously (100 LT-HSCs/mouse) into sub-lethally irradiated (2.5 Gy) 6- to 8-week-old NSG mice (CD45.1) together with 2.5 × 10 [5] BM competitor-recipient cells (CD45.1). [score:1]
Increased cytokine signalling in miR-193b −/− LT-HSCsNext, we aimed to assess the molecular mechanism by which miR-193b restrains HSPC expansion and LT-HSC self-renewal. [score:1]
This proves that the self-renewal of LT-HSCs leading to an enlarged compartment of competent LT-HSCs is intrinsically promoted in the absence of miR-193b. [score:1]
12), may lead to the observed expansion of LT-HSCs in miR-193b -deficient mice. [score:1]
of phosphorylated STAT3, STAT5, AKT and ERK revealed an increase in the basal signalling levels of STAT5 and AKT in miR-193b [−/−] BM cells (Fig. 4b). [score:1]
The miR-193b -deficient LT-HSCs reconstituted equally well as WT LT-HSCs (Fig. 1d) and exhibited normal production of T, B and myeloid cells (Supplementary Fig. 2g). [score:1]
These results show that the absence of miR-193b increases the number of LT-HSCs in active cell cycle (Fig. 2), but does not alter the cell-cycle progression of proliferating LT-HSCs or their progeny during steady-state haematopoiesis (Fig. 3). [score:1]
As a reference under steady-state haematopoiesis, LT-HSCs, MPPs, KL and Lin [+] cells were isolated from BM of 12-week-old miR-193b [+/+] mice via FACS. [score:1]
Here we could show that STAT5A/B is required for the cytokine -induced miR-193b transcription in LT-HSCs. [score:1]
Meanwhile, most miR-193b -deficient cells remained more immature (CD117 [+], CD16/32 [−]; Fig. 3i,j). [score:1]
Although we did not observed increased cancer incidence in 1-year-old miR-193b [−/−] mice, it would be intriguing to test whether the absence of miR-193b cooperates with known oncogenes. [score:1]
Of note, the recipients that received the miR-193b [−/−] donor cells displayed a slightly lower donor cell chimerism in the BM (Supplementary Fig. 2f,h), indicating that although they received more LT-HSCs from primary recipients and again showed an enhanced self-renewal and expansion of LT-HSCs, the ability of these LT-HSCs to produce the same output on mature cells seemed altered. [score:1]
After a rapid induction already at 5 min of stimulation, the levels of pSTAT5 and pAKT further increased to a maximum at 20 min in LT-HSCs from miR-193b [+/+] and miR-193b [−/−] mice. [score:1]
Moreover, there was no decrease of cell death events in the absence of miR-193b (Fig. 3f). [score:1]
Two prominent signalling pathways guiding LT-HSC self-renewal and proliferation, STAT5A/B and PI3K/AKT, are hyperactivated in the absence of miR-193b leading to a more active LT-HSC population that expands over time (Supplementary Fig. 7). [score:1]
A total 10,000 LSK cells (CD117 [+] Sca1 [+] Lineage [−]) from four miR-193b [−/−] and miR-193b [+/+] mice were isolated via FACS. [score:1]
We recently reported the expansion of mammary epithelial stem cells in the absence of miR-193b 14, which suggests a general miR-193b function in restricting adult stem cell proliferation. [score:1]
The expansion of the LT-HSC population may indicate that an increased proportion of LT-HSCs are actively cycling in the absence of miR-193b. [score:1]
Next, we determined the kinetics of STAT5 and AKT signalling in temporal relation to miR-193b expression in LT-HSCs upon cytokine stimulation, and investigated changes in STAT5 and AKT signalling in the absence of miR-193b (Fig. 4e). [score:1]
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[+] score: 167
Low-dose radiation induced mild oxidative stress and led to the enhancement of histone deacetylation of miR-193b-3p promoter regions, which caused the down-regulation of miR-193b-3p expression and negatively regulated the expression of the miR-193b-3p target gene, Rad51 (a homolog recombinase), without inducing DNA damage. [score:11]
As expected, the down-regulation of miR-193b-3p expression, up-regulation of Rad51 expression, and decreased deacetylation of histone that were observed in response to LDIR were restored to basal levels in the presence of the antioxidant (Fig. 4C,D). [score:11]
Moreover, Rad51 protein expression was not correlated with miR-193b-3p expression or negatively regulated when miR-193b-3p expression increased in response to pretreatment with BIX01294 and 0.01 Gy irradiation (Supp. [score:8]
Compared with the decreased miR-193b-3p expression upon exposure to radiation alone, the expression of miR-193b-3p was increased following pretreatment with BIX01294 (a histone methyltransferase inhibitor) alone or in combination with BIX01294 and 0.01 Gy irradiation (Supp. [score:6]
Therefore, the down-regulation of miR-193b-3p expression was not associated with histone methylation on the miR-193b-3p promoter in response to LDIR. [score:6]
For example, miR-877-5p and miR-5114 were up-regulated, whereas miR-3963, miR-378a-3p, miR-193b-3p, miR-125a-5p, miR-378b, miR-365-3p, let-7e-5p, and miR-712-5p were down-regulated in the 0.01 Gy-irradiated mouse spleens compared with the sham spleens. [score:6]
In addition, the up-regulation of miR-193b-3p expression observed upon exposure to NaB alone was reduced when the HepG2 cells were treated with a combination of NaB and 0.01 Gy irradiation. [score:6]
The expression of miR-193b-3p was up-regulated following pretreatment with the HDACi NaB, and the levels of acetylated histone on the miR-193b-3p promoter were reduced in response to LDIR (Fig. 2). [score:6]
To further study the regulation of miRNA expression, we first confirmed the expression of the miRNAs (miR-378a-3p, miR-193b-3p, and miR-125a-5p) in response to LDIR in a normal mouse liver cell line (NCTC), a mouse cancer cell line (Hepa), and a human hepatoma cell line (HepG2). [score:6]
The altered expression of miR-193b-3p (C) and Rad51 protein levels (D) was observed in response to irradiation of the HepG2 cells pretreated with NAC for 24 h. The data were normalized using the mammalian U6 gene and are expressed as the mean ± S. D. GAPDH was used as a loading control. [score:5]
In addition, we predicted the miR-193b-3p target sites on the Rad51 3′UTR using TargetScan 7.0 (http://www. [score:5]
Taken together, these results demonstrate that miR-193b-3p directly regulates Rad51 expression in response to LDIR. [score:5]
To identify the mRNAs targeted by miR-193b-3p, we calculated LDIR-specific genome-wide gene expression profiles from GEO microarray datasets and identified 14 potential LDIR-related miR-193b-3p target genes (Supp. [score:5]
