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31 publications mentioning rno-mir-203a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-203a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 154
Other miRNAs from this paper: rno-mir-146a, rno-mir-203b
B. Downregulation of miR-203expression in response to TGF-β1 (0, 5, 10 ng/ml) for 24 h. The miR-203 expression was analyzed by one-step quantitative real-time PCR. [score:8]
It has also been shown that miR-203 could up-regulate NO expression in female rat MCCs via targeting TRPV4 [31]. [score:8]
Recently the microarry analysis revealed that the expression of miR-203 was significantly downregulated in chronic liver disease and HCC [29], [30]. [score:8]
Moreover, our experiments demonstrated that miR-203 overexpression resulted in significantly decreased TRPV4 expression, suggesting the inhibitory role of miR-203 in liver fibrosis may be correlated to function of TRPV4. [score:7]
In our study, miR-203 expression was downregulated dose -dependently in response to TGF-β1, MTT assay showed that transfection of miR-203 mimics led to a significant inhibition of cell proliferation in TGF-β1 -treated HSC. [score:7]
To determine the potential role of miR-203 in mediating TGF-β1 -induced HSC proliferation, potential targets that are components of TGF-β1 signaling pathway were identified by using miRbase Targets, miRanda, and TargetScan 5.1. [score:7]
C. Upregulation of miR-203 expression in transfected HSC. [score:6]
These results indicated that overexpression of miR-203 inhibited TGF-β1 -induced HSC proliferation. [score:5]
Overexpression of miR-203 inhibited of TGF-β1 -induced HSC proliferation. [score:5]
Moreover, it appeared that the expression of TRPV4 was directly regulated by miR-203 in TGF-β1 -induced HSC (As shown in Fig. 6). [score:5]
3.4 Overexpression of miR-203 inhibits TGF-β1 -induced HSC proliferation. [score:5]
A. Downregulation of miR-203 expression in liver fibrotic tissues compared with vehicle -treated groups. [score:5]
In this experiment, we observed a remarkable declined of miR-203 in response to TGF-β1, in addition, as shown in Fig. 4B, the expression of miR-203 was suppressed by TGF-β1 in a dose -dependent manner (range from 5 to 10 ng/ml at 24 h). [score:5]
Downregulation of miR-203 expression in liver fibrotic tissues compared with vehicle -treated groups. [score:5]
D. MiR-203 overexpression significantly inhibited proliferation of TGF-β1 -induced HSC. [score:4]
These findings convincingly indicated that miR-203 was down-regulated dose -dependently in TGF-β1 -induced HSC. [score:4]
To determine whether TRPV4 gene is a true directly target of miR-203, luciferase reporter vectors encoding a fragment of wild TRPV4 mRNA 3′-UTR, namely, TRPV4-wt was subcloned into a reporter vector downstream of the luciferase gene in HSC. [score:4]
These results demonstrated that TRPV4 is likely a direct target of miR-203. [score:4]
The miR-203 expression of HSC was analyzed by one-step quantitative real-time PCR. [score:3]
The cells transfection with miR-203 mimics significantly increased mature miR-203 expression (Fig. 4C). [score:3]
TRPV4 is a target of miR-203 in HSC. [score:3]
Here, our study provided the initial evidence that, as the target of miR-203, TRPV4 is significantly increased in fibrotic rat livers and plays a critical role in controlling HSC activation. [score:3]
0101179.g005 Figure 5 A. The region of the rat TRPV4 mRNA 3′UTR predicted to be targeted by miR-203. [score:3]
miR-203, a tumor suppressor microRNA, is often silenced in different malignancies, but the roles of miR-203 during liver fibrosis remain obscure at the present. [score:3]
The miR-203 expression was analyzed by one-step quantitative real-time PCR. [score:3]
A. The region of the rat TRPV4 mRNA 3′UTR predicted to be targeted by miR-203. [score:3]
To our surprise, miR-203 was downregulated in rat liver fibrotic tissues compared with the normal liver tissues by one-step quantitative RT-PCR (Fig. 4A). [score:3]
Among the candidate miR-203 targets, we paid more attention to TRPV4 (Fig. 5A). [score:3]
The present study was destined to determine whether miR-203 could play a functional role in regulating HSC proliferation in response to TGF-β1 stimulation. [score:2]
In order to investigate the roles of miR-203 in regulating TGF-β1 -induced HSC proliferation, we tested the effect of miR-203 overexpression on the proliferation of TGF-β1 induced HSC. [score:2]
To investigate whether miR-203 has a role in TGF-β1 induced HSC activation, we firstly sought to determine whether TGF-β1 regulates miR-203 expression in activated HSC. [score:2]
3.5 TRPV4 is a Target of MiR-203 in HSC. [score:2]
Real-time PCR analysis revealed that TRPV4 expression was significantly lower in miR-203 transfected HSC compared with the NS-miRNA -transfected cells (Fig. 5B). [score:2]
Moreover, we explored the potential function of miR-203 in the regulation of TRPV4 in vitro. [score:2]
The MTT assay showed that introduction of miR-203 caused a significant inhibition of cell proliferation in TGF-β1 -induced HSC (Fig. 4D). [score:2]
Briefly, HSC-T6 cells (5×104cells/well) were cultured into 24-well plates and co -transfected with 200 ng DNA of TRPV4-UTR wt plasmid in the presence of 60 nmol of miR-203 mimics and NS-miR-203 (Gene Pharma, Shanghai, China), using 2.5 uL lipofectamine 2000 and 100 uL Opti-MEM (Invitrogen, USA). [score:1]
The role of miR-203 in regulating TGF-β1 -treated HSC proliferation was tested by MTT assay. [score:1]
