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56 publications mentioning mmu-mir-194-2

Open access articles that are associated with the species Mus musculus and mention the gene name mir-194-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 196
Further, ectopic expression of miR-194 also augmented E-cadherin expression and lowered AKT2 expression by targeting 3′UTR of AKT2. [score:9]
Maximal suppression of SPRY2 in clone 7522 resulted in a more than twofold upregulation of miR-194-5p, -4423 and -3925 and downregulation of miR-21 and −491 (corresponding to at least ±1.0  log fold change) (Supplementary Table 1). [score:9]
SPRY2 and miR-194 -dependent suppression of AKT2 and other repressors of E-cadherin may account for upregulation of E-cadherin and inhibition of cancer cell migration and invasion. [score:8]
[19] We, therefore, extended our studies to assess E-cadherin repressors such as SNAIL1 and SNAIL2 that are not the direct targets of miR-194 as predicted by miR databases (picTar, miRanda and TargetScan). [score:6]
Further, SPRY2 downregulation had no significant effect on miR-194-3p expression levels in cancer cells (Supplementary Figure S2). [score:6]
The miR-194 -dependent downregulation of AKT2 and SNAILs may account for increased expression of E-cadherin in these studies. [score:6]
In the present study, increased miR-194 expression in SPRY2 -downregulated cells may indicate increased cancer cell differentiation. [score:6]
Collectively, above results demonstrate that SPRY2 suppression by two different methods significantly upregulated miR-194-5p contents of colon cancer cells. [score:6]
In miR-194 -transfected cells, downregulation of E-cadherin repressors other than AKT2 may represent an indirect regulation of E-cadherin repressors by miR-194 without any involvement of 3′UTR of these genes. [score:6]
[35] SPRY2 -dependent regulation of E-cadherin is the end-organ effect of reduction of both direct and indirect targets of miR-194. [score:6]
demonstrate that miR-194 also affects targets, other than AKT2, by direct or indirect mechanisms involved in E-cadherin induction. [score:5]
To further confirm that SPRY2 suppression affects miR-194-5p expression levels, HCT116 and SW480 cells were transiently transfected with SPRY2 siRNA. [score:5]
Collectively, data indicate that miR-194 may inhibit EMT by increasing expression and membrane localization of E-cadherin and partial association of E-cadherin with AKT2. [score:5]
In order to confirm SPRY2's role on miR-194 -induced regulation of E-cadherin, we assessed E-cadherin induction during SPRY2 downregulation alone or in combination with miR-194 transfection (Figure 2d). [score:5]
Hypermethylation of this cluster promoter and epigenetic downregulation of miR-194 has been suggested in multiple myeloma. [score:4]
MiR-194 mimics significantly increased E-cadherin expression in HCT116 (4.1-fold, P<0.05) and SW480 cells (5.3-fold, P<0.05), whereas miR-194 inhibitor reduced E-cadherin levels in HT29 cells (>70%, P<0.05) as compared with control transfections (Figure 2c). [score:4]
AKT2 is a direct target of miR-194. [score:4]
A complete reversal of E-cadherin induction indicates that miR-194 is a major downstream effector of SPRY2 -dependent upregulation of E-cadherin (Figure 2e). [score:4]
For example, methylation of miR-194-2 and -192 cluster promoter regulates miR-194 expression in cancer cells. [score:4]
To test whether AKT2 is a direct target gene of miR-194, we used a dual luciferase reporter, which has a conserved sequence of mRNA that is complimentary to the seed sequence of miR-194. [score:4]
[25] Suppression of SPRY2 may positively regulate various transcription factors that bind to promoter for increased miR-194 transcription. [score:4]
We identified that knockdown of SPRY2 expression increases miR-194-5p contents in colon cancer cells. [score:4]
A significant downregulation of SNAILs was also observed in miR-194 mimic -transfected HCT116 cells (Supplementary Figure S7). [score:4]
To further confirm miR-194's role on AKT2's induced upregulation of E-cadherin, we assessed E-cadherin induction with siAKT2 or miR-194 transfection or in combination (Figure 3f). [score:4]
Other intracellular factors may also regulate miR-194 expression in CRC. [score:4]
As discussed above, SPRY2 downregulation significantly increased miR-194-5p levels, altered cancer cell morphology and decreased cell migration and invasion. [score:4]
We further validated our results by confocal microscopy and demonstrated a significant upregulation and redistribution of E-cadherin in miR-194 -transfected HCT116 (Figure 4a) and SW480 (Figure 4b) cells. [score:4]
Suppression of SPRY2 also decreased AKT2 expression though to a lesser extent when compared with miR-194 effects (>40%, P<0.05) (Figure 3b). [score:4]
[26] Hepatocyte nuclear factor has been reported to induce miR-194 expression during intestinal epithelial cell differentiation. [score:3]
[24] An increased miR-194 expression in differentiating Caco-2 colon cancer cells has been reported. [score:3]
MiR-194-5p levels were significantly upregulated (threefold, P<0.05) in HCT116 and SW480 cells (Figure 2a). [score:3]
22, 23 Reduced miR-194 expression was noted in CRC. [score:3]
Inverse correlation of miR-194-5p with SPRY2 expression. [score:3]
Several genes of interest were predicted by the search programs of miRanda and TargetScan, and the effect of miR-194 on Talin2, SOX5, Musashi, AKT2, Rac1, HBEGF and IGF-1 R was tested by quantitative real-time (RT–PCR) and western blotting (Supplementary Figure S6). [score:3]
The role of miR-194 has been analyzed in normal and malignant cells of the gastrointestinal tract as high levels of miR-194 are expressed in the intestine and liver. [score:3]
Therefore, in subsequent experiments HCT116 and SW480 cells were used for miR-194 mimic transfection, whereas HT29 cells were used for miR-194 inhibitor experiments. [score:3]
Thus regulation of miR-194 by SPRY2 and suppression of AKT2 and other EMT markers by miR-194 could be considered as a potential anticancer therapeutic strategy. [score:3]
In this study, we provided the experimental evidence that SPRY2 regulates miR-194. [score:2]
The results demonstrate that miR-194 may negatively regulate AKT2 posttranscriptionally in HCT116 and SW480 cells. [score:2]