Thus, in this study, we examined the regulation of the expression of miR-193b-3p and its target gene, Rad51, and investigated histone deacetylation in the presence of an antioxidant. [score:4]
The modification of histone deacetylation on the miR-193b-3p promoter regulated miR-193b-3p expression in response to LDIR. [score:4]
Consistent with the results of the microarray analysis, the expression levels of miR-378a-3p, miR-193b-3p, miR-125a-5p, and miR-712-5p decreased in the 0.01 Gy-irradiated mouse spleens compared with the sham group, whereas the expression of miR-3963 did not change significantly. [score:4]
The down-regulation of miR-193b-3p after exposure to 0.01 Gy irradiation (Fig. 2A) was confirmed in various liver cell lines, including a mouse normal liver cell line (NCTC), a mouse hepatoma cell line (Hepa), and a human hepatoma cell line (HepG2). [score:4]
How to cite this article: Lee, E. -S. et al. Low-dose irradiation promotes Rad51 expression by down -regulating miR-193b-3p in hepatocytes. [score:4]
Identification of the mechanism that regulates miR-193b-3p expression in HepG2 cells exposed to 0.01 Gy irradiation. [score:4]
We also tested the involvement of mild oxidative stress in the regulation of miR-193b-3p and Rad51 expression. [score:4]
To determine whether the down-regulation of miR-193b-3p occurs at the transcriptional level, we measured the abundance of miR-193b-3p in cells pretreated with a histone deacetylase inhibitor (HDACi). [score:4]
These results indicate that the down-regulation of miR-193b-3p is caused by histone deacetylation and the involvement of mild oxidative stress in histone modification in response to LDIR. [score:4]
The results showed that the regulation of miR-193b-3p and Rad51 expression in the 0.01 Gy-irradiated HepG2 cells was restored by pretreatment with NAC (Fig. 4C,D). [score:4]
Among the 3 miRNAs, only miR-193b-3p presented an expression pattern in all three cell lines that was consistent with the in vivo results (Fig. 2A). [score:3]
As shown in Fig. 2B, miR-193b-3p expression was restored to basal levels in the HepG2 cells pretreated with the HDACi sodium butyrate (NaB). [score:3]
We found that the expression of miR-193b-3p was commonly decreased in response to LDIR in the spleen and liver as well as in three liver cell lines. [score:3]
As shown in Fig. 3C, the increased levels of Rad51 protein expression were restored in the cells treated with the miR-193b-3p mimic alone and in the cells treated with both the miR-193b-3p mimic and 0.01 Gy irradiation. [score:3]
In addition, we showed a correlation between miR-193b-3p and Rad51 expression after treatment with 0.01 Gy irradiation. [score:3]
In the case of DNA methylation on the miR-193b-3p promoter, HepG2 cell lines expressed low basal levels of DNMT1 33. [score:3]
These results indicated that histone deacetylation promotes the alteration of miR-193b-3p expression in response to LDIR. [score:3]
Because the human Rad51 mRNA (NM_0011642) contains 3 miRNA response elements (MREs) targeted by miR-193b-3p (246-270nt MRE1, 704-724 nt MRE2, and 745-768 nt MRE3) (Fig. 3D), we generated luciferase reporter constructs harboring these MREs, the full-length 3′UTR, and mutated MREs after the luciferase coding sequence. [score:3]
Thus, we also investigated whether the expression of miR-193b-3p is epigenetically regulated in response to LDIR. [score:2]
To further confirm these results, we next investigated the down-regulation of miR-193b-3p in response to LDIR using ChIP to explore the possible effects of histone deacetylation on the miR-193b-3p promoter (Fig. 2C). [score:2]
We also investigated whether Rad51 expression could be regulated by miR-193b-3p by using a miR-193b-3p mimic. [score:2]
Moreover, there were no miR-193b-3p biding site on 3′UTR of ATAD2, CDCA2, FAM101B and TPX2, when they compared the common target mRNAs from public databases (miRTarBase, miRDB and miRBase). [score:2]
Investigation of miR-193b-3p target genes in HepG2 cells exposed to 0.01 Gy irradiation. [score:1]
HepG2 cells were co -transfected 20 nM of the miR-193b-3p mimic (Bioneer, Daejeon, Korea) or miRNA mimic negative control (mock) (Bioneer) with 50 ng of psiCHECK2-Rad51 plasmid (wild type-, mutant-, MREs 3′ UTR of Rad51) using lipofectamine 2000 transfection reagent (Invitrogen, Carlsbad, CA). [score:1]
Involvement of histone deacetylation at the miR-193b-3p promoter regions in HepG2 cells exposed to 0.01 Gy irradiation. [score:1]
miR-193b-3p and its predicted seed binding site in the 3′UTR of Rad51 is shown in the top panel; the three miR-193b-3p MREs predicted to be located in the 3′UTR of Rad51 are shown in the middle panel; and the Rad51 3′UTR mutant without a seed binding region for miR-193b-3p is shown in the bottom panel. [score:1]
The levels of both H3K9ac and H4K16ac on the miR-193b-3p promoter decreased in the 0.01 Gy-irradiated HepG2 cells. [score:1]
Investigation of miR-193b-3p target genes in the HepG2 cells exposed to 0.01 Gy irradiation. [score:1]
In our qRT-PCR analysis (Fig. 1A), only 5 miRNAs (miR-378a-3p, miR-193b-3p, miR-125a-5p, miR-712-5p, and miR-3963) generated acceptable Ct values, whereas the other 5 miRNAs (miR-877-5p, miR-5114, miR-378b, miR-365-3p, and let-7e-5p) fell below the minimum threshold because of their lower abundance. [score:1]
In addition, the possibility of histone methylation on the miR-193b-3p promoter was also excluded from this study. [score:1]
The levels of miR-378a-3p, miR-193b-3p, miR-125a-5p, and miR-712-5p decreased in response to LDIR, although the level of miR-3963 did not (Fig. 1B). [score:1]
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3
[+] score: 132
ICC intrahepatic cholangiocarcinoma, HNSCC head and neck squamous cell carcinoma MicroRNA Liver disease Target gene(s) miR-155Protective role against non alcoholic steatosis [33]LXR-α[33] C/EBPβ, FOXP3 [35– 37]Up-regulated in NASH [34]Up-regulated in HCC [35]MiR-155 deficiency attenuates steatosis and fibrosis [36] miR-193bDown-regulated in HBV+ HCC [43]CCND1, ETS1 [43]NF1 (HNSCC) [46]Smad3 (glioma) [47] miR-20aDown-regulated in HCC [49]Mcl-1 [49] miR-200aUp-regulated in NAFLD [51]ZEB1, ZEB2 [54]Down-regulated in HCC [52] miR-200cUp-regulated in NAFLD [51]ZEB1, ZEB2, NCAM1 [54]Down-regulated in HCC and ICC [54] miR-27aUp-regulated in HBV+ HCC [55]RXRα, PPARα/γ, FASN, SREBP1, SREBP2 [58, 59] miR-31Up-regulated in fibrosis [60]FIH1 [60]Up-regulated in HCC [17, 53] miR-93Up-regulated in HCC [61, 62]PTEN, CDKN1A [62] miR-99bUp-regulated in HCC [69]mTOR (pancreatic cancer) [66]CLDN11 [69] miR-125a-5pDown-regulated in HCC [89]SIRT7 [89]Biomarker in liver disease [93] miR-182Up-regulated in NAFLD-fibrosis [98]FOXO3 [98]MTSS1 [94], Cebpa [95],Up-regulated in HCC [94– 97]EphrinA5 [96], FOXO1 [97] MiR-193b was down-regulated after 3 and 6 months of HF regimen and revealed over -expression in tumor samples. [score:60]