2.4 Cell transient transfection of miR-203 mimics and siTRPV4. [score:1]
The sequences of oligonucleotides used are as follows: miR-203 mimics: 5′-GUGAAAUGUUUAGGACCACUAG-3′ 5′-AGUGGUCCUAAACAUUUCACUU-3 NS-miRNA: 5′-UUCUCCGAACGUGUCACGUTT-3′ 5′-ACGUGACACGUUCGGAGAATT-3′ Si-TRPV4: 5′- CCGUGUCCUUCUACAUCAATT -3′ 5′- UUGAUGUAGAAGGACACGGTT -3′ si-control: 5'-UUCUCCGAACGUGUCACGUTT-3' 5'-ACGUGACACGUUCGGAGAATT-3' Ru was dissolved in Dulbecco's modified Eagle's medium (DMEM, Gibco, USA) with 10% fetal bovine serum and used at a concentration of 1 uM. [score:1]
Luciferase reporter assays showed that the relative luciferase activity of the reporter that contained wild-type 3′-UTR of TRPV4 mRNA was significantly decreased in miR-203 -overexpressed cells compared to control cells (Fig. 5C). [score:1]
Reporter construct containing wt TRPV4 3′-UTR was cotransfected with miR-203 mimics or NC-miRNA. [score:1]
The sequences of oligonucleotides used are as follows: miR-203 mimics: 5′-GUGAAAUGUUUAGGACCACUAG-3′ 5′-AGUGGUCCUAAACAUUUCACUU-3 NS-miRNA: 5′-UUCUCCGAACGUGUCACGUTT-3′ 5′-ACGUGACACGUUCGGAGAATT-3′ Si-TRPV4: 5′- CCGUGUCCUUCUACAUCAATT -3′ 5′- UUGAUGUAGAAGGACACGGTT -3′ si-control: 5'-UUCUCCGAACGUGUCACGUTT-3' 5'-ACGUGACACGUUCGGAGAATT-3' Ru was dissolved in Dulbecco's modified Eagle's medium (DMEM, Gibco, USA) with 10% fetal bovine serum and used at a concentration of 1 uM. [score:1]
HSC-T6 cells were cultured in serum-free DMEM for 12 h and then subjected to transfection with miR-203 mimics, (NS)-miRNA (GenaPharma, China) and Si-TRPV4, Si-control using Lipofectamine 2000 (Invitrogen, USA)according to the manufacturer's instruction. [score:1]
[1 to 20 of 43 sentences]
[+] score: 122
Other miRNAs from this paper: rno-mir-27a, rno-mir-203b
Further mechanistic studies using cortical neuron cultures revealed that RF treatment induced increased miR-203 expression which in turn inhibited c-Jun expression and increased neuronal cell survival. [score:7]
We further identified c-Jun as a target of miR-203 and its inhibitory effect on c-Jun expression in agreement with earlier studies [21, 22]. [score:7]
The evaluation of the direct effects of RF and UV-B-RF treatments on c-Jun expression revealed that RF or miR-203 overexpression significantly inhibited c-Jun protein expression in SH-SY5Y cells subjected to OGD and cortical neuron cells and cortical brain tissue subjected to ischemic injury, compared to that of the UV-B-RF treatment (Figure  6A). [score:7]
As c-Jun is a negative regulator of miR-203, the circuit constitutes a feedback loop, whereby RF treatment in neuronal cells had increased levels of miR-203 expression, inducing an inhibition of c-Jun resulting in neuroprotection [23, 24], where as UV-B irradiated RF was devoid of this effect. [score:6]
The neuroprotective miR-203 is known to inhibit c-Jun [20- 22] and the inhibition of c-Jun is known to have neuroprotective effects [23]. [score:5]
Interestingly, we found RF treatment both in vivo and in vitro significantly increased miR-203 expression and subsequent c-Jun inhibition leading to neuroprotection. [score:5]
alters the neuroprotective ability of RF through modulation of the miR-203/c-Jun signaling pathwayThe neuroprotective miR-203 is known to inhibit c-Jun [20- 22] and the inhibition of c-Jun is known to have neuroprotective effects [23]. [score:5]
differentially regulates RF induced expression of miR-203 in-vivo and in-vitroExperimental evidence has established the role of miRNAs as critical regulators of neuronal cell survival and cell death [3- 7]. [score:5]
The RF induced increase neuronal cell survival was comparable to the over expression of miR-203, pharmacological and genomic inhibition of c-Jun in cortical neurons (Figure  6). [score:5]
Thus, our results suggest a novel notion: RF preconditioned neuronal cells have increased while UV-B-RF preconditioned neuronal cells have no marginal change in miR-203 expression thereby leading to differential effects on c-Jun inhibition and neuroprotection. [score:5]
The miRNA PCR array analysis indicated that the RF preconditioning increased expression of miR-203, whereas UV-B-RF treatment induced only 0.25 and 0.50 fold change in its expression in cortical neuron cells and cortical brain tissue respectively (Table  1). [score:5]
This was further confirmed through the over expression of miR-203, in cortical neurons which led to significant decrease in the c-Jun expression (Figure  5D). [score:5]
These results clearly indicated that, RF treatment sustained the increased expression of miR-203 in neuronal cells while UV-B-RF has no significant effect on its expression. [score:5]
UV-B irradiation differentially regulates RF induced expression of miR-203 in-vivo and in-vitro. [score:4]
Figure 5 differentially regulates RF induced expression of miR-203 in vivo and in vitro. [score:4]
This finding may possibly due to the existence of a regulatory circuit, in which miR-203 and c-Jun mutually inhibit each other. [score:4]
25miR-10b-1.30.20-1.100.30miR-1451.10.400.940.35miR-3501.40.351.100.50 miR-27a -1.3 0.44 -1.20 0.49 miR-203 expression level increases significantly (p<. [score:3]
The relative decrease in the miR-203 expression with respect to the controls in the cultured neuronal cells or brain tissues treated by UV-B-RF was 0.25 and 050 folds respectively. [score:3]
Therefore, we next explored the effects of increased miR-203 expression on c-Jun levels. [score:3]
Importantly, further studies are required to assess the translational value of the therapeutic activation of the miR-203/c-Jun signaling pathway for neuroprotection. [score:3]
