sort by

7 publications mentioning gga-mir-194

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-194. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 233
Indeed, inhibition of miR-194 elicited to decreasing Runx2 expression and increasing PPAR γ expression in mesenchymal cells under adipogenic conditions (Supplementary Figure S6), suggesting inhibition of miR-194 may commit MSC into adipocytes over osteoblasts. [score:9]
Furthermore, miR-194 expression was upregulated during the differentiation of MSCs toward an osteogenic lineage, while downregulated during adipogenesis. [score:9]
Transfection of miR-194 precursor elicited to increasing Runx2 and OC mRNA expressions, whereas inhibition of miR-194 with anti-miR-194 suppressed the expression in the presence or absence of OM (Figures 3c and e). [score:9]
Furthermore, introduction of miR-194 led to a decrease in COUP-TFII protein level, whereas suppression of endogenous miR-194 increased in C3H10T1/2 cells (Figure 2c), suggesting that miR-194 targeted the COUP-TFII mRNA to suppress its protein expression. [score:9]
[24] In addition, miR-194 inhibits chondrogenic differentiation of human adipose-derived stem cells by targeting Sox5, [25] and suppresses osteosarcoma cell proliferation and metastasis in vitro and in vivo by targeting CDH2 and IGF1R. [score:9]
Collectively, these results suggested miR-194 as a positive regulator of osteoblast differentiation, possibly by the downregulation of COUP-TFII expression. [score:7]
In conclusion, we demonstrated as a novel regulatory mechanism of mesenchymal progenitor cells that miR-194 stimulated osteogenesis and inhibited adipogenesis from MSC via regulating COUP-TFII expression (Figure 5e). [score:7]
The expression of COUP-TFII mRNA was reduced by enhanced expression of miR-194, whereas it was increased by inhibition of miR-194 (Figure 2b). [score:7]
In addition, inhibition of COUP-TFII by siRNA also produced the same phenomenon (Supplementary Figure S5), and COUP-TFII overexpression inhibited the effects of miR-194 on osteogenesis and adipogenesis. [score:7]
To further verify whether miR-194 could regulate osteogenesis through the regulation of COUP-TFII, the expression of miR-194 was altered by transfecting C3H10T1/2 cells with a specific synthetic miRNA precursor or inhibitor (Supplementary Figure S1). [score:7]
These results suggested that miR-194 negatively regulates adipocyte differentiation through suppressing COUP-TFII expression. [score:6]
[12] In the study, we also found that miR-194 overexpression was accompanied by decreased levels of COUP-TFII expression, whereas knockdown of miR-194 increased the COUP-TFII protein level (Figure 3). [score:6]
[26] These findings suggest that miR-194 might be a putative target molecule for regulating metabolic and bone disease. [score:6]
To further determine whether miR-194 directly targets the 3′-UTR of COUP-TFII mRNA, sequences of wild type COUP-TFII-3′-UTR luciferase reporter plasmid (WT), containing the putative miR-194 binding site and mutant COUP-TFII-3′-UTR (MT), with a 4 bp mutation in the seed region, were synthesized (Figure 2d). [score:5]
In addition, the supplementation relived the miR-194 inhibition of lipid droplet formation with the increased expression of aP2 and PPAR γ in mesenchymal lineage cells (Figures 5c and d). [score:5]
The supplementation of COUP-TFII inhibited the promoting effect of miR-194 on mineralization with attenuating miR-194 -induced Runx2 and OC expression (Figures 5a and b). [score:5]
Overexpression of miR-194 also promoted osteoblast differentiation of primary osteoblasts and mesenchymal lineage cells with and inhibited adipocyte differentiation of 3T3-L1. [score:5]
In gain- or loss-of-function experiments, introduction of miR-194 elicited to decreasing expression of PPAR γ, aP2 and adiponectin mRNA, whereas the inhibition of miR-194 increased them (Figures 4c and e, Supplementary Figure S2). [score:5]