Mir-155 level increased after 12 months of HF treatment; miR-193b, which was down-regulated after 3 months of treatment, showed weak ascending expression, whereas miR-31 and miR-93 revealed fluctuant levels during the treatment, with slight down-regulation after 12 months. [score:9]
A number of dysregulated microRNAs in this mo del were already described in the pathogenesis of liver disease and showed concordant level of expression with respect to that already described in literature (miR-155, miR-20a, miR-182, miR-200a, miR-200c, miR-27a, miR-31, miR-99b) or discordant expression level (miR-193b, miR-93, miR-125a-5p). [score:8]
Some miRNAs were overexpressed in tumors (miR-155, miR-193b, miR-27a, miR-31, miR-99b, miR-484, miR-574-3p, miR-125a-5p, miR-182), whereas others displayed down-regulation (miR-20a, miR-200c, miR-93, miR-340-5p, miR-720) or a comparable level of expression (miR-200a) with respect to non tumor tissues. [score:8]
MiR-193b over -expression was also detected in head and neck squamous cell carcinoma [46], where neurofibromin1 (NF1) was described as a target, and in glioma [47], where this miR acted as an oncomiR by targeting Smad3, one of the major TGF-β signaling transducers. [score:7]
Li HF Yan PJ Shao ZM Downregulation of miR-193b contributes to enhance urokinase-type plasminogen activator (uPA) expression and tumor progression and invasion in human breast cancerOncogene. [score:6]
org: miR-SVR score −0.1684 and −0.0002; PhastCons 0.5285 and 0.5702, respectively), leaving hypothesize that miR-193b over -expression could be involved in hepatocarcinogenesis through Smad3 down-regulation. [score:6]
The role of this miR in carcinogenesis is quite controversial: miR-193b was described as a tumor suppressor and appeared down-regulated in several cancers, such as melanoma, breast, prostate carcinoma, and human HCC tissues, mainly HBV -positive [38– 43]. [score:6]
Yang Z He M Wang K Sun G Tang L Xu Z Tumor suppressive microRNA-193b promotes breast cancer progression via targeting DNAJC13 and RAB22AInt J Clin Exp Pathol. [score:5]
This evidence could be in agreement with miR-193b down-regulation detected in our mo del during the first 6 months of HF diet treatment. [score:4]
In vitro and in vivo experimental data demonstrated that miR-193b directly targeted CCND1 (cyclin D1) and the transcription factor ETS1 [43]. [score:4]
With this regard, two miR-193b target sites are predicted on mouse Smad3 3′-UTR (microRNA. [score:3]
On the other hand, miR-193b over -expression was described by Braconi et al. [45] in HCV -positive HCC tissues and cells. [score:3]
Zhong Q Wang T Lu P Zhang R Zou J Yuan S MiR-193b promotes cell proliferation by targeting smad3 in human gliomaJ Neurosci Res. [score:2]
With this regard, ETS1/miR-193b 3′UTR alignment can be identified in Mus musculus (microrna. [score:1]
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4
[+] score: 54
The downregulation of mR-193 is quantitatively comparable with the upregulation achieved in panel A. (D) HepG2 cells were transfected with GAPMER control or GAP1 alone or in association with anti-miR-193b, and cell viability assessed by CellTiter-Blue at 48 hours. [score:7]
Among these nine miRNAs, miR-615, miR-193b and miR-346 were upregulated after inhibition of uc. [score:6]
We have previously shown that miR-193b mediates apoptosis through targeting of mcl-1, 12 and the overexpression of uc. [score:5]
158− in Huh-7 cells induced downregulation of miR-193b (figure 7C). [score:4]
Indeed, miR-193b was shown to be downregulated in human HCC. [score:4]
158− in HCC nicely fits with these data as well as with the previous work that found downregulation of miR-193b in a subgroup of HCCs. [score:4]
miR-193b was found to be overexpressed in Huh-7 versus HepG2 cells (in line with uc. [score:3]
158− changed miR-193b expression in human malignant hepatocytes. [score:3]
158− in HepG2 cells, with miR-193b showing the most significant increase and having higher values of expression (figure 7A). [score:3]
158− inhibitor and anti-miR-193b rescued the effect of uc. [score:3]
In three independent experiments, miR-193b expression was higher in Huh-7 in comparison with HepG2. [score:3]
Bars represent logarithmic expression of miR-193b in Huh-7 versus HepG2. [score:3]
We then looked at the level of miR-193b in the sera of patients with HCC (n:10) who were naive for any treatment. [score:1]
Patients with low circulating miR-193b had mainly alpha-fetoprotein (AFP) negative tumours, in line with previous reports of observed lower levels of AFP in CTNNB1-mutated HCC 41 (figure 7E). [score:1]
Co-transfection of GAP1 and anti-miR-193b could rescue the biological effect of uc. [score:1]
miR-193b was predicted to have binding sites within the uc. [score:1]
χ [2] test was used to assess the correlation between miR-193b and alpha-fetoprotein (AFP) groups. [score:1]
158− and miR-193b was assessed by real-time PCR. [score:1]
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5
[+] score: 45
In this study, there were 8 upregulated miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133a-1-5p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p) and 1 downregulated miRNA (mir-215-5p) present as potential targets for differentiation between gram -negative and gram -positive bacterial infection. [score:9]
Following exposure to gram -positive bacteria in the injection and skin graft mo dels, 7 upregulated miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p) and 1 downregulated miRNA (mir-215-5p) were found. [score:7]
Therefore, we focused on these 3 differentially-expressed miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p), and their expression with sequence reads is illustrated in Figure  3. Obviously, the expression of mir-133a-1-3p and mir-133a-2-3p is similar in the 12 libraries. [score:7]
Among them, mir-193b-3p, mir-133a-1-3p, and mir-133a-2-3p presented the most common miRNA targets expressed in the mice exposed to gram -positive bacterial infection. [score:5]
Upon gram -positive bacterial infection, 9 miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133a-1-5p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p, mir-215-5p) showed upregulation greater than 4-fold with a p-value < 0.01. [score:4]