This finding was further confirmed by the comparable reduction in LDH secretion through miR-203 over expression in cortical neurons (Figure  5B). [score:3]
RF significantly increased the expression of miR-203 compared to that of UV-B-RF (B) RF treatment or miR-203 overexpression significantly decreased the LDH secretion compared to that of UV-B-RF treatment. [score:3]
Collectively, these results showed that alters the RF induced increase in the expression of miR-203 in neuronal cells both in vivo as well as in vitro. [score:3]
The miR-203 has neuroprotective effects [20] and it is known to regulate cell proliferation, differentiation and death [21, 22]. [score:2]
Functional assays clearly demonstrated that the UV-B-RF preconditioning failed to sustain the increased expression of miR-203 and the decreased levels of c-Jun, mediating the neuroprotective effects of RF. [score:2]
of the luciferase assay indicated that the miR-203 targeted the 3′-UTR of c-Jun (Figure  5C). [score:2]
Consistent with this finding, our study showed that the RF treatment in neuronal cells induced significantly increased expression of miR-203, decreased OGD induced LDH secretion and increased cell survival compared to that of the UV-B-RF treatment. [score:2]
The luciferase reporter plasmids containing the wild-type 3′UTR with the miR-203 binding site of c-Jun was obtained from Genecopoeia (Rockville, MD, USA). [score:1]
UV-B irradiation alters the neuroprotective ability of RF through modulation of the miR-203/c-Jun signaling pathway. [score:1]
Cortical neuron cells were transfected with the luciferase constructs (100 ng per 24-well) and pre-miR-203 or pre-miR-Control (10 nM, Applied Biosystems) using Lipofectamin 2000 (Invitrogen). [score:1]
Finally we tried to confirm the role of the miR-203/c-Jun signaling on cortical neuron cell survival in the conditions of OGD. [score:1]
Taken together our studies suggest that (i) induces attenuation of the neuroprotective effects of RF (ii) through the modulation of the miR-203/c-Jun signaling pathway. [score:1]
Figure 6 modulates the miR-203/c-Jun signaling pathway for altering the neuroprotective effect of RF. [score:1]
attenuated the neuroprotective effects of RF through modulation of the miR-203/c-Jun signaling pathway. [score:1]
Collectively, these results suggested that the alters the neuroprotective effects of RF through modulation of the miR-203/c-Jun signaling pathway. [score:1]
Immunoblotting analysis of (A) p-H2AX and (B) Cleaved caspase-3 in cell lysates prepared from the cortical regions of the brain subjected to ischemic injury and pretreated with either vehicle (saline), RF (10 mg/kg i. p. ), UV-B-RF(10 mg/kg, i. p. ) or miR-203 mimic (200 nM/kg i. p. ). [score:1]
[1 to 20 of 36 sentences]
[+] score: 120
Consistent with these reports, the current results in isolated rats showed that gene expression for SOCS3 was suppressed while miR-203 was upregulated on days 3 and 5. Thus, as reported here in conditions of isolation stress, miR-203 overexpression may have contributed to the delay and eventual prolongation of inflammation, and reduced expression of angiogenic factors, via its actions on VEGFA. [score:12]
Our results confirmed that VEGFA is a direct target of these miRNAs, as both miR-29a,c and miR-203 strongly and specifically suppressed endogenous VEGFA expression in vitro. [score:8]
Although there are presumably additional targets regulated by miR-29 and miR-203, our experiments suggest that VEGFA suppression is mediated, at least in part, by overexpression of these miRNAs. [score:8]
Overexpression of miR-29b was detected on days 3 and 5. Expression level of miR-203 was also markedly higher on days 3 and 5 (4.2-fold and 2.6-fold, respectively) (Figure 3B). [score:5]
Based on bioinformatics analysis, a highly conserved miR-29 isoform -targeting sequence and a miR-203 -targeting sequence were identified in the VEGFA mRNA 3’ UTR (Figure 4A). [score:5]
Relative expression levels of miR-29 family members (A) and miR-203 (B) in isolated (ISO) rats are in comparison to control levels expressed as 1 on the graph. [score:5]
Cells were co -transfected with constructs containing the predicted targeting sequence (WT) or mutated targeting sequence (Mutant) cloned into the 3’-UTR of the reporter gene, along with miRNA mimics of miR-29 or miR-203. [score:5]
0072359.g004 Figure 4(A) The predicted miR-203 and miR-29 targeting sequences located in the 3’-untranslated region (3’-UTR) of VEGFA mRNA. [score:5]
These data suggest that overexpression of miR-29 and miR-203 contributes to isolation -induced delays of wound healing, partially by suppressing VEGFA. [score:5]
MiR-203 and miR-29 directly target VEGFA mRNA. [score:4]
miR-29a, miR-29c (Figure 4B) and miR-203 (Figure 4C) significantly reduced activity of firefly luciferase by directly targeting the rat VEGFA 3′ UTR. [score:4]
miR-29a,c and miR-203 Suppress Endogenous VEGFA. [score:3]
In accordance with these findings, our results demonstrate that miR-29 family members and miR-203 were persistently overexpressed across healing in isolated rats. [score:3]
Suppression of SOCS3 by miR-203 results in increased and prolonged skin inflammatory responses [39]. [score:3]
In this study, VEGFA was the only healing -associated mRNA targeted by miR-29 and miR-203 (out of the nine that were tested). [score:3]
For functional analysis, miR-29 (a, b, c) mimics, miR-203 mimics and non -targeting miRNA mimics (Dharmacon, Lafayette, CO, USA) were transfected into cells using DharmaFECT Transfection Reagent 1 (Dharmacon) per the manufacturer’s instructions. [score:3]