The miR-194 reduction of COUP-TFII expression induced osteogenesis and inhibited adipogenesis (Figures 3 and 4). [score:5]
Therefore, miR-194 may prove to be a promising therapeutic target for treatment of metabolic and bone disease, including osteoporosis or obesity. [score:5]
Collectively, these results revealed that miR-194 negatively regulate the expression of COUP-TFII by directly binding to the COUP-TFII-3′-UTR. [score:5]
These findings provided evidence that COUP-TFII may regulate osteogenic differentiation by directly interacting with the Runx2 protein to suppress osteogenic-related genes, which could be considered as one of the mechanisms underlying miR-194 -mediated regulation of osteogenic differentiation. [score:5]
To further confirm whether COUP-TFII directly mediates the miR-194 control of mesenchymal cell differentiation, we examined the effects of COUP-TFII overexpression on the miR-194 control of osteogenesis and adipogenesis. [score:4]
All the above results suggest that COUP-TFII may be a direct target of miR-194. [score:4]
Expression of miR-194 was differentially regulated during osteoblast and adipocyte differentiation. [score:4]
In addition, overexpression of miR-194 promoted matrix mineralization, whereas knockdown reduced mineralization (Figures 3g and h), as evidenced by alizarin red staining. [score:4]
The miR-194 is preferentially expressed in bone compared with other tissues in mice (Supplementary Figure S4), suggesting that it may also have a regulatory role in bone development and homeostasis. [score:4]
When the miR-194 was co -transfected with the empty vector or MT reporter, no decrease in luciferase activity was observed, confirming that the predicted site is a direct target of miR-194. [score:4]
Collectively, these results revealed that COUP-TFII and miR-194 expression was reversible during osteogenesis and adipogenesis of MSCs, suggesting that miR-194 may be a regulator of COUP-TFII in these cells. [score:4]
[12] By in silico analysis, COUP-TFII-3′-UTR was found to have a putative miR-194 binding site (UGUUACA; 92–98 bp far from stop codon; TargetScan). [score:3]
Furthermore, introduction of miR-194 decreased COUP-TFII protein levels, while inhibition of miR-194 caused them to increase. [score:3]
The miR-194 expression increased following osteogenic differentiation, reaching a high on the 4th day (Figure 3a). [score:3]
29, 30 Our study also revealed that miR-194 controlled adipogenesis as well as osteogenesis with alteration of COUP-TFII and PPAR γ expression. [score:3]
COUP-TFII expression vector, not including 3′-UTR, was co -transfected with miR-194 or control miRNA into mesenchymal C3H10T1/2 cells, after which qRT-PCR was performed (Supplementary Figure S3). [score:3]
Consistently, overexpression of miR-194 reduced lipid droplet formation in 3T3-L1, and reversely anti-miR-194 enhanced it (Figures 4g and h), as evidenced by the. [score:3]
The miR-194 control of osteoblast and adipocyte differentiation was related to the expression of COUP-TFII, Runx2 and PPAR γ (Figures 3 and 4). [score:3]
The effects of miR-194 on COUP-TFII expression were further examined by gain- and loss- of-function experiments in C3H10T1/2 cells. [score:3]
During the adipocyte differentiation, expression of miR-194 decreased and reached a minimum on day 4 (Figure 4a). [score:3]
The expression levels of miR-194 were first examined at different time-points of osteogenic differentiation in primary osteoblasts. [score:3]
Because miR-194 was found to have an inhibitory effect on COUP-TFII expression, we investigated whether miR-194 controls osteoblast differentiation. [score:3]
Oligonucleotides (pri-miR negative control (miR-CTL), anti-miR negative control (anti-miR-CTL), pri-miR-194 precursor (miR-194), and miR-194 inhibitor (anti-miR-194)) and mirVana miRNA isolation kits were purchased from Ambion (Austin, TX, USA). [score:3]
These results suggest that miR-194 is critical for maintaining the balance of adipocyte and osteoblast differentiation from MSC through the regulation of COUP-TFII (Figure 5e). [score:2]