Furthermore, combination of siAKT2 and miR-194 accentuated E-cadherin expression when compared with siAKT2 or miR-194 responses alone (Figure 3f). [score:2]
Further, miR-194 transfection also induced E-cadherin expression to a greater extent as compared with siAKT2 response only. [score:2]
In summary, studies demonstrate a significant role of miR-194 in negative regulation of EMT in CRC. [score:2]
Cancer cells were transfected with miR-control or miR-194 mimics, and transfection was confirmed by increased miR-194 levels as assessed by RT–PCR (Supplementary Figure S9). [score:1]
Cells were co -transfected with miR-194 plasmid or empty vector and AKT2 wild-type 3′UTR or AKT2 mutant 3′UTR. [score:1]
Mir-194 -dependent regulation of AKT2 has been recently demonstrated. [score:1]
MiR-194 is transcriptionally regulated in intestinal epithelial cells. [score:1]
In miR-194 -transfected cells, the immunoreactive E-cadherin appears in small vesicles that have a tendency to concentrate in the cell periphery in the area of plasma membrane. [score:1]
Mir-194 precursor is processed into miR-194-5p and miR-194-3p. [score:1]
Conversely, the luciferase activity of the mutant reporter was not affected in response to miR-194 plasmid treatment (Figure 3c). [score:1]
Mir-194-5p is the major mature form of miR-194. [score:1]
Briefly, cells were seeded in six-well plates, co -transfected with miR-194 precursor vector (p-CMV-miR-194) or empty vector control (Origene, Rockville, MD, USA) and a wild-type AKT2 3′UTR reporter construct (pmiR-GLO-AKT2-3′UTR) or pmir-GLO-AKT2-3′UTR mutant or empty vector with the firefly luciferase reporter and the control vector Renilla luciferase, pRL-TK (Promega, Madison, WI, USA) using lipofectamine 2000 following the manufacturer's protocol. [score:1]
[20] However, miR-194 transfection moderately increased the association of AKT2 with E-cadherin on the cell membrane, but no nuclear translocation of AKT2 was noted. [score:1]
[15] We focused our investigation on miR-194, because this is mainly expressed in the gastrointestinal tract. [score:1]
The highest efficiencies of miR-194 transfection were achieved at 96 h posttransfection at 100 n m final concentration (data not shown). [score:1]
We then investigated endogenous contents of miR-194-5p in three different colon cancer cell lines that express different levels of SPRY2. [score:1]
HCT116 and SW480 cancer cells have significantly lower contents of miR-194-5p than HT29 cells (Supplementary Figure S3). [score:1]
MiR-194 negatively regulates EMT and colon cancer cell migration and invasion. [score:1]
[1 to 20 of 57 sentences]
[+] score: 182
Our in vitro results suggest that both GYY and miR-194 mimic upregulated miR-194 expression suggesting that GYY regulates miR-194 expression in HG condition (Fig.   6B). [score:9]
Downregulated miR-194 expression in diabetes was normalized by GYY4137 (GYY) treatment. [score:6]
We observed downregulation of miR-194 and GYY treatment normalized miR-194 expression in both in vivo and in vitro hyperglycemic (HG) condition (Fig.   6A and B). [score:6]
Studies have also shown that miR-194 is highly expressed in the kidney [13] and the expression level diminished in progressive CKD [65]. [score:5]
Since miR-194 was downregulated in diabetic condition (Fig.   6A and B) and miR-194 mimic decreased ROS production in HG condition (Fig.   6C), we determined whether miR-194 regulates ROMO1 and MMPs under in vitro HG condition using MGECs. [score:5]
We also demonstrate that pro-fibrogenic molecules i. e., MMPs and PARP-1 are the target genes of miR-194 since miR-194 mimic reverse expressed these molecules in HG condition (Figs  7 and 8). [score:5]
The major finding from our study is that miR-194 downregulation leads to increased ROS activity in diabetic kidney. [score:4]
On the other hand, HG cells that was treated without or with GYY in the presence of inhibitor showed a significant reduction in miR-194 expression compared to NG, and these results were comparable to HG alone. [score:4]
Increased ROS, in turn causes imbalance of MMPs and upregulation of PARP-1. The alterations of H [2]S, miR-194, ROS, MMPs and PARP-1 in diabetic kidney lead to collagen accumulation and re-alignment resulting in kidney fibrosis and renovascular constriction. [score:4]
On the other hand, downregulation of miR-194 in the kidney have been reported following renal ischemia-reperfusion injury (IRI) [60]. [score:4]
Nonetheless, the cause and effect relationship of miR-194 downregulation and amelioration by GYY treatment in diabetic kidney was not clear from our in vivo studies. [score:4]
Overall, our results suggest that the above-mentioned genes are the possible target of miR-194 in diabetic renal fibrosis. [score:3]
Regulation of miR-194 by GYY may therefore be considered as a potential target to halt or slow debilitating kidney remo deling in DN. [score:3]
In the present study, we therefore sought to delineate the mechanism of miR-194 -mediated collagen realignment and fibrosis in type-1 diabetic kidney and whether H [2]S generating compound, GYY4137 can modulate the remo deling process to ameliorate disease progression. [score:3]
miR-194 mimic normalized PARP-1, Col1a and Col IV expression in HG condition. [score:3]
obtained from MGECs experiment following HG condition and transfected with both mimic and inhibitor of miR-194 for 72 hours were compiled in Fig.   6B. [score:3]
Figure 6 (A, B) Increased miR-194 expression in diabetic condition was normalized by GYY4137 treatment. [score:3]
Figure 7Altered ROMO1, MMP-9, -13 and -14 mRNA and protein expression was ameliorated by miR-194 mimic in HG condition. [score:3]
These results are in agreement with our in vivo results of GYY -mediated molecular changes in diabetic kidney, and suggest that while GYY regulates miR-194 in diabetic kidney, mirR-194 in turn regulates these above ECM protein and their modulators in HG condition. [score:3]
Altered expression of HIF1α, PLOD2 and P4HA1 in HG condition was ameliorated by miR-194 mimic transfection. [score:3]
No significant changes, in terms of mRNA and protein expression of these molecules, were observed in NG condition without or with miR-194 mimic transfection (Fig.   7A,B,C,D,E and F). [score:3]