Figure 3 Comparison of the sequence reads as the expression levels of 3 dominant circulation miRNAs (mir-133a-1-3p, mir-133a-2-3p, and mir-193b-3p) in the sera of the mice receiving bacterial infection. [score:3]
Therefore, the 3 most common circulating miRNAs (mir-193b-3p, mir-133a-1-3p, and mir-133a-2-3p) expressed in the mice exposed to Staphylococcus aureus in the absence or presence of Escherichia coli may be potential biomarkers for gram -positive bacterial infection. [score:3]
Although miR-193b has been considered a tumor suppressor gene, and modulates proliferation, migration, and invasion of the cancer cells [22- 25], it has been reported to be associated with death from sepsis in an analysis of 214 sepsis patients (117 survivors and 97 non-survivors based on 28-day mortality) [26]. [score:2]
A functional role of miR-133a and miR-193b was recently revealed in systemic inflammatory responses associated with infections, myocardial infarction, and cancer. [score:1]
It was revealed that a total of 9 miRNAs (mir-193b-3p, mir-133a-1-3p, mir-133a-2-3p, mir-133a-1-5p, mir-133b-3p, mir-434-3p, mir-127-3p, mir-676-3p, mir-215-5p) showed differences greater than 4-fold with p-value < 0.01 between the 2 libraries (Table  1). [score:1]
This study identified mir-193b-3p, mir-133a-1-3p, and mir-133a-2-3p as potential circulating miRNAs for gram -positive bacterial infections. [score:1]
Significant alterations of miR-133a, miR-193b, miR-150, and miR-155 were found in mice after cecal pole ligation and puncture -induced sepsis [12]. [score:1]
Among these miRNAs, mir-193b-3p had the highest fold-change of 61.5-fold and 40.4-fold in the injection and skin graft mo dels of gram -positive bacterial infection, respectively, and of 13.9-fold and 13.0-fold in the injection and skin graft mo dels of mixed bacterial infection, followed by mir-133a-1-3p and mir-133a-2-3p in the gram -positive or mixed bacterial infection. [score:1]
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6
[+] score: 34
Specifically, during severe Plasmodium infection, miR-146a and/or miR-193b regulate functions such as production of inflammatory cytokines (also involving miR-467a), recruitment of macrophages, increased nitric oxide production, disruption of neuronal function, as well as modulation of the expression of surface molecules controlling interactions between circulating cells and endothelial cells [4, 64]. [score:4]
Within the malaria pathway, miR-193b promotes the THBS1, THBS2, and TGFβ2 genes; and regulates apoptosis by targeting myeloid leukaemia cell differentiation protein 1, among others [57]. [score:4]
Dot plots show the expression levels of miR-146a, miR-193b, miR-205, miR-215, miR-467a, miR-150, and miR-486 measured for MV, MV-free plasma, and brains from NI, NCM, and CM conditions, expressed as normalized values as compared to the expression of a panel of control miRNA in each case. [score:4]
The direction of regulation in CM conditions was the opposite for MV and brain tissue in the case of miR-150, miR-205, miR-193b, and miR-467a. [score:3]
The differential expression profiles of these selected miRNA (miR-146a, miR-150, miR-193b, miR-205, miR-215, miR-467a, and miR-486) were analyzed in mouse MV, MV-free plasma, and brain tissue by quantitative reverse transcription PCR (RT-qPCR). [score:3]
Upon verification, two miRNA were confirmed as significantly dysregulated in CM MV: miR-146a and miR-193b, suggesting a role for these miRNA in cerebral pathology, as the same significant changes were not observed in NCM mice [47]. [score:2]
NI MV OpenArray RT-qPCR hsa-miR-328 − 2.5* ± 0.93Not tested [a] hsa-miR-335* − 3.0* ± 1.13Not tested [a] mmu-miR-16* 2.8** ± 0.65Not tested [a] mmu-miR-21* 5.0** ± 0.88Not tested [a] mmu-miR-297a* 5.8* ± 1.60Not tested [a] mmu-miR-685 3.0* ± 1.00Not tested [a] mmu-miR-1949 5.0* ± 1.69Not tested [a] hsa-miR-590-5p Unique to NINot validated [b] rno-miR-450 Unique to CMNot validated [b] mmu-miR-10b 2.7* ± 0.85Not validated [b] hsa-miR-146a 3.2** ± 0.68 7.2* ± 2.74 hsa-miR-150 1.8* ± 0.64 2.7 (ns) ± 2.26 hsa-miR-205 2.3* ± 0.75 − 0.5 (ns) ± 1.89 hsa-miR-486 2.3*** ± 0.18 4.7 (ns) ± 1. 45 mmu-miR-193b − 2.7** ± 0.62 − 7.5* ± 0 62 mmu-miR-215 2.1* ± 0.554.6 (ns) ± 99.39 [c] mmu-miR-467a − 2.0* ± 0.69 − 5.6 (ns) ± 0.96 The list of significantly differentially expressed miRNA in CM vs NI MV from the was compared with the results obtained by. [score:2]
Specifically, miR-193b is decreased in abundance in amyotrophic lateral sclerosis [58], and in sepsis [59], for which it has been identified as a biomarker. [score:1]
The database was searched with the full names of each murine miRNA as per the ThermoFisher Scientific product information and miRBase version 21: mmu-miR-16-1-3p, mmu-miR-21a-3p, mmu-miR-146a-5p, mmu-miR-150-5p, mmu-miR-193b-3p, mmu-miR-205-5p, mmu-miR-215-5p, mmu-miR-297a-3p, mmu-miR-328-3p, mmu-miR-335-3p, mmu-miR-467a-5p, mmu-miR-486a-5p, mmu-miR-685, mmu-miR-1949, and rno-miR-10b-5p. [score:1]
Specifically, miR-146a and miR-193b were both significantly dysregulated in the MV from CM mice compared with NI-increasing 3.2- or 7.2-fold in the case of miR-146a, or decreasing 2.7- or 7.5-fold (miR-193b) in array and, respectively (Table  1). [score:1]
The results of these are denoted as * = 0.05–0.01, ** = 0.01–0.0001, *** ≤ 0.0001 No significant change in the abundance of miR-150, miR-205, miR-215, miR-467a, and miR-486 in MV following Plasmodium infectionOf the seven miRNA of interest tested by RT-qPCR, miR-146a and miR-193b showed the same significant change in abundance as in the OpenArray (from Fig.   2b). [score:1]
The results of these are denoted as * = 0.05–0.01, ** = 0.01–0.0001, *** ≤ 0.0001 Of the seven miRNA of interest tested by RT-qPCR, miR-146a and miR-193b showed the same significant change in abundance as in the OpenArray (from Fig.   2b). [score:1]
Significantly changed abundance of miR-146a and miR-193b in MV following P. berghei infection. [score:1]
d Venn Diagram shows the overlap between statistically significant miRNA as determined by all normalization methods Significantly changed abundance of miR-146a and miR-193b in MV following P. berghei infectionVerification by RT-qPCR was performed on newly generated samples. [score:1]
miR-193b plays a role in the TGFβ2 signaling pathway [55], and in monocyte-macrophage differentiation [56], both of which have been explored in relation to CM [50]. [score:1]