These results suggest that miR-194 might be a critical regulator in maintaining the balance between osteogenesis and adipogenesis. [score:2]
In the present study, we identified a novel function of miR-194 concerning the regulation of COUP-TFII -mediated osteogenesis and adipogenesis. [score:2]
[13] Bioinformatic analyses informed us that 3′-UTR of COUP-TFII mRNA has complementary sequence to miR-194, and luciferase assays provided evidence that miR-194 targets the COUP-TFII mRNA in cellular level (Figure 2). [score:2]
In addition, our results consistently showed that the levels of COUP-TFII mRNA and protein were regulated by miR-194 in osteogenesis and adipogenesis processes. [score:2]
In contrast, the knockdown of miR-194 produced the opposite effects. [score:2]
MiR-194 acts as an attenuator of COUP-TFII expression. [score:2]
MiR-194 inhibits adipocyte differentiation. [score:2]
also revealed that miR-194 reduced PPAR γ and COUP-TFII protein levels, and that anti-miR-194 increased them (Figures 4d and f). [score:1]
To confirm interaction between miR-194 and the COUP-TFII-3′-UTR region, cells were transfected with 100 ng of pmirGLO wild type (or 100 ng mutant type) or empty pmirGLO vector (100 ng) in the presence of 10 nM miR-194 precursor (or 10 nM miR-CTL) using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:1]
For functional analysis of miR-194, pmirGLO-COUP-TFII-3′-UTR-Luc constructs containing a partial fragment of COUP-TFII-3′-UTR and luciferase reporter genes were made. [score:1]
Among those detected, miR-194 showed the greatest changes in both osteogenesis and adipogenesis, revealing a twofold induction by osteogenic and a 50% reduction by AM treatment, respectively. [score:1]
MiR-194 regulates lineage specification of mesenchymal cells via COUP-TFII. [score:1]
The introduction of miR-194 enhanced Runx2 protein levels, and transfection with anti-miR-194 reduced Runx2 protein levels (Figures 3d and f). [score:1]
Introduction of miR-194 or anti-miR-194 was confirmed by qRT-PCR (Figure 2a). [score:1]
Cells were transfected with miR-194 precursors or anti-miR-302a using Lipofectamin RNAiMAX (Invitrogen), and then cultured in AM for 8 days. [score:1]
A total of eight miRNAs were identified, including let-7d, miR-17, miR-24, miR-194, miR-195, miR-298, miR-374 and miR-721, which could potentially bind to the 3′-UTR of COUP-TFII mRNA (Figure 1a). [score:1]
Cells were transfected transiently with the indicated plasmids, 20 nM miR-194 (or 20 nM miR-CTL) and 40 nM anti-miR-194 (or 40 nM anti-miR-CTL) using Lipofectamin RNAiMAX (Invitrogen). [score:1]
[1 to 20 of 59 sentences]
2
[+] score: 154
Other miRNAs from this paper: gga-mir-30b, gga-mir-10b, gga-mir-29c, gga-mir-143
Indeed, lentivirus -mediated overexpression of pre-miR-194 abrogated α-MSH’s inhibition on caspase 3 or 7 activities, (Fig. 6), suggesting that down-regulation of miR-194 is necessary for α-MSH’s protection in the glutamate-stimulated retinal explants. [score:8]
The array results demonstrated that the expression levels of miR-10b, miR-192, miR-194, and miR-197 were up-regulated more than 10-fold; whereas those of miR-143, miR-150, miR-28, miR-29c, miR-30b, miR-320a, miR-328, and miR-451a were up-regulated 5- to 10-fold in the glutamate -treated group as compared to α-MSH + glutamate -treated group (Supplementary Table S3, Fig. 5A). [score:8]
Under pathological conditions, excessive excitatory neurotransmitter glutamate binds to ionotropic and metabotropic receptors and causes dramatic up-regulation of miR-194, which may lead to down-regulation of a survival factor and subsequent cell death. [score:7]
On the other hand, lentivirus -mediated expression of miR-194 in osteosarcoma and colorectal cancer cells reduces proliferation, increases apoptosis, and suppresses migration and invasion of these cells, thereby leading to the inhibited tumor growth and metastasis in vivo 50 51. [score:7]
