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22 publications mentioning rno-mir-194-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-194-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 241
Effect of miR-194 inhibition on protein expression of the oxidative phosphorylation complexes expression in L6 cells. [score:7]
In summary, our data indicate that miR-194 is down-regulated early in the development of insulin resistance and that this regulation is maintained through the progression towards type 2 diabetes. [score:6]
When miR-194 was down-regulated in vitro, western blot analysis showed an increased phosphorylation of AKT and GSK3β in response to insulin, and an increase in expression of proteins controlling mitochondrial oxidative phosphorylation. [score:6]
When studying the effects of miR-194 inhibition in L6 myocytes, we found that down-regulation of miR-194 resulted in an increased glucose uptake into the muscle cells and incorporation into glycogen both basally and in response to insulin. [score:6]
Our functional experiments in vitro have provided strong evidence of the effects of miR-194 down-regulation on glucose metabolism; additional studies examining the effects of miR-194 inhibition in vivo are now warranted to confirm our data. [score:6]
A computational prediction of miR-194 target genes has suggested several targets linked to T2DM signaling pathways (ATM, AKT2, KCNJ11, MAPK1, SOCS2), insulin signaling (AKT2, ATM, CRK, FOXO1, GRB10, INPP5K, MAPK1, PRKAR1A) and AMPK signaling (ADRAP1A, AKT2, ATM, CHRNAS, MAPK1, PPAT, PPP2R2C, PRKAR1A). [score:5]
Our combined experimental and clinical approach allowed us to identify changes of miR-194 expression across multiple species and metabolic tissues (skeletal muscle, adipose tissue) at different stages of the disease progression suggesting that miR-194 may be involved in the initial cellular responses to hyperglycemia and be part of the early cellular events related to the pathogenesis of type 2 diabetes. [score:5]
Phosphorylation of AKT (Ser473) and GSK3β (Ser9), relative to total expression, in response to insulin were increased by 43±9% and 71±4% respectively (p<0.05) in L6 cells transfected with the miR-194 inhibitor (Fig 4). [score:5]
We firstly assessed basal and insulin-stimulated glucose uptake in the L6 muscle cell line after inhibiting miR-194 expression. [score:5]
Interestingly, miR-194 was a unique miRNA that appeared regulated across different stages of the disease progression, from the early stages of insulin resistance to the development of T2DM. [score:5]
The expression levels of miR-194 were validated by qPCR, demonstrating a 50% reduction in expression in the skeletal muscle of individuals with pre-diabetes and diabetes (Fig 1A) and a 25% decrease in the skeletal muscle of insulin resistant rats (Fig 1B). [score:5]
Effect of miR-194 inhibition on AKT and GSK3β expression in L6 cells. [score:5]
Down-regulation of miR-194 identified by microarray was indeed validated by qPCR, showing good correlation between microarray and qPCR, and discarding the possibility of a false positive which can be high with microarray studies. [score:4]
Interestingly, a unique microRNA was regulated across both species: indeed, miR-194 expression was significantly reduced by 25 to 50% in both mo dels. [score:4]
Down-regulation of miR-194 in vitro activates the insulin signaling pathway and oxidative phosphorylation. [score:4]
To investigate the functional effect of down-regulation of miR-194 expression in the development of T2DM, we performed in vitro functional assays. [score:4]
miR-194 down-regulation promotes multiple aspects of glucose metabolism in skeletal muscle. [score:4]
We identified miR-194 as being commonly down-regulated in humans and rats. [score:4]
We have also shown an increased glycolysis in response to the down-regulation of miR-194, as indicated by an elevated lactate production in transfected cells. [score:4]
We investigated the functional role of miR-194 in skeletal muscle cells and showed that miR-194 down-regulation is associated with: 1) increased basal and insulin-stimulated glucose uptake, 2) increased glycolysis and incorporation into glycogen, 3) increased AKT and GSK3β phosphorylation in response to insulin stimulation, 4) increased glucose oxidation capacity, and 5) increased basal protein expression of mitochondrial oxidative phosphorylation complexes in skeletal muscle. [score:4]
Down-regulation of miR-194 in vitro promotes glucose metabolism. [score:4]
Among these, only one miRNA was similarly regulated: miR-194 expression was significantly reduced by 25 to 50% in both the rat mo del and in human with pre-diabetes and established diabetes. [score:4]