The results are presented as follows: significant changes in MV – miR-146a and miR-193b, significant changes in the brain—miR-205, miR-215, and miR-467a, no significant changes—miR-150 and miR-486. [score:1]
To summarize, three miRNA: miR-146a, miR-193b, and miR-467a, control 10 genes within the malaria pathway: CD40 ligand (CD40L, CD154), CXCL8 (IL-8), IFNγ, Integrin β2 (ITGβ2), Transforming Growth Factor β2 (TGFβ2), Thrombospondin genes (THBS1/TSP1, THBS2/TSP2), Toll-Like Receptors (TLR2, TLR4), and TNF. [score:1]
All the remaining miRNA (Table  1, miR-146a, miR-150, miR-193b, miR-205, miR-215, mir-467a, and miR-486) were tested on MV samples as per the and also on MV-free plasma and brain tissue from NI, NCM, and CM mice. [score:1]
Notably, miR-193b is a predictor of mortality in several other severe inflammatory conditions with associated neurotropic complications. [score:1]
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7
[+] score: 27
Other miRNAs from this paper: mmu-mir-125b-2, mmu-mir-193a, mmu-mir-125b-1
Figure 5 MiR-193a-3p inhibited GC cells proliferation in vitro(A) qRT-PCR revealed that the expression of miR-193a-3p was increased in the mimics group and decreased in the inhibitor group; linc00152 could reverse the increased miR-193-3p level of mimics group in AGS and BGC-823 cells, respectively. [score:7]
It has been shown that down-regulation of miR-193-3p inhibits proliferation, migration, and chemotherapy resistance of tumor cells in GC through regulating PTEN gene [13]. [score:7]
LINC00152 relieved cells proliferation inhibition induced by miR-193a-3p To investigate the influence of miR-193a-3p on GC cells proliferation and the negative regulation effect of LINC00152 on miR-193-3p, we transfected mimics NC, miR-193a-3p mimics, miR-193a-3p inhibitor, miR-193a-3p mimics, and pcDNA3.1-LINC00152 into AGS and BGC-823 cells, respectively. [score:4]
Moreover, the overexpressed LINC00152 increased MCL1 level, while the silenced LINC00152 increased miR-193-3p level. [score:3]
Previous studies revealed that MCL1 was inversely correlated with the level of some miRNAs such as miR-193b [32] and miR-125b [3], and MCL1 expression could induce epithelial–mesenchymal transition (EMT) via some signaling pathways, which subsequently stimulated the invasive and migratory capacity of human GC cells [4]. [score:3]
To investigate the influence of miR-193a-3p on GC cells proliferation and the negative regulation effect of LINC00152 on miR-193-3p, we transfected mimics NC, miR-193a-3p mimics, miR-193a-3p inhibitor, miR-193a-3p mimics, and pcDNA3.1-LINC00152 into AGS and BGC-823 cells, respectively. [score:2]
MiR-193-3p could also negatively regulate MCL1 level (P<0.01, Figure 4E). [score:1]
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8
[+] score: 19
The high expression of miR-122 and miR-705 combined with the downregulation of miR-193 and miR-27a might decrease the levels of fatty acid synthesis and lipid metabolism, which might be important in inhibiting the growth and development of S. japonicum in the host environment. [score:9]
Some differentially expressed miRNAs in liver had important functions, such as involvement in nutrient metabolism, including a cholesterol metabolism regulator (miR-122), a lipid metabolism regulator (miR-705), an adipocyte differentiation and regulation factor (miR-27a and miR-193), and erythrocyte differentiation (miR-223 and miR-451). [score:6]
miR-193 is a key regulator in adipogenesis [35], and miR-27a is known as an important negative regulator of adipocyte differentiation [36]. [score:3]
Among them, miR-122, miR-705, miR-193 and miR-27a were related to nutrient metabolism. [score:1]
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9
[+] score: 19
The expression of miR-342-3p was unchanged while miR-193b expression was slightly induced during the monocyte-to-macrophage transition, while both increased significantly in response to IL-4. In contrast, miR-99b and miR-125a-5p showed a significant induction during monocyte–macrophage differentiation. [score:5]
We examined miR-193b and miR-342-3p as two of the highly expressed IL-4 -induced miRNAs. [score:3]
The IL-4 -dependent induction of mir-193b expression is known, hence we used it as an adequate control of our differentiation method [24]. [score:3]
In contrast, miR-193b expression did not change upon IL-4 treatment. [score:3]
We found IL-4 -dependent induction of miR-342-3p and miR-193b and repression of miR-99b and miR-125a-5p. [score:1]
Some miRNAs from our study, including miR-342-3p and miR-193b, may be promising candidates as potential biomarkers in combination with other well characterized alternative macrophage activation-specific genes and proteins in human diseases. [score:1]
a Stem-loop RT-qPCR -based measurement of miR-342-3p, miR-193b, miR-99b, and miR-125a-5p expression in IL-4-stimulated and unstimulated mouse bone marrow-derived macrophages. [score:1]
Finally, miR-193b has been found to be induced by IL-4 in human macrophages, although its function remains unknown [24]. [score:1]
c Stem-loop RT-qPCR -based measurement of miR-342-3p, miR-193b, miR-99b, and miR-125a-5p expression in human monocytes, 72-h nontreated, and IL-4-stimulated macrophages. [score:1]
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10
[+] score: 16
Furthermore, qPCR was performed again to validate the downregulated and upregulated expression of selected miRNAs that may be relevant to development and confirmed that miR-135, miR-302, miR-449a, miR-200b, miR-200c, miR-193b, miR-130, and miR-141 were downregulated, whereas miR-10a, miR-181, and miR-470 were upregulated by RA treatment (Fig 4C and 4D). [score:16]
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11
[+] score: 16
Of these, eight (miR-193b, miR-199a-3p/hsa-miR-199b-3p, miR-455-3p, miR-210, miR-381 (also known as miR-381-3p), miR-92a, miR-320c, and miR-136) were upregulated, while the other four (miR-490-5p, miR-4287, miR-BART8*, and miR-US25-1*) were downregulated during this process [22]. [score:7]
We demonstrated that miR-193b regulates early chondrogenesis by targeting transforming growth factor β 2 (TGFB2) and TGFBR3 [23], and that miR-455-3p might promote early chondrogenesis by targeting RUNX2 [24]. [score:6]
Hou C. Yang Z. Kang Y. Zhang Z. Fu M. He A. Zhang Z. Liao W. MiR-193b regulates early chondrogenesis by inhibiting the TGF-β2 signaling pathway FEBS Lett. [score:3]
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[+] score: 14
While the cluster miR-193–365 is up-regulated by Prdm16, partially through Pparγ [14], they are not required for brown fat development and function [24]. [score:5]