At 80% confluence, cells were transfected with miR-194 mimic or inhibitor using Lipofectamine RNAiMAX reagent at a final concentration of 10 nM following the manufacturer’s protocol for 48 h. We used 250 µM concentration of GYY4137 for 24 hours along with HG or NG before the cells were processed for qPCR, Western blot, DHE or immunostaining analysis. [score:3]
Overall, the expression of miR-194 in HG cells was 7-fold higher in the presence of mimic and GYY treatment than the HG cells treated only with GYY (Fig.   6B). [score:3]
It is also reported that miR-194 expression was significantly reduced in both rodent and human diabetic condition [66]. [score:3]
The bar diagram represents expression of miR-194 in mouse kidney (A) and in mouse glomerular endothelial cells (MGECs) (B). [score:3]
In summary, our findings suggest that intraperitoneal injections of GYY to Akita mice alleviate diabetic renal remo deling by increasing the expression of miR-194. [score:3]
Therefore, to determine the cause and effect relationships between H [2]S and miR-194, and to determine whether GYY regulates downstream molecular cascades leading to ECM deposition and remo deling in diabetic condition, we compared results using mouse glomerular endothelial cells (MGECs) treated without or with GYY along with miR-194 mimic and inhibitor in HG and NG condition. [score:3]
Our present finding is in agreement with these previous studies and demonstrated significant reduced expression of miR-194 in the diabetic kidney (Fig.   6A). [score:3]
Figure 8Increased PARP-1, Col 1a and Col IV transcript and protein expression was mitigated by miR-194 mimic transfection in HG condition. [score:3]
Increased miR-194 was accompanied with decreased ROS, MMPs-9 and -13, and PARP-1. In addition, increased accumulation and alignment of collagen was mitigated in Akita mice following GYY treatment as it was evidenced by diminished fibrosis and decrease in the expression of PLOD-1, P4HA and HIF1α. [score:3]
The expression of miR-194 was decreased in both diabetic kidney tissue as well as in hyperglycemic (HG) conditions. [score:3]
Among the known ~2,500 miRNA by deep sequencing of human genome [12], miR-192, miR-194, miR-204, miR-215 and miR-216 are highly expressed in kidney than other human tissues [13]. [score:3]
In these sets of experiment, we determined whether miR-194 mimic could modulate expression of PARP-1, Col1a and Col IV in HG condition. [score:3]
Further, our results demonstrate that supplementation of GYY (i. e., GYY4137), as a source of H [2]S ameliorates diabetic kidney remo deling through reversing miR-194 expression. [score:3]
MGECs were transfected with miR-194 mimic and miR-194 inhibitor for 72 hours. [score:3]
Transfection of miR-194 mimic normalized altered expression of ROMO-1, MMP-9, -13 and -14 in hyperglycemic (HG) MGECs. [score:3]
Figure 9Increased expression of HIF1α, PLOD2 and P4HA1 in HG condition was normalized by miR-194 mimic transfection. [score:3]
Results obtained from MGECs experiment following HG condition and transfected with both mimic and inhibitor of miR-194 for 72 hours were compiled in Fig.   6B. [score:3]
When MGECs were transfected with miR-194 mimic, the expression of these molecules were normalized in HG condition. [score:3]
Studies have shown that increased expression of miR-194 in the kidney have a protective role in the prevention of diabetic renal injury [59]. [score:3]
Using miR-194 mimic and inhibitor, we also demonstrate that miR-194 is involved in matrix remo deling in HG condition. [score:3]
When MGECs were transfected with miR-194 mimic, the expression of these molecules were almost normalized in HG condition compared to non -transfected cells (Fig.   9A,B,C,D and E). [score:2]
These results suggest that miR-194 regulates ROMO1, MMP-9, -13 and -14 in HG condition in vitro. [score:2]
These results indicate that ROS production in HG condition was in part, mediated by H [2]S and miR-194, and H [2]S regulates miR-194 in HG condition. [score:2]
These results suggest that miR-194 regulates PARP-1, Col1a and Col IV in MGECs under HG condition. [score:2]
These results indicate that miR-194 regulates HIF1α, PLOD2 and P4HA1 in HG condition. [score:2]
Regulatory role of miR-194 on HIF1α, PLOD2 and P4HA1 under HG condition was assessed by transfecting MGECs with miR-194 mimics. [score:2]
Further to demonstrate the proof-of-concept whether miR-194 regulates oxidative stress and its modulator, MMPs, collagens and their modulating molecules in HG condition, we performed experiments as reported in Figs  7, 8 and 9. indicated that similar to GYY, miR-194 mimic also attenuated ROS in MGECs under HG condition (Fig.   6C). [score:2]
In Fig.   10A, we depict possible protein-protein and chemical-protein interactions, and in Fig.   10B, we highlight major findings with regulatory cascades of ECM remo deling involving miR-194 and H [2]S in diabetic condition. [score:2]
This result highlights possible regulatory role of miR-194 by H [2]S in protecting diabetic kidney. [score:2]
In diabetic kidney, diminished H [2]S and decreased miRNA-194 induces increased production of ROS. [score:1]
In HG condition miR-194 mimic or GYY4137 (GYY) mitigated ROS production in MGECs. [score:1]
indicated that miR-194 mimic mitigated superoxide (ROS) production in HG condition (Fig.   6C). [score:1]
Thus, our findings provide evidence that in genetic diabetic kidney, H [2]S ameliorates collagen realignment and renal fibrosis, and therefore improves vascular density possibly in miR-194 -dependent pathway. [score:1]
Similar result was obtained in HG cells in the presence of miR-194 mimic. [score:1]
In our present study, we report beneficial effect of miR-194 in diabetic renal fibrosis is in part through altered MMPs -mediated PARP-1 induction (Figs  2 and 3). [score:1]
Thus, a strong relationship of H [2]S and miR-194 exists in diabetic kidney in which GYY in concert with miR-194 modulates fibrotic vasculopathies. [score:1]
GYY4137, a H [2]S donor, treatment normalizes miR-194 and ROS -dependent downstream pathways of renovascular remo deling, and thus preserves renovascular architecture in diabetes. [score:1]
Cells in NG condition without or with miR-194 mimic had basal level of DHE fluorescence indicating NG cells are not in stress (Fig.   6C). [score:1]
However, the specific roles of miR-194 in DN are still incompletely understood. [score:1]
In a recent study, Jia et al. have demonstrated that miR-194 could be used as a potential predictor for early-stage diabetic nephropathy [61]. [score:1]