Importantly, lentivirus -mediated overexpression of pre-miR-194 abolished the inhibitory effects of α-MSH on the glutamate -induced elevation in the normalized caspase activity, whereas overexpression of the empty vector did not (Fig. 6G, p < 0.001, miR-194 + α-MSH + glu vs α-MSH + glu; p < 0.001, miR-194 + α-MSH + glu vs RFP + α-MSH + glu; p = 0.757, RFP + α-MSH + glu vs α-MSH + glu). [score:7]
Among the up-regulated miRs, miR-194 exhibited the most dramatic change (Supplementary Table S3, Fig. 5A, 33.76-fold up-regulation in the glu vs α-MSH + glu). [score:7]
Whereas α-MSH binds to MC4R on the cell surface, and inhibits the up-regulation of miR-194 through a currently unknown pathway, hence antagonizing the pro-cell death role of miR-194 (Supplementary Fig. S4). [score:6]
α-MSH down-regulated miR-194 expression during glutamate excitotoxicity in retinal explants. [score:6]
Importantly, a previously unrecognized molecular target, miR-194, downstream MC4R was identified (Fig. 5), and down-regulation of miR-194 during glutamate excitotoxicity was essential for α-MSH’s protection (Fig. 6D). [score:6]
It is possible to speculate that miR-194 targets ZIC1 gene, up-regulation of miR-194 may lead to reduced ZIC1 protein abundance, and then cell death in glutamate-stimulated developing chick retina. [score:6]
At 4 DIV, immunofluorescence (IF) showed that RFP reporter gene carried by both viruses expressed across the retina, including the ONL, INL, and GCL (Fig. 6C), suggesting the efficient viral transduction and overexpression of miR-194 in the explants. [score:5]
miR-194 overexpression abrogated the suppressing effects of α-MSH on caspase activity in glutamate-stimulated retinal explants. [score:5]
As for the downstream target of miR-194, bioinforamtics searches using Pictar and Targetscan reveal 3 potential miR-194 binding sites on the 3′-UTR of chicken ZIC1 gene. [score:5]
Although we do not provide the direct evidence that the molecular mechanism also underlies the protective effects of α-MSH in chick retinas, the approaches employing MC4R antagonist and lentivirus -mediated overexpression of miR-194 have been successfully applied in several animal mo dels. [score:4]
Therefore, both high-throughput and regular qPCR revealed the glutamate -induced miR-194 up-regulation that can be precluded by α-MSH in the retinal explants, providing the hint for the molecule downstream MC4R. [score:4]
Although the signaling pathway mediating MC4R’s regulation on miR-194 and the downstream target of miR-194 are beyond the scope of this study, clues can be gleaned from the studies in similar mo del systems. [score:4]
α-MSH prevented the glutamate -induced upregulation of miR-194 in retinal explants. [score:4]
These results suggest that down-regulation of miR-194 during glutamate -induced excitotoxicity is essential for the anti-cell death effects of α-MSH, and implicate that miR-194 may be the molecule downstream MC4R mediating the α-MSH’s protective effects. [score:4]
Therefore, the α-MSH’s protection against glutamate -induced cell death (Fig. 7) and visual dysfunctions (Fig. 8) in chick retinas is likely due to the MC4R -mediated down-regulation of miR-194 during glutamate excitotoxicity. [score:4]
How to cite this article: Zhang, Y. et al. α-Melanocyte-stimulating hormone prevents glutamate excitotoxicity in developing chicken retina via MC4R -mediated down-regulation of microRNA-194. [score:4]
In a separate experiment, quantitative RT-PCR (qPCR) confirmed the significant up-regulation of miR-194 in the glutamate-stimulated explants in comparison to the α-MSH + glutamate -treated explants and normal controls (Supplementary Fig. S3, Fig. 5B, both p < 0.01, glu vs α-MSH + glu; glu vs normal). [score:4]
Therefore, it would be interesting to ascertain in the future experiments if cAMP-PKA pathway is involved in the MC4R’s regulation on miR-194 expression under glutamate excitotoxicity in our retinal explant cultures. [score:4]