As shown in Figure 4D, ectopic transfection of miR-29a, miR-29c and miR-203 in HEK293 cells led to a significant decrease in VEGFA protein expression. [score:3]
0072359.g003 Figure 3 Expression of miR-29 family members, miR-203 and SOCS3 mRNA in wounded tissues by. [score:3]
miR-29a,c and miR-203 Target VEGFA. [score:3]
Expression of miR-29 family members, miR-203 and SOCS3 mRNA in wounded tissues by qRT-PCR. [score:3]
Furthermore, co-transfection of miR-29c and miR-203 mimics produced an additive effect on reducing VEGFA expression in vitro. [score:3]
Interestingly, in this study, we identified a negative correlation between levels of VEGFA and the expression of miR-29a,c and miR-203 in wounds. [score:3]
Wound closure was assessed daily and tissues were collected for determination of gene expression levels and miRNAs (i. e., miR-29a,b,c and miR-203). [score:3]
Corresponding to the higher miR-203 levels, mRNA levels of SOCS3, which is a known direct target of miR-203, were found to be lower in isolated rats on days 3 and 5 (0.32 ± 0.04 and 0.75 ± 0.09, respectively) compared to control rats. [score:3]
As expected, mutation of the putative miR-203 binding site abolished the effect of miR-203 while leaving the action of all three miR-29 isoforms unaffected (Figure 4B). [score:2]
Intriguingly, both miR-29 and miR-203 are important regulators of wound-specific cell functions and the cytokine network [38, 39]. [score:2]
Mutation of the putative miR-203 binding site abolished the effect of miR-203 while leaving the action of all three miR-29 isoforms unaffected (B). [score:2]
Both miR-29a and miR-203 reduced luciferase activity by ≥ 40% (p<0.001) (Figure 4B, C). [score:1]
In this study, we hypothesized that social isolation delays oral mucosal wound healing, and healing -associated genes and miRNAs (i. e., miR-29 and miR-203) play a role in this process. [score:1]
Considering the important role of miR-29 and miR-203 in both dermal and mucosal repair, these results suggest a putative mechanism for isolation -induced healing impairments through the modulation of VEGFA. [score:1]
In both the putative miR-29 and miR-203 binding sites, the 6 to 8 nucleotides of the “seed region” were replaced with a restriction enzyme site with minimal complementarity to the miRNA sequence (see Materials and). [score:1]
Intriguingly, the isolated rats persistently exhibited higher levels of miR-29 family members and miR-203. [score:1]
To test this, we selected and determined the levels of two miRNAs in wounds: miR-29 and miR-203. [score:1]
Isolation Stress and Levels of miR-29 and miR-203. [score:1]
MiR-203 is the first identified skin- and keratinocyte-specific miRNA. [score:1]
This suggests there are novel roles of miR-29 and miR-203 in isolation-impaired healing. [score:1]
[1 to 20 of 36 sentences]
[+] score: 60
Other miRNAs from this paper: rno-mir-203b
Only ten of these 39 microRNAs were up-regulated by TNF-α and these are listed in Table 4. In silico analysis using the miRanda algorithm [35] next identified one of the ten up-regulated microRNAs (miR203) as having the potential to target mouse lysyl oxidase mRNA. [score:9]
TNF-α down-regulated lysyl oxidase at the post-transcriptional level in C3H10T1/2 cells by reducing the half-life of lysyl oxidase mRNA mediated by miR203, and not by inhibition of lysyl oxidase transcription as originally predicted. [score:6]
We next functionally verified the up-regulation of miR203 in Wnt3a-stimulated C3H10T1/2 in response to TNF-α in the presence or absence of Wnt3a pretreatment using a miR203 luciferase reporter (miR203-RenSPL) which generates an mRNA that can be targeted by a functional and fully processed miR203. [score:6]
TNF-α was found to inhibit lysyl oxidase expression, but not through the expected transcriptional mechanism, but rather through miR203. [score:5]
0100669.g006 Figure 6 A) miR203 down-regulates lysyl oxidase mRNA levels: C3H10T1/2 cells were transfected with miR203 mimic or non-specific control micro RNA. [score:4]
Analysis of miR203 functionality to down-regulate lysyl oxidase mRNA levels. [score:4]
Figure S3 TNF-α up-regulates miR203 in Wnt3a-stimulated pluripotent progenitor cells. [score:4]
A) miR203 down-regulates lysyl oxidase mRNA levels: C3H10T1/2 cells were transfected with miR203 mimic or non-specific control micro RNA. [score:4]
B) To functionally evaluate TNF-α up-regulation of functional miR203 in C3H10T1/2 cells, cells were transfected with the miR203 reporter plasmid miR203-RenSPL and R01-RenSPL (control) constructs. [score:2]
miR203 mimic is a synthetic double stranded RNA, and can be directly transfected into cells. [score:2]
C3H10T1/2 cells were transfected with a miR203 mimic or control microRNA (AllStars siRNA). [score:1]
Cells were seeded in a 6-well plate at the density of 1×10 [6] per well, and the next day, were incubated with 2 ml per well of transfection master mix [Eagle's MEM supplemented with 5 nM siRNAs (miR203 mimic or negative control mimic), 20 µl Hi-perfect reagent, and 0.1% BSA] for 8 hours. [score:1]
C3H10T1/2 cells were transfected with miR203 mimic (Syn-mmu-miR-203 miScript microRNA Mimic, Qiagen cat#MSY0000236) or a control microRNA mimic (AllStars Negative Control siRNA, Qiagen cat#1027280) using Hi-Perfect (Qiagen cat#301705). [score:1]
The results revealed that TNF-α induces miR203 in C3H10T1/2 cells under both Wnt3a-stimulated (Figure 6B, panel i) and non-stimulated conditions (Figure 6B, panel ii, evident as reduced luciferase activity in these groups. [score:1]