Additionally, a clear link between miR-194 and ROS in mediating renovascular fibrosis, and whether H [2]S may impede fibrosis by modulating miR-194 in diabetic kidney is unknown. [score:1]
The expression level of miR-194 was evaluated using the Roche LightCycler® 96 software version 1.1. [score:1]
Similar effect was observed with miR-194 mimic treatment (bottom panel). [score:1]
No significant changes were observed in NG cells without or with miR-194 mimic transfection. [score:1]
In addition, miR-194 mimic normalized ROMO-1, MMP-9, -13, -14 (Fig.   7A,B,C,D,E and F); PARP-1, Col1a, Col IV (Fig.   8A,B,C,D and E); HIF1α, PLOD2 and P4HA1 (Fig.   9A,B,C,D and E) in HG condition. [score:1]
No significant changes were observed in cells without or with miR-194 mimic transfection in NG condition (Fig.   8A,B,C,D and E). [score:1]
The decreased levels of miR-194 in diabetic kidney was normalized with GYY4137 treatment (A), and in MGECs transfected with miR-194 mimic (B). [score:1]
[1 to 20 of 68 sentences]
[+] score: 35
Notably, miR-122, miR-194, miRNA-101b, and miRNA-705 were upregulated and miRNA-376a, miRNA-127, miRNA-34a, miRNA-300 and miRNA-342-3p were downregulated in the liver tissue of MCD-fed mice treated with or without metformin (Table IB and Fig. 6). [score:7]
The four upregulated miRNAs, i. e., miR-122, miR-194, miRNA-101b and miRNA-705, in mice treated with or without metformin were consistent with four of the 60 downregulated miRNAs from the control group and MCD-fed mice. [score:7]
By contrast, miRNA-122 and miRNA-194 were significantly upregulated by metformin out of the nine miRNAs that were downregulated in the NASH liver of MCD-fed mice. [score:7]
Similar to miRNA-122, downregulation of miRNA-194 enhances the expression of frizzled-6 (FZD6) and promotes tumorigenesis in the adult liver (26). [score:6]
In various types of cancer, such as gastric (28), endometrial cancer (29, 30), renal cell carcinoma (31) and colorectal cancer (32) miRNA-194 inhibits tumor invasion and metastasis. [score:3]
Taken together, it is suggested that one of the downstream targets of the metformin -induced pathway is miRNA-122 and/or miRNA-194. [score:3]
miRNA-194 is also considered to be a marker of hepatic epithelial cells and inhibits the metastasis of liver cancer cells (27). [score:2]
[1 to 20 of 7 sentences]
[+] score: 24
Mmu-miR-695, mmu-miR-31, mmu-miR-190, mmu-miR-183, mmu-miR-182, and mmu-miR-194 were the most significantly downregulated miRNAs, whereas mmu-miR-34c and mmu-miR-124 were the most significantly upregulated miRNAs. [score:7]
The most significantly downregulated (mmu-miR-31, mmu-miR-455, mmu-miR-744, mmu-miR-695, mmu-miR-181a, mmu-miR-181d, mmu-miR-182, mmu-miR-190, mmu-miR-194) and upregulated miRNAs (mmu-miR-34c, mmu-miR-124, mmu-miR-142–3p, mmu-miR-706, mmu-miR-29c) were analyzed. [score:7]
The results showed that the expression of mmu-miR-31, mmu-miR-695, mmu-miR-183, mmu-miR-182, mmu-miR-194, and mmu-miR-190 markedly downregulated in the corneal endothelium of old mice compared to young mice. [score:5]
The qRT-PCR results demonstrated a decrease in the expression of mmu-miR-31(34.2±13.4-fold), mmu-miR-695 (19.8±4.79-fold), mmu-miR-183 (26.6±2.53-fold), mmu-miR-182 (55.2±15.3-fold), mmu-miR-194 (42.6±10.2-fold) and mmu-miR-190 (37.1±2.78-fold) in the corneal endothelium of old mice compared to young mice, whereas the expression of mmu-miR-34c and mmu-miR-124 increased 26.4±5.28-fold and 62.7±2.54-fold, respectively (Figure 2). [score:4]
To validate the reproducibility of the results from the miRNA microarray, qRT-PCR analysis of (microRNAs come from mice) mmu-miR-695, mmu-miR-183, mmu-miR-182, mmu-miR-194, mmu-miR-34c, mmu-miR-31, mmu-miR-190, and mmu-miR-124 was performed using the same extracted total RNA as the microarray analysis. [score:1]
[1 to 20 of 5 sentences]
[+] score: 24
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Out of these 25 miRNAs, 18 miRNAs were differentially expressed in a consistent manner between the 2 groups (Figure 4A, highlighted); 8 miRNAs were downregulated in both groups (miR-16, miR-200, miR-205, miR-3064, miR-379, miR-431, miR-485 and miR-491) and 10 miRNAs were upregulated in both groups (miR-194, miR-1894, miR-211, miR-3072, miR- 3077, miR-4436, miR-5128, miR-669a, miR-669c and miR-6967). [score:9]
A triple comparison was also done that included cbs [–/–], cbs [+/–] and STZ retinas, which revealed 6 miRNAs (miR-194, miR-16, miR-212, miR-30c, miR-5128 and miR-669c) that were commonly changed among cbs [–/–], cbs [+/–] and diabetes; 2 of these miRNAs were consistently changed among the three groups (miR-194 was upregulated and miR-16 was downregulated). [score:7]
In the microarray data, 12 miRNAs were consistent in their change either with HHcy or diabetes; of which 4 miRNAs were downregulated in both groups (miR-16, miR-1983, miR-412 and miR-487) and 8 miRNAs (miR-194, miR-188, miR-1896, miR-467e, miR-504, miR-5110, miR-669k and miR-696) were upregulated in both groups. [score:7]
Among those miRNAs, 2 miRNAs (miR-16-5p and miR-194) were consistently changing among the three different groups. [score:1]
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[+] score: 20
However, four miRNAs (miR-194-5p, miR-107-3p, miR-3090-5p, and miR-3077-5p) were commonly and in general consistently regulated at 0.34, 1.3, 4.3, and 13 Gy (Figures 2A and 2B), with the exception of miR-3077 which showed a tendency towards increased expression level with increased absorbed dose. [score:4]
Four differentially expressed miRNAs (miR-15a-5p, miR-92a-3p, miR-107, and miR-194-5p) were selected for verification by QPCR. [score:3]
Similar results were found for the Fga and Rnase6 genes as targets for miR-194. [score:3]
Furthermore, a number of miRNAs were recurrently differentially expressed (miR-194-5p, miR-107-3p, miR-3090-5p, and miR-3077-5p). [score:3]
However, four miRNAs (miR-194, miR-107, miR-3090, and miR-3077) were commonly regulated at the highest four absorbed doses. [score:2]
miR-194, miR-107, miR-3090, and miR-3077 were commonly regulated at 0.34, 1.3, 4.3, and 13 Gy. [score:2]
In the present study, a strong correlation between the microarray and the qRT-PCR results was found for the miRNAs miR-15a-5p, miR-107, and miR-194-5p. [score:1]
Furthermore, a positive correlation between the Per1 gene and miR-194 (correlation >0.8) were found. [score:1]