The relative expression levels of miR-194, the miR exhibiting the most dramatic change in the miR array, were confirmed in a separate experiment by qPCR, n = 5–10/group (B). [score:3]
The relative expression levels of miR-194 were analyzed using a comparative threshold cycle (2 [−∆∆Ct]) method. [score:3]
The mechanistic studies indicate miR-194 as a novel therapeutic target for glutamate excitotoxicity in retina. [score:3]
Overexpression of pre-miR-194 abrogated the protective effects of α-MSH in retinal explants. [score:3]
miR-194 exhibited the most dramatic change between the two groups in the array analyses, its expression levels were confirmed by us in a separate experiment. [score:3]
Both high throughput miR qPCR array and regular qPCR revealed the striking difference in miR-194 expression levels between the glutamate-stimulated explants pre -treated with or without α-MSH (Fig. 5), implicating that miR-194 may act as a downstream molecule of MC4R. [score:3]
Pre-miR-194, including mature miR-194 and flanking sequences, was amplified, confirmed by sequencing, and cloned into a lentiviral expression vector (Fig. 6A). [score:3]
The standard curves (Supplementary Fig. S3) served as the positive controls for qPCR, and demonstrated the similar priming efficiency between miR-194 and U6 (Supplementary Fig. S3). [score:1]
The sequence of chicken pre-miR-194 (A) contains the mature miR-194 sequence (bold) and flanking sequences. [score:1]
Representative dot plots of untransduced, lenti-RFP-, and lenti-miR-194-transduced 293T cells were shown in (B). [score:1]
The linear standard curves were generated as described above between miR-194 or U6 Ct values and the logarithm of the cDNA template concentrations (Supplementary Fig. S3). [score:1]
On the next day, 2 μg mixture of endotoxin-free plasmids, including lenti-pre-miR-194 or lenti-RFP, RRE, REV, and VSVG (mass ratio 4:2:1:1.2) were transfected into the 293T cells with the assistance of X-tremeGENE HP DNA Transfection Reagent (Roche, Branford, CT, USA) and chloroquine (Sigma-Aldrich, St. [score:1]
The recombinant vector was termed lenti-pre-miR-194, and the empty vector lenti-RFP. [score:1]
Furthermore, this study identifies a novel mechanism underlying the protective effects of α-MSH that links MC4R to miR-194. [score:1]
On 4 DIV, the transduced and untransduced explants (n = 5/group) were collected for cryosections; On the other hand, the explants were divided into normal, glu, α-MSH + glu, miR-194 + α-MSH + glu, and RFP + α-MSH + glu groups (n = 5–12/group). [score:1]
The cDNA content of miR-194 was normalized to internal standard U6. [score:1]
The titers for lenti-pre-miR-194 and lenti-RFP were 6.4 × 10 [6] TU/ml and 1.3 × 10 [7] TU/ml, respectively. [score:1]
The titers of lenti-pre-miR-194 and lenti-RFP were 6.4 × 10 [6] TU/ml and 1.3 × 10 [7] TU/ml, respectively, as determined by flow cytometry (Fig. 6B). [score:1]
The retinal explants were then divided into normal, glu, α-MSH + glu, RFP + α-MSH + glu, and miR-194 + α-MSH + glu groups. [score:1]
Cloning of chicken pre-miR-194. [score:1]
The titters of lenti-pre-miR-194 and lenti-RFP were equally adjusted. [score:1]
[1 to 20 of 43 sentences]
3
[+] score: 17
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-9-2, mmu-mir-151, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-122, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-214, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-194-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-10a, mmu-mir-210, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-151a, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-16-1, gga-mir-10b, gga-mir-199-2, gga-mir-16-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-199-1, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-122-1, gga-mir-122-2, gga-mir-9-2, mmu-mir-365-2, gga-mir-9-1, gga-mir-365-1, gga-mir-365-2, hsa-mir-151b, mmu-mir-744, gga-mir-21, hsa-mir-744, gga-mir-199b, gga-mir-122b, gga-mir-10a, gga-mir-16c, gga-mir-214, sma-let-7, sma-mir-71a, sma-bantam, sma-mir-10, sma-mir-2a, sma-mir-3479, sma-mir-71b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, gga-mir-365b, sma-mir-8437, sma-mir-2162, gga-mir-9-3, gga-mir-210a, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-mir-10c, gga-mir-210b, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-9b-2, gga-mir-122b-2