Thus, cells were transfected with miR203 or R01 (control) luciferase, starved overnight, and treated with Wnt3a- or control-conditioned media for 24 hours. [score:1]
Lysyl oxidase mRNA levels were reduced down to 20% of control levels in cells transfected with the miR203 mimic (Figure 6A). [score:1]
To functionally assess for TNF-α -induced miR203, 80% visually confluent cells were transfected with miR203 RenSP-luciferase construct (miR203-RenSPL, cat#S880167) or R01 scrambled control RenSP-luciferase construct (R01-RenSPL, cat#S790001), using FuGene-6 as described above. [score:1]
Taken together, the results from these two experiments confirmed that miR203 is induced by TNF-α and reduces lysyl oxidase mRNA levels in a mo del of pluripotent mesenchymal cells. [score:1]
The mature miR203 sequence is 5′UGAAAUGUUUAGGACCACUAG. [score:1]
The luciferase activity of miR203 reporter is inversely correlated with the levels of fully processed and functional miR203 because the transcript of miR203-RenSP construct has a specific binding site for miR203. [score:1]
Panel (iii) is from cells treated only with or without Wnt3a showing that this reporter for miR203 activity is not affected by Wmt3a alone, as expected. [score:1]
FuGene-6 reagent (Roche# 11914443001) was used to transiently transfect cells with various constructs: (i) lysyl oxidase promoter firefly-luciferase construct (pLOXFFL); (ii) TCF/LEF mutated lysyl oxidase promoter firefly-luciferase constructs (pmLOXFFL); (iii) pCS2+DKK1-flag (plasmid 16690) and SOST/pcDNA3.1+ (plasmid 10842) both from Addgene; (iv) miR203 RenSP-luciferase construct (miR203-RenSPL); (v) R01 control RenSP-luciferase construct (R01-RenSPL); (vi) Renilla luciferase thymidine kinase (pRL-TK, Promega cat#E2241). [score:1]
The data presented as a ratio of miR203-RenSPL reporter to R01-RenSPL reporter. [score:1]
Figure 6B panel iii shows that Wnt3a treatment does not affect the activity of this miR203 reporter, as expected. [score:1]
[1 to 20 of 24 sentences]
[+] score: 50
Other miRNAs from this paper: mmu-mir-203, rno-mir-203b
It has been reported that p63 expression is strongly inhibited during low-calcium culture of primary mouse keratinocytes transfected with wild-type miR-203, which indicates that miR-203 regulates p63 by translational suppression [46]. [score:10]
MiR-203 regulates p63 by suppressing translation, and strongly inhibits p63 expression. [score:9]
With regard to early-stage protein expression, we found increased m -RNA transcription in CD29, p63, VEGF-A, sustained expression of high levels of CK15 and low levels of the regulatory factor miR-203, suggesting that the chitin membrane promotes early-stage protein synthesis at the wound surface and enhances the healing speed together with ESCs which is play an important role in this process, perhaps because the signaling molecules secreted by these cells may induce ESCs differentiation, resulting in self-repair and regeneration of tissues after activation. [score:6]
Quantitative RT-PCR was used to analyze the mRNA expression levels of CD29, CK15, p63 and VEGF-A throughout the ESCs -modified chitin membrane skin repair process and to track changes in the regulatory factor microRNA-203 (miR-203). [score:4]
Regulatory factor miR-203 did not show a significant difference between the two groups before day 7, but its expression increased in the group C-CBM at day 28 and the two groups significant difference (P<0.01) (Figure 5B, f). [score:4]
MiR-203 expression is obvious during epidermis differentiation and development. [score:3]
Over-expressed miR-203 reduces Np63 mRNA [45]. [score:3]
After the defects of miR-203, p63 translation in the basal epidermis will increase. [score:3]
If expressed too early in epidermal cells in the basal layer, miR-203 may result in premature differentiation and defects of proliferative potential. [score:3]
MiR-203 targets Np63 mRNA, and acts as a switch in the proliferation and differentiation of keratinocytes in the adult epidermis. [score:2]
MiR-203 is a regulation gene of ESCs differentiation. [score:1]
Therefore, miR-203 is a key molecule controlling the differentiation of keratinocytes from the basal state to the basal layer. [score:1]
Quantitative RT-PCR Analysis and miR-203. [score:1]
[1 to 20 of 13 sentences]
[+] score: 46
Additionally, miR-203 is known to directly target suppressor of cytokine signaling 3 (SOCS3) and block its role as an inhibitor of cytokine signal transduction [42]. [score:8]
fcgi?artid=1860071&tool=pmcentrez&rendertype=abstract Accessed 2013 February 5. 42Ru P, Steele R, Hsueh EC, Ray RB (2011) Anti-miR-203 Upregulates SOCS3 Expression in Breast Cancer Cells and Enhances Cisplatin Chemosensitivity. [score:6]
com query, 374 genes are predicted targets of rno-miR-142-5p and 386 genes are predicted targets of rno-miR-203. [score:5]
Intraperitoneal administration of the α [1]-ADR antagonist prazosin (2.0 mg/kg) 30 min prior to Stress attenuated the stress -induced down-regulation of miR-142-5p, but not miR-203. [score:4]
Down-regulation of miR-203 is also capable of inducing TNF-α and IL-6 synthesis by enabling myeloid differentiating factor 88 (MyD88) activation [43]. [score:4]
45Ding X, Park SI, McCauley LK, Wang C-Y (2013) Signaling between transforming growth factor β (TGF-β) and transcription factor SNAI2 represses expression of microRNA miR-203 to promote epithelial-mesenchymal transition and tumor metastasis. [score:3]