The miRNAs miR-15a-5p (r = 0.92), miR-107 (r = 0.91), and miR-194-5p (r = 0.72) showed a strong correlation whereas the miR-92a-3p (r = −0.11) revealed no correlation. [score:1]
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[+] score: 19
We previously suggested that of the miRs analyzed, nine (miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805 and miR-194) stand out as being differentially expressed in C57BL/6 mice undergoing IRI compared to the expression observed in mice undergoing a sham procedure [14]. [score:4]
Movie showing the rotation of a three-dimensional plot of the first three PCs obtained by performing PCA on all expression data obtained for kidneys from C57BL/6 mice following IRI (blue line) or sham surgery (red lines) in which we eliminated miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805 and miR-194 from the analysis. [score:3]
Shown is a three-dimensional plot of the first three PCs obtained by performing PCA on expression data for miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805 and miR-194 obtained for kidneys from C57BL/6 mice following IRI (blue line) or sham surgery (red lines). [score:3]
Shown is a three-dimensional plot of the first three PCs obtained by performing PCA on expression data for miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805 and miR-194 obtained for kidneys from C57BL/6 mice following IRI (blue line) or sham surgery (red lines) (Movie S3). [score:3]
Panel C, Shown is a three-dimensional plot of the first three PCs obtained by performing PCA on all expression data obtained for kidneys from C57BL/6 mice following IRI (blue line) or sham surgery (red lines) in which we eliminated miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805 and miR-194 from the analysis. [score:3]
Our previous work showed that in C57BL/6 mice, expression of miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805 and miR-194 is significantly different between IRI and sham control groups at all times analyzed [14]. [score:3]
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[+] score: 18
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
We also found miR-194 abundantly expressed in the liver, and its level of expression was comparable with that of miR-122 (Figure 2B). [score:5]
Several miRNAs (miR-1, miR-133, miR-499, miR-208, miR-122, miR-194, miR-18, miR-142-3p, miR-101 and miR-143) have distinct tissue-specific expression patterns. [score:3]
Additionally, miR-1 and miR-133 in the heart, miR-181a and miR-142-3p in the thymus, miR-194 in the liver, and miR-143 in the stomach showed the highest levels of expression. [score:3]
miR-194 has been implicated in intestinal epithelial cell differentiation and maturation [54], and our finding of miR-194 expression in stomach of the pig is consistent with this previous report [54]. [score:3]
The liver -associated expression of miR-194 in the mouse has been reported recently [53]. [score:3]
We also detected a trace amount of miR-194 in pig stomach (Figure 2B). [score:1]
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[+] 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, 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-194, 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]
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[+] score: 15
miR-96 is the only miRNA demonstrated to cause hearing loss when mutated [21, 28]; miR-140 is highly and selectively expressed in hair cells during development and targets Jag1 and RARβ, both important for hair cell and inner ear development [22, 30]; miR-194 targets Fgf10, which is essential for the development of the otic vesicle [27, 47, 48]. [score:10]
With these criteria a set of 11 miRNAs (miR-17, miR-33, miR-96, miR-140, miR-181b, miR-183, miR-191, miR-194, miR-199b, miR-341, and miR-1192) were selected that might participate to coordinate with NR2F1 to regulate inner ear gene expression. [score:4]
Additionally, miR-96, miR-140, and miR-194 were included for the following reasons. [score:1]
[1 to 20 of 3 sentences]
[+] score: 14
Reduced expression of miR-709 (a highly expressed miRNA), miR-122, miR-192, miR-194, miR-26a, let-7a, let7b and let-7c, miR-494 and miR-483* (reduced by ~4.9 fold) was validated by qPCR. [score:5]
Several key proteins involved in epigenetics are predicted targets for miRNAs, in particular, methyl-CpG binding protein 2 are predicted targets for 5 miRNAs (miR-709, let-7s, miR-122, miR-194 and miR-26a) showing reduced levels in maternal HF fed offspring. [score:5]
We found that methyl-CpG binding protein 2 was the common predicted target for miR-709, miR-let7s, miR-122, miR-194 and miR-26a using our own purpose-built computer program. [score:3]
We found that ZSWIM3 (zinc finger, SWIM domain containing 3), a protein whose function was yet to be characterised [56], was targeted by 5 miRNAs namely miR-122, miR-192, miR-194, miR-709 and miR-483*. [score:1]
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[+] score: 13
On the other hand, miR-192 and miR-194 were highly expressed in the kidney and small intestine, and miR-449a was highly expressed in the lung (Figures 3(d) and 3(e)). [score:5]
The expression of miR-200a, miR-200b, miR-200c, miR-192, miR-194, and miR-449a was validated with real-time RT-PCR in rat tissues in order to discriminate the kidney from other tissues with a tubular structure. [score:3]
miR-192 and miR-194 were highly expressed in the kidney and in the small intestine. [score:3]
A significant increase in plasma miR-200a/b/c, miR-192, and miR-194 levels was observed in the AKI mo del. [score:1]
Consistently, the plasma concentrations of the miR-200 family members and miR-192 and miR-194 increased significantly. [score:1]
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[+] score: 11
Our recent data revealed that miR-30e is a downstream target of beta-catenin during intestinal crypt cell differentiation [15]; Hino et al. showed that miR-194 expression was induced by HNF-1alpha during intestinal epithelial cell differentiation [16], suggesting active roles for miRNAs during intestinal development. [score:6]
No statistically significant regulations were found for miR-143 or miR-194. [score:2]
Cell Mol Life Sci DOI: 10.1007/s00018-010-0366-y 16 Hino K Fukao T Watanabe M 2007 Regulatory interaction of HNF1-alpha to microRNA-194 gene during intestinal epithelial cell differentiation. [score:2]