Indeed, we identified miR-194 as being down-regulated in skeletal muscle of insulin resistant rats from HF fed dams, high fat fed mice, and humans with pre-diabetes and T2DM. [score:4]
Although we have not examined the mechanism by which miR-194 is down-regulated in skeletal muscle in the current study, it could involve selective packaging into exosomes. [score:4]
Among these, one miR was similarly regulated; indeed, miR-194 expression was significantly reduced in both mo dels. [score:4]
Thus, miR-194 could be down-regulated in patients with early features of diabetes as an adaptive response to facilitate glucose metabolism in the face of insulin resistance. [score:4]
Expression of the phosphorylated and total forms of AKT (A) and GSK3β (B) were measured by Western blot in L6 cells 48 hours after transfection with a miR-194 inhibitor. [score:3]
When stimulated with insulin, lactate production increased by 18±7% in control cells while there was no further increase in cells transfected with the miR-194 inhibitor (p<0.05, Fig 3C). [score:3]
For instance, miR-194 expression was found increased in C2C12 cells treated with palmitate, and restored with oleate [52]. [score:3]
miR-194 expression was validated by qPCR in human (A) and rat samples (B) (n = 4–6 per group). [score:3]
To determine the optimal concentration, experiments using varying miR-194 inhibitor concentrations (5–100 nM) were performed. [score:3]
miR-194 expression in the skeletal muscle of human participants and rat offspring and correlations with HOMA-IR. [score:3]
Indeed, our study revealed augmented levels of insulin-stimulated phosphorylation of AKT and GSK3β by miR-194 inhibition. [score:3]
Expression of the oxidative phosphorylation (OXPHOS) complexes I to V of the electron transport chain was measured by western blot in L6 cells 48 hours after transfection with a miR-194 inhibitor. [score:3]
Effect of miR-194 inhibition on glucose homeostasis in L6 cells. [score:3]
Transfection of miR-194 inhibitor. [score:3]
Of note, we also found a decreased miR-194 expression in the adipose tissue from our human cohort (-21% in patients with pre-diabetes, -38% in patients with T2DM, data not shown). [score:3]
Fully differentiated L6 cells were transfected with either a miR-194 inhibitor or a negative control (Applied Biosystems, #MH10004 and #4464076) using Lipofectamine RNAiMAX (Invitrogen) following the manufacturers’ recommended protocol. [score:3]
MiR-194 could be down-regulated in patients with early features of diabetes as an adaptive response to facilitate tissue glucose uptake and metabolism in the face of insulin resistance. [score:3]
Correlation between miR-194 expression and HOMA-IR in human (C) and rat (D) was assessed using Pearson’s or Spearman’s correlation test as appropriate. [score:3]
Although there was no effect of miR-194 inhibition on the basal glucose oxidation rate, we found an increased glucose oxidation when the cells were treated with the mitochondrial uncoupler FCCP (Fig 3D). [score:3]
The microarray data from humans and rats provided a basis for the a priori hypothesis that miR-194 would be differentially expressed between the various mo dels when assessed by qPCR. [score:3]
In line with our oxidative phenotype, L6 muscle cells transfected with a miR-194 inhibitor had higher protein expression of several complexes of the mitochondrial oxidative phosphorylation (OXPHOS) chain, a proxy measure for mitochondrial volume. [score:3]
A negative correlation between miR-194 expression and the HOMA-IR also indicated an inverse association of this miR with insulin resistance. [score:3]
There was no effect on phosphorylation of these proteins by miR-194 inhibition under basal conditions. [score:3]
Moreover, we identified a negative correlation between homeostatic mo del assessment index of insulin resistance (HOMA-IR, reported in Table 1) and miR-194 expression levels (r = -0.69, p = 0.01 in humans, r = -0.65, p = 0.04 in rats, Fig 1C and 1D), indicating an association of miR-194 with insulin resistance. [score:3]
Measuring circulating miR-194 in the blood at different stages of the disease progression could inform on the potential of miR-194 as an early biomarker of diabetes, long before the onset of the disease. [score:3]
A role for miR-194 in type 2 diabetes has not yet been described in the literature; however, Zhang J. et al. showed a decreased hepatic expression of miR-194 in the adult offspring of high fat fed dams [29]. [score:3]
0155108.g005 Fig 5Expression of the oxidative phosphorylation (OXPHOS) complexes I to V of the electron transport chain was measured by western blot in L6 cells 48 hours after transfection with a miR-194 inhibitor. [score:3]
0155108.g004 Fig 4Expression of the phosphorylated and total forms of AKT (A) and GSK3β (B) were measured by Western blot in L6 cells 48 hours after transfection with a miR-194 inhibitor. [score:3]