For example, exposure to the same stressor tested here is known to modulate genes involved in the TGF-β pathway [44], which is a prime target of miR-203. [score:3]
KEGG analysis also revealed that miR-203 targets metabolic pathways, which is in line with cortisol mediation of metabolic pathways during the stress response [46]. [score:3]
Activation of SOCS3 terminates the innate immune response; therefore, stress -induced reductions in exosomal miR-203 could prevent activation of SOCS3 and its downstream suppression of pro-inflammatory cytokines. [score:3]
Pathway enrichment analyses of rno-miR-142-5p and rno-miR-203. [score:1]
MiRNA from stressed, control, stress + prazosin, and control + prazosin rats were analyzed for changes in miR-142-5p, miR-150, miR-155, and miR-203. [score:1]
Functionally enriched pathways impacted by miR-142-5p and miR-203. [score:1]
Stress reduces exosomal miR-142-5p and miR-203. [score:1]
KEGG and Wiki analyses revealed that rno-miR-142-5p and rno-miR-203 are related to several functional categories, including metabolic pathways (25 genes), mRNA processing (12 genes), cancer pathways (10 genes), ubiquitin mediated proteolysis (9 genes), mitogen-activated protein kinase (MAPK) signaling (8 genes), transforming growth factor-β (TGF-β) signaling pathway (6 genes), and TGF-β receptor signaling pathway (6 genes). [score:1]
Therefore, stress -induced reductions in miR-203 likely promote elevations in TGF-β activity, which may be crucial for constraining stress -induced immunomodulation. [score:1]
In addition, miR-203 is known to repress the anti-inflammatory properties of TGF-β [45]. [score:1]
[1 to 20 of 16 sentences]
[+] score: 22
Inhibition of FGF signaling through SU5402 -treated primitive streak regions of chick embryos identified up-regulation of let-7b, miR-9, miR-19b, miR-107, miR-130b, miR-148a, miR-203, and miR-218 and down-regulation of miR-29a and miR-489 (Bobbs et al. 2012). [score:9]
Down-regulation of Dicer1, predicted by miR-152, miR-203 and miR-222, could be a part of a complex regulation related to the global abundance of miRNAs and their requirements for processes such as cell-cycle exit control and onset of cell differentiation. [score:5]
In contrast, expression of miR-9 and miR-203 was induced by FGF2 in lens, although they were induced via inhibition of FGF receptors in the embryonic chick mo del (Bobbs et al. 2012). [score:5]
Ten miRNAs, miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351. [score:1]
Similarly, the highest ranking “late” -induced miRNAs, including miR-203, miR-182, miR-181a, miR-369-3p, and miR-29c (Figure 6B), also make the greatest number of connections with the 12 genes analyzed in Figure 6B. [score:1]
Similar analysis of “late” group, including c-Maf, Ets1, N-Myc, Nfat5, and Nfib, yielded 10 miRNAs: miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351, with multiple connections. [score:1]
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[+] score: 21
For these miRNAs, both platforms reported them to be similarly regulated; miR-320 was up regulated while let-7d and miR-203 were down regulated (Tables  1 and 4). [score:4]
Regardless of platform differences, the three miRNAs identified by both platforms, let-7d, miR-203 and miR-320, hold promise as tubular injury biomarkers due to their strong functional associations with cellular process or pathways relevant to renal disease. [score:3]
This led to identification of several additional renal activities, including a link between the third common miRNA identified by both platforms, miR-203, and polycystic kidney disease (Figure  5A). [score:3]
Network analysis was performed on the three conserved miRNAs (let7a-5p, miR-203-3p, and miR-320b) using IPA’s ‘Grow’ function to add genes experimentally linked downstream of the miRNAs via ‘RNA/RNA interactions analysis: miRNA targeting’ relationship. [score:3]
However, all three miRNAs: let-7d, miR-203, and miR-320 were reliably detected by qRT-PCR in every sample with low mean C [t] values (miR-let-7d: 27.52 ± 0.77; miR-203: 24.66 ± 0.3; miR-320: 24.69 ± 1.1) which suggests relatively high levels of urinary expression. [score:3]
Out of the 14 miRNAs that were detected to be differentially expressed using NGS (Table  4), five (rno-let-7d-5p, rno-miR-100-5p, rno-miR-203a-3p, rno-miR-21-5p, rno-miR-320-3p) were represented on the TLDA-A, while nine (rno-miR-378a-3p, mmu-miR-5100, rno-miR-30e-3p, rno-miR-125b-2-3p, rno-miR-320-5p, rno-miR-3473, rno-miR-21-3p, rno-miR-455-5p, and hsa-miR-7641) were not. [score:3]
miRNAs identified by both platforms, let-7d, miR-203, and miR-320, may potentially serve as promising novel urinary biomarkers for drug induced renal tubular epithelial injury. [score:1]
Three miRNAs, rno-miR-320-3p, rno-miR-203a-3p, and rno-let-7d-5p, were found to be significantly altered by both the qRT-PCR and in the gentamicin treated urine specimens. [score:1]
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[+] score: 20
Several studies suggest that miR-203 also acts as a tumor suppressor in the liver [86– 88] by inhibition of liver cell proliferation. [score:5]
Altered expression of miRNA-203 has also been found to be associated with alcoholic steatohepatitis [89]. [score:3]
The expression of miRNAs (miR-18a, miR-99a, and miR-203, miR-451) was also found to associate with specific sexually dimorphic hepatic histopathology. [score:3]
The expression of specific miRNAs (miR-451, miR-18a, miR-99a, and miR-203) was found to associate with sexually dimorphic histopathology findings of basophilic foci and bile duct hyperplasia. [score:3]