Takada et al. [27] showed high abundance of miR-143 and miR-194 in mouse small intestine and Hino et al. [16], [28] further showed induction of miR-194 by HNF-1 during differentiation of intestinal epithelial Caco-2 cells. [score:1]
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[+] score: 10
Of the 113 miRNAs with significantly aberrant expressions after RDX exposure, the expression levels of 10 miRNAs were significantly increased in both mouse liver and brain (p < 0.01): miR-99a, miR-30a, miR-30d, miR-30e, miR-22, miR-194, miR-195, miR-15a, miR-139-5p, and miR-101b. [score:5]
In addition to the 43 liver-specific miRNAs, five miRNAs (miR-148a, miR-192, miR-194, miR-122, and miR-21) were highly expressed in the liver but at low levels in the brain; four of them (miR-148a, miR-192, miR-194, miR-122) were expressed at levels at least 10-fold greater in the liver than in the brain. [score:5]
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[+] score: 10
The expression of miR-150 and miR-194 were both down-regulated in the fibrotic livers of rats induced by bile duct-ligation (BDL), while over -expression of miR-150 and miR-194 could inhibit the proliferation of LX-2 cells [15]. [score:10]
[1 to 20 of 1 sentences]
[+] score: 10
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 A. Scatterplot showing relative expression of miRNAs by macroarray. [score:4]
Mature ID Fold Regulation miR-135b −2.6965 miR-363 −2.5995 miR-98 −2.543 miR-132 −2.355 miR-103 −2.1776 miR-99b −2.044 miR-135a −1.8734 let-7d −1.7861 miR-130a −1.6538 miR-152 −1.6246 miR-129-5p −1.6232 miR-298 −1.6169 miR-185 −1.6035 miR-214 −1.5746 miR-140 −1.5688 miR-134 −1.5667 miR-18b −1.5607 miR-194 −1.5509 let-7f −1.5107 miR-149 −1.51 Because miRNAs typically regulate translation in animal cells, we compared CXCL10 and STAT1 protein levels in both control and Dicer [d/d] animals and cells. [score:4]
This indicates that Stat1 mRNA could be controlled in a miRNA -dependent manner, and indeed, the miRanda algorithm predicts potential binding sites in its 3’ UTR for numerous miRNAs including miR-214, miR-194 and miR-140, which are listed in Table 2. An alternative hypothesis for differential gene expression in Dicer [d/d] splenocytes compared to wild-type could reside in a modification in the proportion of the cellular content if this organ. [score:2]
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[+] score: 10
The commonly upregulated miRNAs included those of 34 known tumor suppressor genes (e. g., miR-16, miR-96, miR-150, miR-183, miR-186, miR-194, miR-320, and miR-371), nine miRNAs of oncogenes (e. g. miR-454), and 14 miRNAs that show both tumor suppressive and oncogenic function(Supplementary Table S1). [score:8]
In addition, to examine whether these candidate miRNAs regulate CCR6, we transiently transduced 12 miRNAs including miR-150, miR-96, miR-183, miR-194-5p, miR-320a, miR-371a-5p, miR-3135b, miR-3652, miR-4534, miR-4698, and miR-6088. [score:2]
[1 to 20 of 2 sentences]
[+] score: 9
Of the multiple miRNAs which had terminal uridines that required Zcchc11 in our deep sequencing datasets and were predicted to target the 3′ UTR of IGF-1 (Figure 3B), we examined the ability of 4 (miR-126-5p, miR-194-2-3p, miR-379 and Let-7d) to suppress IGF-1 expression. [score:7]
MiR-126-5p, miR-194-2-3p, and miR-379, but not Let-7d, significantly silenced the IGF-1 reporter (Figure 5A). [score:1]
The uridylation of miR-126-5p or miR-379 significantly diminished IGF-1 silencing by these miRNAs, while uridylation of miR-194-2-3p had no effect (Figure 5B). [score:1]
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[+] score: 8
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Both ACTH and 17α-E2 up-regulated the expression of miRNA-212, miRNA-132, miRNA-154, miRNA-494, miRNA-872, miRNA-194, and miRNA-24-1, but reduced the expression of miRNA-322, miRNA-20b, miRNA-339, miRNA-27a, miRNA-551b, and miRNA-1224. [score:8]
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[+] score: 8
For example, miR-106b and miR-194 were predicted to target the transcription factor gene, Mef2c, which is a confirmed target of miR-223 [14, 49]. [score:5]
Expression of miR-106b and miR-194 may act in concert with that of miR-223, which may explain a previous observation whereby granulopoiesis was not completely impaired in miR-223 null mice [14]. [score:3]
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[+] score: 7
Direct targets of p53 include the already mentioned miR-34 and also miR-192, miR-194 and miR215, which then modulate MDM2 expression [15]. [score:6]
One of the most elegant works provided evidence that miR-192, miR-194 and miR-215 can be transcriptionally activated by p53 [15]. [score:1]
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[+] score: 7
[14] and miR-21a, miR-26b, miR-30b, miR-103, miR-194, miR-449a found to be upregulated in both the present study and in that of Gapp et al. [60] In addition, let7f, let7g and let7i were found to be upregulated in both this study and Gapp et al. [60] It is important to emphasize that we are not discounting the importance of other small RNAs not common between the studies to-date because they are potentially acting as secondary molecular mediators of the offspring phenotypes under specific study conditions. [score:7]
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[+] score: 7
Of the 20 miRNAs downregulated in crypts, 8 showed a >4.0 fold difference (miR-142-5p, miR-16-5p, miR-22-3p, miR-194-3p, miR-33-5p, miR-223-3p, miR-32-5p, miR-140-5p; Fig. 4a1, blue spots), whereas, of the 15 miRNAs upregulated in crypts, 2 showed a >3.0 fold difference (miR-192-5p, miR-98-5p) (Fig. 4a2, blue spots). [score:7]
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[+] score: 7
For example, miR-194 and miR-206 were previously found to be involved in osteoblast [62] and muscle differentiation, [63] respectively, while miR-101, whose expression was decreased in p53R172H iPS cells, is a well-characterised tumour suppressor that inhibits tumour growth and metastasis. [score:5]
Among the miRNAs that are regulated by p53R172H during the MEF to iPS cell transition, several have known functions in stemness and differentiation, for example miR-186, miR-194 and miR-206. [score:2]