Interestingly, the absence of further increase of lactate production when transfected cells are treated with insulin may indicate that the glycolytic rate within miR-194 inhibited cells is already operating at maximal capacity. [score:3]
Conversely, we observed that decreased expression of miR-194 for a short term (48 hours in vitro) is able to increase muscle mitochondrial oxidative capacity potential through increased mitochondrial OXPHOS. [score:3]
Differentiated L6 cells were transfected with either a miR negative control or miR-194 inhibitor. [score:3]
Taken together, our data suggest that the decrease in miR-194 expression observed in insulin resistant muscle is an adaptive response to facilitate tissue glucose uptake and metabolism in the face of insulin resistance. [score:3]
rates were unaffected by miR-194 inhibition under basal conditions, but in the presence of the mitochondrial uncoupler FCCP, cells had an increased oxidative capacity. [score:3]
A concentration of 100 nM proved optimal, giving robust and consistent efficacy inducing a 35 fold decrease in miR-194 expression in the cells (qPCR, data not shown). [score:3]
Considering glucose oxidation was assayed under basal conditions, it might be interesting to determine whether miR-194 inhibition can increase glucose oxidation under simulated nutrient excess. [score:2]
Basal or insulin-stimulated glucose uptake (A), glycogen synthesis (B) and lactate production (C) were assayed in L6 cells 48 hours after transfection with a miR-194 inhibitor. [score:2]
Under basal conditions, we found lactate production was significantly increased following miR-194 inhibition compared to control (9±4%, p<0.05, Fig 3C). [score:2]
Compared to control, miR-194 inhibition increased glycogen synthesis by 34±3% under basal conditions and 23±13% with insulin stimulation (p<0.05 for both, Fig 3B). [score:2]
MiR-194 expression in the skeletal muscle of mice fed a high fat diet. [score:2]
To further confirm down-regulation of miR-194 in the insulin resistant state, we measured its expression in skeletal muscle from mice fed a HFD for 8 weeks, a well characterized mouse mo del of insulin resistance [18]. [score:2]
To address the possible mechanisms by which miR-194 regulates glucose metabolism, we examined components of signaling pathways contributing to glucose metabolism. [score:2]
0155108.g003 Fig 3Basal or insulin-stimulated glucose uptake (A), glycogen synthesis (B) and lactate production (C) were assayed in L6 cells 48 hours after transfection with a miR-194 inhibitor. [score:2]
Inhibition of miR-194 induced a 53±8% increase in basal glucose uptake and a 40±20% increase in insulin-stimulated glucose uptake into the muscle cells compared to the transfection control (p<0.05 for both, Fig 3A). [score:2]
Knockdown of miR-194 in L6 skeletal muscle cells induced an increase in basal and insulin-stimulated glucose uptake and glycogen synthesis. [score:2]
Complexes I (NADH dehydrogenase, NDUFB8), II (succinate dehydrogenase, SDHB), IV (cytochrome c oxidase, MTCO1), and V (ATP synthase, ATP5A) were increased by between 30 to 85% (p<0.05) when miR-194 was inhibited compared to control (Fig 5). [score:2]
The results of this study reveal an important role of miR-194 in influencing glucose metabolism in association with the progression from insulin resistance to type 2 diabetes. [score:1]
Thus, reduced miR-194 may elevate glucose uptake and its incorporation into glycogen by activating AKT and inactivating GSK3 through phosphorylation. [score:1]
These data suggest a reduction in miR-194 may allow greater oxidation of substrate, specifically glucose, under periods of increased substrate supply or under metabolic stress where greater ATP turnover is required. [score:1]
Moreover, we measured miR-194 expression in the skeletal muscle of high fat fed mice with established insulin resistance [18] and also showed a 37% decrease in the skeletal muscle of these animals. [score:1]
Furthermore, in vitro experiments showed miR-194 is involved in glucose uptake, glycolytic breakdown and its incorporation into glycogen, as well as mitochondrial oxidative capacity through mechanisms involving modulation of AKT, GSK3 and oxidative phosphorylation complexes. [score:1]
We have shown miR-194 is involved in multiple aspects of skeletal muscle glucose metabolism from uptake, through to glycolysis, glycogenesis and glucose oxidation, potentially via mechanisms involving AKT, GSK3 and oxidative phosphorylation. [score:1]
A greater mitochondrial volume provides a likely explanation for the increase in oxidative capacity we observed in miR-194 silenced cells. [score:1]
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[+] score: 42