Increased expression of both miR-99a and miR-203 was associated with the presence of hepatic bile duct hyperplasia, a common aging lesion [83]. [score:3]
Using the same analysis described above, the expression of 2 miRNAs was found to associate with the presence and absence of liver bile duct hyperplasia, miR-99a and miR-203 (Table  4). [score:3]
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[+] score: 20
Specifically, miR-195 potentially regulates vesicle -associated membrane protein 1 (VAMP1), miR-30a targets actinin, alpha 1 (ACTN1), miR-21 targets paired-like homeodomain 2 (PITX2) in D6; miR-132 potentially regulates solute carrier family 2, member 1 (SLC2A1), nuclear receptor subfamily 4, group A, member 2 (NR4A2) and Cdc42 guanine nucleotide exchange factor 9 (ARHGEF9), miR-203 targets calcium binding protein 7 (CABP7), miR-17-5p targets early growth response 2 (EGR2) in S6; miR-330 potentially regulates CD247, nerve growth factor receptor (NGFR) and FAT tumor suppressor homolog 3 (FAT3), miR-338 targets ADAM metallopeptidase domain 17 (ADAM17), miR-218 targets src kinase associated phosphoprotein 1 (SKAP1), miR-185 targets calcium channel, voltage -dependent, N type, alpha 1B subunit (CACNA1B) in S9. [score:20]
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[+] score: 17
Individual target analysis suggests that chaperone proteins FKBP4 and FKBP5 that are critical for the binding affinity of GR and consequent corticotropin-releasing hormone -mediated stress response are targets of a set of miRNAs: miR-203, 721, 29a, and 137. [score:5]
For example, miR-324-5p, miR-365 localized on chromosome 10 and miR-153 and miR-203 localized on chromosome 6 showed significant upregulation. [score:4]
[57] Another synaptic plasticity-related gene CREB is a target of multiple miRNAs (miR-101a, miR-203, miR-218, miR-721, miR-409-5p). [score:3]
[64] Serotonergic genes HTR2A and HTR2C, and SLC6A4 (5HTTLPR) are targeted by miR-203 and miR-324-5p, respectively. [score:3]
For example, miR-218, miR-324-5p, miR-365 and miR-146a were localized on chromosome 10; miR-764-5p and miR-351 on chromosome X; miR-101 and miR-30e on chromosome 5; miR-582 and miR-137 on chromosome 2; miR-153 and miR-203 on chromosome 6; miR-124 and 181a on chromosome 3 and miR-135a*/miR-135a-3p and let-7i on chromosome 7. Some of the miRNAs that were localized on the chromosome and in close proximity showed the same direction of changes. [score:2]
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[+] score: 17
Based on previous work, the expression of the two increased miRNA species miR-375 and miR-210 and the three decreased miRNAs, miR-203, miR-185 and miR-450a, is involved in the regulation of insulin secretion and pancreatic β cell function [11, 26, 27, 28]. [score:4]
The expression of miR-133a was persistently increased, and the level of miR-203 was persistently decreased (Figure 4). [score:3]
In a recent study, decreased miR-203 and miR-210 expressions were detected in pancreatic islets of young pre-diabetic and diabetic db/ db mice and in mice fed with a high fed diet [26] and were strongly associated with β cell dysfunction [20, 22]. [score:3]
miR-203 levels were strongly decreased at all time points during the progression of the disease. [score:3]
When β cell failure occurred, the circulating level of miR-133a remained high, and additionally, the level of miR-122 was significantly increased, whereas miR-203, miR-450a and miR-434-3p were decreased at this time point (Figure 4). [score:1]
Therefore, a similar regulation of miR-203 was observed in db/ db mice and high fat diet-fed mice (HFD mice) compared to our study. [score:1]
Diminution in circulating levels was detected for miR-140, miR-151-3p, miR-185, miR-203, miR-434-3p and miR-450a (Figure 5). [score:1]
At late-stage diabetes, the circulating level of 12 miRNAs was specifically altered; the circulating level of miR-375, miR-210 and miR-133a was increased, and the circulating levels of let-7i, miR-140, miR-450a, miR-185, miR-186, miR-151-3p, miR-203, miR-16 and miR-685 were strongly diminished versus their levels at the pre-diabetes stage (Figure 4). [score:1]
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[+] score: 14
Other miRNAs from this paper: rno-mir-140, rno-mir-16, rno-mir-23b, rno-mir-203b, rno-mir-15a
MyD88, a key adaptor protein for IL-1R and Toll-like receptors that was recently found to modulate myoblast fusion [33], is targeted by miR-203, and this results in the downregulation of MyD88 expression [34]; miR-15a and miR-16 were shown to repress the expression of Wnt3a [35]; and the miRNA-23b cluster was reported to inhibit the expression of Smad4 [36]. [score:14]
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[+] score: 12
The analysis based on their fold changes showed a significant (P < 0.05) upregulation of miR-200c-3p (predicted to regulate IL-13 and VEGF-alpha), miR203a-3p (predicted to regulate IL-24 and PRKC α), miR29-3p (predicted to regulate TNFRS1A), and miR-21-5p (predicted to regulate NFk-B activity), in ocular tissues of LPS+RvD1 -treated rats compared to the vehicle+LPS group (Figure 4). [score:7]
These were miR-21-5p that is predicted to regulate NFk-B activity; miR-200c-3p that is predicted to negatively regulate IL-13, LEPR, NTF3, PRKC α, RIPK2, and VEGFA indicating decreased of proinflammatory cytokines [29]; miR-203a-3p predicted to regulate IL-24 and PRKC α; miR-29b-3p predicted to negatively regulate HDAC4, IL-1RAP, Lif, PDGF α, PDGFc, VEGFA, and TNFRSF1. [score:5]