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infectionBetween weeks 6 and 12, female parasites continue to produce ∼300 eggs per day [51], resulting in an increase in the number of granulomas in the liver and the development of fibrosis [45]. [score:4]
As shown in Fig. 2, the levels of miR-192, miR-194 and miR-122 in serum do not change between 4–12 weeks post infection, whereas five of the miRNAs that are up-regulated in the liver are also significantly elevated in serum at 12 weeks post infection (p<0.05), ranging from 2.6 fold (miR-21) to 4.7 fold (miR-214) (Table S2). [score:4]
However, according to our analysis, although miR-192, miR-122 and miR-194 were down-regulated in the liver during infection, their levels in serum did not change significantly (Fig. 1– 2). [score:4]
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infection. [score:3]
Consistent with the array results, there was an increase in miR-199-5p, miR-199-3p, miR-214, miR-21, miR-210, and a reduction of miR-192, miR-194, miR-365, miR-122 and miR-151 in the liver tissue of S. mansoni infected mice as compared to naïve mice; miR-9 and miR-744 did not display differential expression and were not analysed further (Table 1). [score:2]
[1 to 20 of 5 sentences]
4
[+] score: 11
Target genes of 14 differentially expressed miRNAs (gga-miR-122-5p, gga-miR-193a-5p, gga-miR-194, gga-miR-215-5p, gga-miR-217-3p, gga-miR-375, gga-miR-1559-3p, gga-miR-1769-3p, gga-miR-1788-3p, gga-miR-1798-5p, gga-miR-2954, gga-miR-3525, and gga-miR-3531-3p) were predicted by using the miRDB and TargetScan programs. [score:7]
A total of 14 differentially expressed miRNAs were detected (gga-miR-2954, gga-miR-215-3p, gga-miR-1798-5p, gga-miR-194, gga-miR-217-3p, gga-miR-1769-3p, gga-miR-1788-3p, gga-miR-1559-3p, gga-miR-3531-3p, gga-miR-215-5p, gga-miR-3525, gga-miR-193a-5p, gga-miR-122-5p, and gga-miR-375). [score:3]
On the other hand, miR-215-3p, miR-194, miR-217-3p, miR-215-3p, miR-193a-5p, miR-122-5p, and miR-375 are more conservative miRNAs in vertebrate animal species. [score:1]
[1 to 20 of 3 sentences]
5
[+] score: 9
Other miRNAs from this paper: gga-mir-302a, gga-mir-302b, gga-mir-302c, gga-mir-302d
MicroRNA-194 reciprocally stimulates osteogenesis and inhibits adipogenesis via regulating COUP-TFII expression. [score:5]
Recent studies have shown that COUP-TFII expression is regulated by Shh, Wnt3a, miR-302a, and miR-194 during the differentiation process; however, it is restricted to adipogenesis and osteodifferentiation events [5– 8]. [score:4]
[1 to 20 of 2 sentences]
6
[+] score: 6
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-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, 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-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
Mdm2 is negatively regulated by several miRNAs including miR-192 (Pichiorri et al., 2010), miR-194 (Pichiorri et al., 2010), miR-215 (Pichiorri et al., 2010), miR-221 (Kim et al., 2010), and miR-17 (Li and Yang, 2012) in different cellular contexts; however, whether these or other miRNAs regulate Mdm2 expression during the CNS development must be determined. [score:6]
[1 to 20 of 1 sentences]
7
[+] score: 5
Top amongst them were miRs reported to decrease tumor metastasis and invasion (miR-194, miR-103, miR-29) [21, 22], inhibit cell proliferation (let-7 family, miR-215) [23], induce apoptosis (miR-125) [24], and tumor suppressors (let-7 family, miR-125, miR-106) [25, 26] to mention but a few. [score:5]
[1 to 20 of 1 sentences]