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[+] score: 7
Among these, miR-31 is consistently upregulated [12]– [17], [20], [22], [23], [25] and microRNA clusters miR-143/-145 [18], [21]– [23], [37]– [40] and miR-194/-215 [18], [21]– [23], [37], [38], [41] downregulated in colon cancer. [score:7]
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[+] score: 6
Liver fibrosis causes downregulation of miRNA-150 and miRNA-194 in hepatic stellate cells, and their overexpression causes decreased stellate cell activation. [score:6]
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[+] score: 6
We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
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[+] score: 6
Hepatology 17 Venugopal SK Jiang J Kim TH Li Y Wang SS 2010 Liver fibrosis causes downregulation of miRNA-150 and miRNA-194 in hepatic stellate cells, and their overexpression causes decreased stellate cell activation. [score:6]
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[+] 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, 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-194, 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]
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[+] score: 5
Kim et al. [64] found that p53 up-regulated miR-200 and miR-192 family members and described the role of p53 in regulating epithelial-mesenchymal transition (EMT) in HCC through the induction of specific effector microRNAs including miR-141, miR-192, miR-194, miR-200b, miR-200c, and miR-215. [score:5]
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[+] score: 5
As an example, inhibition of TSP-1 by miR-194 promoted angiogenesis and tumor growth of colonic carcinoma xenografts [13]. [score:3]
In colon cancers, p53 seems to regulate TSP-1 by a posttranscriptional mechanism that involves miRNA-194 [13]. [score:2]
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[+] score: 5
The array uncovered the induction of 117 miRNAs with the signal intensity ≥500 (the fluorescence amount of each miRNA probe is measured by a photo multiplier tube or charge-coupled device and signal scaled across the range of detection for the platform) in GA muscle (Table 1, Fig. 1A and 1B), including the highly downregulated miRNAs (≥1.5-fold) miR-194-5p, miR-101b-3p, miR-148a-3p, miR-199b-5p, miR-335-5p, miR-127-3p, miR-379-5p, miR-541-5p, miR-382-5p, miR-329-3p, miR-299-5p and miR-434-3p, and the highly up-regulated miRNAs (≥1.5 fold), miR-146b-5p and miR-146a-5p (Fig. 1C). [score:5]
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[+] score: 5
Recently, miRNA expression profiles [19] revealed that several miRNAs (miR-192, miR-194, miR-204, miR-215, and miR-216) are highly and nearly exclusively expressed in the kidney. [score:5]
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[+] score: 5
The miRNAs (miR-203, miR-194, miR-98, let-7 g, and miR-155) predicted to have seed sites in the 3’UTR of Rictor were stably over expressed in the ERα [+] MCF-7 cell line and screened by qPCR for Rictor expression levels. [score:5]
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[+] score: 4
Although we found that mimics of miR-125b-5p, miR-194-5p miR-21-5p and miR-122-5p restored GSH levels significantly (Fig. 1d), inhibitors of only miR-125b-5p and miR-122-5p led to significant reduction in GSH levels (Fig. 1e). [score:3]
We found seven miRNAs fulfilling these two criteria: miR-194-5p, miR-125b-5p, miR-21-5p, let-7a-5p, miR-122-5p, miR-30c-5p and miR-193a-3p (Fig. 1c). [score:1]
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[+] score: 4
Some miRNAs have been identified to regulate the expression of FoxM1, including miR-149, miR-134, miR-370, miR-494, miR-194, and miR-24-1 [37– 43]. [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-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, 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-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The prospect that a similar function may extend to other miRNAs is suggested by the conservation of several miRNAs (e. g. miR-25, miR-34a/b/c, miR-135a/b, miR-194, and miR-200a) that are capable of directly targeting the Wnt/β-catenin, a signaling pathway that has been wi dely implicated in the control of oncogenic hallmarks such as cell proliferation, metastasis, angiogenesis, telomerase activity, and apoptosis (reviewed by [49]). [score:4]
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[+] score: 4
Hepatocyte -associated miRNAs, such as miR-122, miR-145, miR-192, and miR-194, were also upregulated (Figure 3B). [score:4]
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[+] score: 3
Three probesets aligned to regions that contain structural variants among CC founder strains (miR-148b, miR-192, and miR-194), but the observed patterns of expression were not correlated with the strain distribution of structural variants. [score:3]
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[+] score: 3
miRNA nameIL10 [−/−] mice mo del Intestinal Inflammation Inflammation mmu-miR-29b-3p x mmu-miR-122-5p x x x mmu-miR-148a-3p x mmu-miR-150-5p x x mmu-miR-192-5p x mmu-miR-194-5p x mmu-miR-146a-5p x mmu-miR-375-3p x x x mmu-miR-199a-3p x We showed that our nine-miRNA signature could discriminate between the different forms of colitis and arthritis, as well as between non-colitic mice with and without a genetic predisposition to develop the disease (WT mice versus non-colitic IL10 [−/−] mice). [score:3]
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[+] score: 3
For example, miR-192 and miR-194 are abundantly expressed in normal human kidneys, and their levels in rats are higher in the renal cortex than in the medulla [1], [2]. [score:3]
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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-15a, hsa-mir-17, hsa-mir-21, hsa-mir-29a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-194-1, mmu-mir-200b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-140, hsa-mir-194-1, 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-21a, mmu-mir-29a, mmu-mir-96, mmu-mir-34a, mmu-mir-135b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-376c, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-135b, mmu-mir-181b-2, mmu-mir-376b, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-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-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-29a, dre-mir-96, 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-140, dre-mir-181c, dre-mir-194a, dre-mir-194b, dre-mir-200b, dre-mir-200c, hsa-mir-376b, hsa-mir-181d, hsa-mir-507, dre-let-7j, dre-mir-135b, dre-mir-181a-2, hsa-mir-376a-2, mmu-mir-376c, dre-mir-34b, dre-mir-34c, mmu-mir-181d, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, mmu-mir-124b