Of these miRNAs, 145 were expressed in both human and mouse BAT (Additional file 4), including 23 miRNAs that had the same name but their sequences differed by few nucleotides between the species (i. e. miR-155, miR-193b, miR-455). [score:3]
Homeobox C9 (HOXC9) is predicted to be targeted by miR-193, 150 and -26b. [score:3]
However, miR-193b null mice, that are also deficient in miR-365, have normal BAT development, differentiation and function [24]. [score:2]
miR-193b null mice have elevated levels of miR-455 suggesting a compensatory effect in the absence of the miR-193b-365 cluster. [score:1]
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13
[+] score: 13
To reveal the role of these miRNAs in the muscular phenotype of myostatin knockout mice, we quantified their expression by qRT-PCR, and observed a significant increase in the expression of miR-411, miR-434-3p, miR-379, and miR-193b in myostatin knockout mice (Figure 1A). [score:7]
However, the expression of the remaining 9 miRNAs (miR-411, miR-434-3p, miR-299*, miR-193, miR-146b, miR-379, miR-193b, miR-22, and miR-223) has not been verified. [score:3]
Figure 1(A) A significant increase in miR-411, miR-434-3p, miR-379, and miR-193b expression in myostatin -deficient skeletal muscle at 13 weeks of age was determined by quantitative RT-PCR. [score:3]
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14
[+] score: 11
In contrast, the upregulation of miR-149 and miR-193b, and the downregulation of miR-122 and miR-200a were not confirmed in DMD patients (not shown). [score:7]
This included the markedly upregulated miR-378, which is another muscle-enriched miRNA [37] as well as miR-193b, miR-149 and miR-30a. [score:4]
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15
[+] score: 11
Some of the results are in accordance with previous studies, such as the up-regulation of mmu-miR-221 and mmu-miR222 cluster and the down-regulation of the mmu-miR-200 family, as well as of mmu-miR-204, mmu-miR-30a*, mmu-miR-193, mmu-miR-378 and mmu-miR-30e*. [score:7]
The down-regulation of mmu-miR-30a*, mmu-miR-30e*, mmu-miR-193 and mmu-miR-378 during HFD -induced obesity is consistent with previous studies [19], [37], [50]. [score:4]
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[+] score: 8
Downregulation of miR-193b contributes to enhance urokinase-type plasminogen activator (uPA) expression and tumor progression and invasion in human breast. [score:6]
For instance, miR-193b is characterized to have a defined role in breast cancer as its down-regulation contributes to tumor progression and invasion (Li et al., 2009). [score:2]
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[+] score: 7
Among these miRNAs, 3 were downregulated (miR-193, miR-30b and miR-29c) and 2 were upregulated (miR-199a-3p and miR-199a-5p) (Figure 9B). [score:7]
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[+] score: 7
Other miRNAs from this paper: mmu-mir-193a, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-331
According to the literatures [26, 27], two truncated fragments of ING5 (aa 1-184 and aa 107-226) can induce cellular senescence and S arrest by down -regulating Cyclin E and Cdk2 expression, while microRNA-193 was found to have pro-proliferation effects for bone mesenchymal stem cells after low-level laser irradiation treatment by targeting ING5 to regulate Cdk2 activity. [score:7]
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19
[+] score: 6
miR-193b directly targets STMN1 and inhibits the malignant phenotype in colorectal cancer. [score:6]
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20
[+] score: 6
Clustered miRNAs and homologous miRNAs had various expression levels (even involved in larger expression divergence), but they always showed consistent dysregulation patterns (For example, mir-15b cluster and mir-193b cluster; mir-15 family) although the fold change may differ. [score:6]
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[+] score: 6
miR-193, -30b, -30c, -26a, and -26b are highly expressed during early development, gestation and late involution; miR-141, -200a, -148a, and -146b are highly expressed during gestation, lactation, and early and late involution. [score:6]
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[+] score: 6
By contrast, the expression of miR-193b and miR-365, previously shown to be direct downstream targets of Prdm16 and required for BAT differentiation [8], were increased in mG [+] compared to mT [+] cells (Fig. 2D). [score:5]
In addition, the cluster of miR-193b and miR-365, downstream signals of Prdm16, are required for brown adipocyte differentiation [8]. [score:1]
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23
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Among them are two polycistronic transcripts (miR-15a~16-1 and miR-193b~365-1), and two expressing single miRNAs (miR-148a and miR-155). [score:3]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
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[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
14-3-3ζ expression can be modulated by miR-193b and miR-375, which target 3′ UTR of 14-3-3ζ mRNA, in cancer cells (33, 34). [score:5]
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[+] score: 5
In our study, the expression of miR-193a and c-kit was decreased by infection with a miR-193 -expressing lentivirus or 5-AZA treatment. [score:5]
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[+] score: 5
The top 10 differentially expressed miRNAs included miR-193b-5p, miR-365-1-5p, miR-129-5p, miR-122-5p, miR-6240 and miR-5130 which had lower expression in both SAT and VAT (WAT) than in BAT. [score:5]
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[+] score: 5
Leivonen reported that five ERα -regulating miRNAs (e. g. miR-18a, miR-18b, miR-193b, miR-302c, and miR-206) directly targeted ERα in the 3′UTR [29]. [score:5]
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[+] score: 5
Hypo -expression was maintained by miR-200c, 93 and 340-5p and overexpression by miR-193b and 182 (Figure 4B). [score:5]
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[+] score: 5
CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer. [score:5]
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[+] score: 4
miR-365 is clustered with miR-193b which shows similar expression patterns to miR-365 in our system (Tables 2 and 3 ), thus suggesting that these miRNAs may be co-regulated. [score:4]