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[+] score: 10
Yan et al. reported that miR-203 expression in tongue exfoliated cells was significantly downregulated in GERD patients compared to controls [15], suggesting that miR-203 testing in tongue coating samples might assist with GERD diagnosis. [score:5]
Yan X. Zhu S. Zhang H. miR-203 expression in exfoliated cells of tongue coating represents a sensitive and specific biomarker of gastroesophageal reflux diseaseGastroenterol. [score:5]
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[+] score: 8
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
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[+] score: 6
Treatment with triptolide enhanced expression of five miRNAs (rno-miR-146b-5p, rno-miR-20b-5p, rno-miR-142-3p, rno-miR-223-3p, and rno-miR-21-5p), while that of five other miRNAs (rno-miR-668, rno-miR-203-3p, rno-miR-382-5p, rno-miR-344b-3p, and rno-miR-30b-3p) was significantly downregulated (Tables 3 and 4, and Figure 8). [score:6]
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[+] score: 6
MiRNA203 suppresses the expression of protumorigenic STAT1 in glioblastoma to inhibit tumorigenesis. [score:6]
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[+] score: 5
Targeting of Runx2 by miR-135 and miR-203 impairs progression of breast cancer and metastatic bone disease. [score:5]
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[+] score: 5
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19b-2, rno-mir-26b, rno-mir-203b
Fish oil/pectin treatment up-regulated miR-19b, miR-26b and miR-203 expression as compared to corn oil plus cellulose (CCA) specifically in Lgr5 (high) cells. [score:5]
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[+] score: 5
Moreover, miR-203 has a proposed role as a stemness inhibitor of glioblastoma stem cells and may contribute to the increased expression of glial and neuronal differentiation markers (Deng et al. 2016). [score:5]
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[+] score: 4
In addition, rno-miR-484, rno-miR-138-1-3p, rno-miR-201-3p and rno-miR-203a-3p are downregulated in the network, nevertheless, previous studies reported these miRNAs to be tumor -associated (Pizzini et al., 2013; Liu et al., 2015; Merhautova et al., 2015; Murray et al., 2014; Yang et al., 2016; Ye et al., 2015). [score:4]
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[+] score: 4
Other miRNAs from this paper: rno-mir-203b
Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression. [score:3]
Indeed, microRNA that reduces ABL1 levels, miR-203, was detected (Bueno et al., 2008). [score:1]
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[+] score: 4
For example, miR-203a-3p was involved in liver regeneration, notably by inhibiting SOCS3, one known regulator of hepatic cell proliferation. [score:4]
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[+] score: 3
Six candidate miRNAs that are predicted to target caspase-3 (let-7, miR-138, miR-30b, miR-129, miR-203, and miR-219-5p) and have an aggregate Pct greater than 0.2 were selected (Fig.   1c). [score:3]
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[+] score: 2
Other miRNAs from this paper: rno-mir-146a, rno-mir-146b, rno-mir-203b, rno-mir-155
MiR-146, miR-155 and miR-203 regulate arthritic inflammatory response and joint destruction 31. [score:2]
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[+] score: 2
Some deregulated miRNAs were identified both in the TLE patients of Kan’s work and in our rat TLE mo del, such as miR-27a, miR-190, miR-203 and miR-301a. [score:2]
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[+] score: 1
At 2 ppm, three miRNAs (miR-142-3p, miR-145 and miR-203) were significantly decreased. [score:1]
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[+] score: 1
[8] These miRNAs include miR-26a, miR-203, miR-22, miR-375, and other. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
Type of site Context+ Context Structure Energy Is experimental validated rno-miR-326-5p MIMAT0017028 3 8mer 7mer-m8 imperfect −0.442 −0.242 431 −65.97 TRUE rno-miR-485-5p MIMAT0003203 2 7mer-m8 −0.343 −0.372 290 −34.96 TRUE rno-miR-300-5p MIMAT0004743 1 8mer −0.338 −0.421 156 −15.16 TRUE rno-miR-702-5p MIMAT0017884 1 8mer −0.317 −0.274 142 −13.86 TRUE rno-miR-203b-3p MIMAT0017800 2 7mer-m8 −0.298 −0.421 295 −29.93 TRUE rno-miR-33-3p MIMAT0017104 2 8mer 7mer-m8 −0.297 −0.813 305 −22.7 TRUE rno-miR-466b-3p MIMAT0017285 1 8mer −0.295 −0.47 159 −15.26 TRUE rno-miR-532-5p MIMAT0005322 1 7mer-m8 −0.268 −0.302 151 −10.71 TRUE rno-miR-511-5p MIMAT0012829 1 7mer-m8 −0.268 −0.302 152 −10.37 TRUE rno-miR-343 MIMAT0000591 1 7mer-m8 −0.262 −0.24 140 −13.75 TRUE rno-miR-203a-3p MIMAT0000876 1 8mer −0.245 −0. [score:1]
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[+] score: 1
9 -45.6 mmu-miR-27b -1.8 -71.4 -462.7 mmu-miR-214* -2.6 -5.0 -43.5 mmu-let-7c-1* -73.2 -204.4 -334.1 mmu-miR-34c -9.4 -26.1 -42.7 mmu-miR-542–3p -5.9 -195.6 -319.8 mmu-miR-706 -9.3 -5.0 -38.7 mmu-miR-487b -2.0 -161.5 -263.9 mmu-miR-467b* -10.1 -2.2 -33.6 rno-miR-17–3p -1.6 -152.0 -248.5 mmu-miR-323–3p -3.7 -23.3 -29.8 mmu-miR-10b -2. 4 -136.6 -223.3 mmu-miR-202–3p -6.5 -5.9 -21.4 mmu-miR-29b -3.0 -135.1 -220.9 mmu-miR-339–5p -1.6 -9.6 -19.6 mmu-miR-297a* -2.4 -128.4 -209.8 mmu-miR-181c -2.0 -10.5 -14.6 mmu-miR-692 -41.5 -115.8 -189.2 mmu-miR-203 -4.6 -6.4 -13.8 mmu-miR-208 -40.6 -113.5 -185.5 mmu-miR-467a* -2.6 -3.9 -11.4 mmu-miR-467c -38.9 -108.6 -177. [score:1]
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