The expression data is based on in situ hybridization experiments of P0 mouse inner ear sections, except for miR-194 at E16.5, miR-140 at P1 and miR-124a and -100a at P5. [score:3]
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Similarly, we found an increased expression of let-7i-5p, miR-29a-3p, miR-29c-3p, miR-30a-5p, miR-98-5p, miR-138-5p, miR-139-5p, miR-140-5p, miR-146b-5p, miR-148b-3p, miR-181a-1-3p, miR-181a-5p, miR-194-5p, and miR-342-3p, all of which have been reported to be altered in different AD tissues (Cogswell et al., 2008; Hebert et al., 2008; Maes et al., 2009; Wang et al., 2011, 2012; Lau et al., 2013). [score:3]
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For example, the miR-202/ miR-202* expression ratio changes from ∼0.5 to ∼0.9 during female gonadogenesis in chicken embryos [16], and mouse miR-194-5p is present at a higher level than miR-194-3p in kidney and stomach, but at a lower level in lung and uterus [17]. [score:3]
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MicroRNAs targeting MDM2: miR-192, miR-194, miR-215, miR-221, miR-605, miR-17-3p, miR-193a, miR-25, miR-32, miR-143, miR-145, miR-18b, miR-661 [reviewed in Ref. [score:3]
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Figure S2 DNA methylation status of Igf2-H19 gene cluster (A) and expression of Let-7a, Let-7d and miR-194 miRNAs (B) in multipotent adult germ-line (maGS) stem cells cultured in two different culture conditions. [score:3]
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In addition, we found that liver-enriched miR-122 and miR-192/194 as well as erythrocyte-enriched miR-451 levels were also detected in the plasma of these mice (miR-122, 34.69 ± 0.07 Ct; miR-192, 27.06 ± 0.17 Ct; miR-194, 30.48 ± 0.10 Ct; miR-451, 21.42 ± −0.16 Ct). [score:1]
Absolute miRNA quantification was performed by reverse transcription of serial dilutions of synthetic oligonucleotides with sequence to mature mmu-miR-375 (5′-UUUGUUCGUUCGGCUCGCGUGA-3′), mmu-miR-16 (5′-UAGCAGCACGUAAAUAUUGGCG-3′), and mmu-miR-194 (5′-UGUAACAGCAACUCCAUGUGGA-3′). [score:1]
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Krützfeldt et al[18] have showed that intravenous administration of blocking locked nucleic acid (LNA) oligonucleotides (antagomirs) against miR-16, miR-122 and miR-194 resulted in marked reduction of corresponding microRNA levels in several different organs of mice. [score:1]
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However, in sheep, the analyzed miRNA sites that are located in the 505 bp 3′ UTR of the ovine s-SCF (+) form belongs to the miRNA families of miR-27a/b, miR-194, miR-128, miR-370, and two sites for miR-132/212, miR-320/320abcd (Figure 9(a)) where as miR-669f/a/o-3p, miR-466b and miR828b are detected on the shorter 3′ UTR segment (144 bp) of ovine m-SCF (−) form (Figure 9(b)). [score:1]
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For absolute quantification of miRNAs, synthetic miRNAs comprising the mature miRNA sequence (Sigma) were serially diluted in water and used as input for RT-qPCR reactions, generating standard curves against which to compare experimental cycle threshold (Ct) values (mmu-miR-375-3p, 5′-UUUGUUCGUUCGGCUCGCGUGA-3′; mmu-miR-200a-3p, 5′-UAACACUGUCUGGUAACGAUGU-3′; mmu-miR-200c-3p, 5′-UAAUACUGCCGGGUAAUGAUGGA-3′; mmu-let-7f-5p, 5′-UGAGGUAGUAGAUUGUAUAGUU-3′; mmu-miR-194-5p, 5′-UGUAACAGCAACUCCAUGUGGA-3′; mmu-miR-122-5p, 5′-UGGAGUGUGACAAUGGUGUUUG-3′; mmu-miR-33-5p, 5′-GUGCAUUGUAGUUGCAUUGCA-3′; and mmu-miR-16-5p, 5′-UAGCAGCACGUAAAUAUUGGCG-3′). [score:1]
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Other miRNAs from this paper: mmu-mir-194-1, hsa-mir-194-1, hsa-mir-194-2
The regions with the proximal HNF4α -binding sites (+ HNF4α) and the regions without HNF4α -binding site (− HNF4α) in the human MIR-194/192 gene were amplified. [score:1]
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This group includes the KSHV pre-miRNAs along with the cellular pre-miRNAs let-7a-1, let-7a-2, let-7a-3, mir-7-1, mir-27a, mir-125b-2, mir-140, mir-152, mir-181c, mir-194-2, and mir-220. [score:1]
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For example, miR-451 and miR-142-3p were much more abundant in exosomes than in MIN6B1 cell extracts, whereas the levels of miR-32 and miR-194 were clearly higher inside the cells. [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-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, 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-203a, 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-344i MIMAT0025049 2 8mer −0.42 −0.334 297 −32.2 TURE rno-miR-6316 MIMAT0025053 2 8mer, 7mer-m8 −0.41 −0.611 308 −29.59 TRUE rno-miR-21-3p MIMAT0004711 2 8mer, 7mer-m8 −0.408 −0.581 289 −25.18 TRUE rno-miR-3120 MIMAT0017900 2 7mer-m8 −0.402 −0.536 289 −24.4 TRUE rno-miR-194-5p MIMAT0000869 3 7mer-m8 offset 6mer −0.381 −0.593 442 −41.91 TRUE rno-miR-126a-3p MIMAT0000832 1 8mer −0.358 −0.248 148 −18.86 TRUE rno-miR-27a-3p MIMAT0000799 3 7mer-m8 −0.357 −0.708 447 −41.04 TRUE rno-miR-26b-5p MIMAT0000797 3 7mer-m8 offset 6mer −0.348 −0.581 444 −30.64 TRUE rno-miR-3557-3p MIMAT0017820 4 8mer 7mer-m8 imperfect −0.346 −0.503 582 −81.21 TRUE rno-miR-27b-3p MIMAT0000798 4 7mer-m8 offset 6mer −0.334 −0.705 588 −55.75 TRUE rno-miR-3569 MIMAT0017849 2 8mer offset 6mer −0.333 −0. [score:1]
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41 mmu-miR-33 −59.71 mmu-miR-222 1.23 mmu-miR-93 −1.52 mmu-miR-124 −97.01 mmu-miR-429 1.07 mmu-miR-192 −1.52 mmu-miR-129-5p −111.43 mmu-miR-100 −1.74 mmu-miR-210 −157.59 mmu-miR-20a −2 mmu-miR-134 −194.01 mmu-miR-137 −2 mmu-miR-215 −222.86 mmu-miR-194 −2.14 mmu-miR-452 −675.59 mmu-miR-196a −2.64 mmu-miR-223 −955.43 Differentiated sample versus control sample [DIF EBs d8/CONTROL EBs d8]. [score:1]
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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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