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[+] score: 4
Other miRNAs from this paper: mmu-mir-193a, mmu-mir-378a, mmu-mir-378b, mmu-mir-378c, mmu-mir-378d
Finally, we profiled microRNA gene expression along the same process, leading to the identification of known general adipogenic microRNAs (e. g. miR-378), brown lineage-specific microRNAs (miR-193), as well as several microRNAs not implicated in adipogenesis so far (S5 Fig and S2 Table). [score:3]
For example, the members of the bone morphogenetic protein (BMP) family, the PPARγ co-factor PGC1α, the transcription factors (TFs) PRDM16, EBF2, KLF11, the protein deacetylase SIRT1, the secreted factors IRISIN and FGF21 as well as lncRNAs Blnc1, lncBATE1, and microRNAs miR193/365 have been shown to be essential for thermogenic fat cell recruitment [6, 10– 13]. [score:1]
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Liu C-G Song J Zhang Y-Q Wang P-C MicroRNA-193b is a regulator of amyloid precursor protein in the blood and cerebrospinal fluid derived exosomal microRNA-193b is a biomarker of Alzheimer’s diseaseMol. [score:4]
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In particular, we identified significant indirect negative correlations between the glutamate receptor signalling and neurogenesis modules with expression indices of miR-193, miR-200, and the miR-34 families (Pearson’s correlation) (Supplementary Fig.   5 and Supplementary Table  3). [score:4]
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For this analysis, we decided to use the eight miRNAs having more than 80 dysregulated targets (miR-23b [50], miR-223, miR-193b [51], miR-424, miR-20a [52], miR-98, miR-891a, and miR-566), see Figure 2. We left the custom degree constraint at the default of 1 for the subsequent ORA. [score:4]
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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-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-411, hsa-mir-378d-2, mmu-mir-146b, 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
In contrast, only one miRNA, hsa-miR-193, was down-regulated in DMD. [score:4]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-193a, mmu-mir-21a, mmu-mir-21b, mmu-mir-21c
The EdU assay showed that overexpression of miR-193 promoted pancreatic cancer cell proliferation, and vice versa (Fig. 2c). [score:2]
Together, we believed that miR-193 promoted cell proliferation and accelerated repopulation through TGF-β2/TGF-βRIII/SMADs/E2F6/c-Myc signaling. [score:1]
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Expression of several miRNAs related to BAT metabolism such as miR-26a, miR-27a, miR-93, miR-193b, miR-365a, and miR-445 were altered in response to the diet in both genotypes while no effect of genotype was observed (Figure S1). [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-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-18a, hsa-mir-22, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-100, 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-30b, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-200b, mmu-mir-203, mmu-mir-204, mmu-mir-205, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-203a, hsa-mir-204, hsa-mir-205, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, 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-18a, mmu-mir-22, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-100, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-375, mmu-mir-375, hsa-mir-335, mmu-mir-335, mmu-mir-133a-2, hsa-mir-424, hsa-mir-193b, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-518f, hsa-mir-518b, hsa-mir-517a, hsa-mir-519d, hsa-mir-516b-2, hsa-mir-516b-1, hsa-mir-517c, hsa-mir-519a-1, hsa-mir-516a-1, hsa-mir-516a-2, hsa-mir-519a-2, hsa-mir-503, mmu-mir-503, hsa-mir-642a, mmu-mir-190b, hsa-mir-190b, mmu-mir-1b, hsa-mir-203b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Yoo KH Kang K Feuermann Y Jang SJ Robinson GW Hennighausen L The STAT5-regulated miR-193b locus restrains mammary stem and progenitor cell activity and alveolar differentiationDev Biol. [score:2]
MiR-193b also has been implicated in regulating mammary stem cell activity in vivo and may serve an additional function in controlling the alveolar differentiation during pregnancy [21]. [score:1]
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[+] score: 3
Interestingly, in the “early” and “late” response phases, Ets1 and Nfat5, are targeted by only a single miRNA, i. e., miR-193 and miR-494, respectively. [score:3]
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Overexpression of miR-193b promotes autophagy and non-apoptotic cell death and thereby significantly impedes the ability of esophageal cancer cells to recover following 5-fluorouracil (5-FU) treatment (Nyhan et al., 2016). [score:3]
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[+] score: 3
miRanda algorithm showed that, activin receptor 1 (ACVR1) is predicted target gene for mmu-mir-193, mmu-mir-294, mmu-mir-295 and mmu-mir132. [score:3]
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42
[+] 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, hsa-mir-411, 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-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
Several miRNAs were found to be highly expressed in particular tissues: miR-204, -218, and -129-2-3p in brain tissues, miR-30a, -30e, -30d, -200a and -200b in kidney, miR-192 in liver, miR-451 in spleen, miR-21 in spleen and thymus, miR-193b, -378 in LDM muscle. [score:3]
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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]
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Most of these miRNAs have been implicated in mechanisms of hepatocellular carcinoma (miR-193b, [13] -195, [14- 16] -200a/b [15, 17- 19]), hepatitis C virus infection of hepatocytes (miR-193b [20] and −320 [21]), and nonalcoholic fatty liver disease and steatohepatitis (miR-200a/b, [22, 23] Table  2). [score:3]
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Few inhibitory miRNAs were identified in melanoma, including miR-34a (uveal melanoma) [16], miR-193b [23], let-7a [24], and miR-211 [25], [26], while miR-182 [27] and miR-221/222 [28]were shown to stimulate metastatic potential of melanoma cells. [score:3]
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Other miRNAs from this paper: hsa-mir-193b, hsa-mir-596, rno-mir-193b
158- was activated by the Wnt/β-catenin pathway in liver cancer and drove cellular growth and migration, possibly by modulating miR-193b expression [18]. [score:3]
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47
[+] score: 2
Several miRNAs, such as miR-33a, miR-26a, miR-193, miR-221/222 and let-7, are regulated by metformin in breast, pancreatic, and lung cancer cells [25– 29]. [score:2]
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The expression of Hsa-miR-101-3p, Hsa-miR-193b-3p, Hsa-miR-21-5p and Hsa-miR-34a-5p was quantified using predesigned primers (Exiqon) and ExiLENT SYBR green master mix (Exiqon Woburn, MA). [score:2]
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Among these 17 dynamically regulated miRNAs, the top 5 with the greatest fold change were miR-126 (23-fold), miR-34c (17-fold), miR-130a (12-fold), miR-574 (9-fold) and miR-193b (8-fold). [score:2]
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50
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miR-30c and miR-193 are a part of the TGF-β -dependent regulatory network controlling extracellular matrix genes in liver fibrosis. [score:2]
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51
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Of the miRNAs that were increased >2-fold in our, only miR-193b had been previously reported to be E2 regulated (in MCF7 cells) [26]. [score:2]
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52
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Although these miRNAs were generally elevated in the mdx samples, for miR-22, miR-30a and miR-193b, the serum miRNA levels dropped below C57Bl/10 levels at the 32-week time point (Supplementary Figure S2A–C). [score:1]
Aside from the established dystromiRs, the four most differentially abundant miRNAs were miR-22, miR-30a, miR-193b and miR-378 (Figure 2A). [score:1]
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Other miRNAs from this paper: mmu-let-7d, mmu-mir-101c
Haetscher N STAT5-regulated microRNA-193b controls haematopoietic stem and progenitor cell expansion by modulating cytokine receptor signallingNat. [score:2]
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54
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However, we found no evidence for that the force reversal of both miR-193-3p and SRSF2/LOXL4 levels in 5637 and H-bc cells have a detectable effect on the level of Nrf2 and its phosphorylated form as well as its nuclear-cytoplasmic distribution (data not shown). [score:1]
It is surprising to find a significant discrepancy between the mRNA level (by qRT-PCR) and protein level (by Western blotting analysis) of SRSF2 and LOXL4 altered by miR-193-3p mimic or antagomiR, the alteration of the protein level is far limited than that of mRNA. [score:1]
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Roy S. Benz F. Vargas Cardenas D. Vucur M. Gautheron J. Schneider A. Hellerbrand C. Pottier N. Alder J. Tacke F. miR-30c and miR-193 are a part of the TGF-β -dependent regulatory network controlling extracellular matrix genes in liver fibrosis J. Dig. [score:2]
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In addition to miR-122-5p, the miRNA species miR-22, miR-29b, miR-29c, miR-130a and miR-193 were increased in both mice and humans. [score:1]
In rats, in addition to miR-122-5p, the increase of miR-22, miR-193 and miR-194 was in accordance with our human data 23. [score:1]
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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, hsa-mir-411, 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
Similar observations were made for miR-124, miR-137, miR-193, miR-210, miR-2, miR-79 and miR87 across species, with miRNAs following the loop-counting rule having lower arm abundances of 5′-isomiRs. [score:1]
Besides shifted seeds, many well-conserved 5′-isomiRs with the same or nearly identical seed regions had different arm abundances among the four species, exemplified by miR-124, miR-193, miR-210, miR-2 and miR-87 (Table 3). [score:1]
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Although it has been previously demonstrated that the microinjection of a single microRNA can both alter the molecular makeup of the embryo and induce phenotypic outcomes in adult offspring (eg microRNA-221/222 [38]; microRNA-1 [37]; microRNA-124 [39]; microRNA-193-5p (partial phenotype) [41]). [score:1]
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This analysis also identified three mouse miRNA homologues: miR-193, miR-10 and miR-200, within the top five most abundant secreted miRNAs. [score:1]
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60
[+] 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-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
99E-0249mmu-miR-185-5pmir-1850.198.912.60E-033.38E-0241mmu-miR-191-5pmir-1910.199.711.25E-031.94E-0228mmu-miR-193-3pmir-1930.256.553.70E-048.12E-0329mmu-miR-1952mir-19520.219.183.70E-048.12E-0372mmu-miR-1961mir-19610.196.581.03E-029.11E-0234mmu-miR-204-5pmir-2040.317.746.87E-041.29E-0226mmu-miR-222-3pmir-2210.2310.222.37E-045.81E-0335mmu-miR-221-3pmir-2210.259.098.47E-041. [score:1]
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Plasma miR-22, miR-101b, miR-122, miR -133a, miR135a*, miR-192, miR193 and miR486 have been shown to be affected by liver damage [39]. [score:1]
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Moreover, another miRNA cluster, miR-193b/365 (ref. [score:1]
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These miRNAs include miR-29a/b, miR-100, miR-107, miR-130b, miR-193b, miR-343-3p, miR-351, and miR-455. [score:1]
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Torres-Ferreira J MiR-193b promoter methylation accurately detects prostate cancer in urine sediments and miR-34b/c or miR-129-2 promoter methylation define subsets of clinically aggressive tumorsMol. [score:1]
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65
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2 mmu-miR-204* mmu-let-7b mmu-miR-30c mmu-miR-500* mmu-miR-219-3p mmu-miR-362-3p mmu-miR-455* mmu-miR-3098-5p mmu-miR-193 DEmiRNAs in bold were confirmed using. [score:1]
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Functions of the other three miRNAs, miR149, miR193 and miR466a-3p, have not been previously examined in the intestinal epithelium in vitro or in vivo. [score:1]
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These are mir-26b, mir-29a, mir-34b, mir-92-1, mir-93, mir-133a-1, mir-133a-2, mir-193, mir-221, mir-223, mir-301, mir-323 and mir-346. [score:1]
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