Cg Down-regulated Fold-change Fold-change Fold-change rno-miR-310.37 [*] 0.42 [*] / rno-miR-1000.45 [*] 0.40 [*] / rno-miR-930.45 [*] 0.48 [*] / rno-miR-1520.38 [*] 0.40 [*] / rno-miR-4970.33 [*] 0.44 [*] / rno-miR-192 /0.24 [*] 0.28 [*] rno-miR-194 /0.14 [*] 0.12 [*] rno-miR-200b /0.19 [*] 0.27 [*] Up-regulated Fold-change Fold-change Fold-change rno-miR-1223.87 [*] 2.49 [*] / *indicates significant difference between the two groups. [score:7]
The miRNA screen identified 8 significantly down-regulated miRNAs (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b) and one highly up-regulated miRNA (miR-122) in the hypertonic dialysate group. [score:7]
The results demonstrated that in the hypertonic dialysate group, miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were all significantly down-regulated whereas miR-122 was highly up-regulated (all P <0.05) (Figure  3). [score:7]
It was found that 8 miRNAs were significantly and consistently down-regulated in the hypertonic dialysate group (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b), and within which miR-192, miR-194 and miR-200b were also down-regulated in the normal saline group (Table  3). [score:7]
Compared with the control and saline groups, both miRNA microarray and real-time PCR analyses demonstrated that miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were significantly down-regulated, and miR-122 was highly up-regulated in the hypertonic dialysate group. [score:6]
These results are consistent with our findings and future studies should focus on elucidating how the targets of miR-194 might be involved with modulation of α-SMA and COL-1 activation. [score:3]
Introduction of miR-194 in hepatic stellate cells resulted in significantly reduced expression of α-SMA and COL-1 [42]. [score:3]
miR-194 has been associated with liver fibrosis in a rat mo del. [score:1]
Taken together, these results suggest to us that the miRNA species identified in our miRNA screen (mir-31, mir-93, mir-192, mir-194 and mir-200b) may be critical in the process of mesothelial cell EMT and in the progression of peritoneal fibrosis. [score:1]
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[+] score: 20
Cumulatively, our results indicated that let-7b expression is upregulated in burn patients, comparatively more than miR-194. [score:6]
It has been earlier shown that miRNA-194 can target IGF1R and silence its expression in burn cases. [score:5]
MiR-194 expression was also higher in serum from burn patients (1.62 ± 0.27) (Figure 1B; p = 0.039) (P<0.05), but the changes were much more with let-7b than miR-194. [score:3]
Furthermore, it has been established that miR-194 can target insulin-like growth factor 1 receptor (IGF1R) and result in hyperglycemia post-burn injury [15]. [score:3]
This induction was overwhelmingly more when compared to increase in expression of the previously reported miR-194 [15]. [score:2]
We assessed the levels of let-7b, let-7e, miR-194, miR-15, miR-133a, miR-15, and miR-195 (as a non-specific control) by real-time PCR. [score:1]
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[+] score: 19
Furthermore, we have also partly elucidated the molecular mechanisms that would explain the elevated circulating levels of glucose and NEFAs observed in the animals exposed to the short photoperiod, which were as follows: (1) a sharp down-regulation of the phosphorylated Akt2 levels in both soleus and gastrocnemius muscles; and (2) decreased expression in the soleus muscle of the glucose metabolism-related microRNA-194 and lower mRNA levels of the genes involved in glucose metabolism (Irs1, soleus, and Glut2, liver), β-oxidation (Had and Cpt1β, soleus) and fatty acid transport (Cd36, soleus and liver). [score:6]
Furthermore, the down-regulation of the soleus mRNA levels of the gene encoding IRS1, a key protein involved in the activation of Akt2 (Long et al., 2011); the lower levels of miR-194 observed in this tissue, which was also reported in insulin-resistant rats and in prediabetic and diabetic humans (Latouche et al., 2016); and the decreased hepatic gene expression levels of Glut2, the main glucose transporter in the liver (Lamia et al., 2008), could also account for the elevated serum glucose levels displayed by L6 rats. [score:6]
In addition, L6 rats presented lower mRNA levels of the insulin receptor substrate 1 (Irs1) (p = 0.007, Student’s t-test) (Figure 1A), a gene encoding a key protein involved in the insulin signaling pathway (Long et al., 2011), and lower expression levels of the glucose metabolism-related microRNA-194 (miR-194) (Latouche et al., 2016) than the L12 rats (p = 0.009, Student’s t-test) (Figure 3B). [score:3]
The Exposure to Different Day Lengths Altered the mRNA Levels of Fatty Acid Transport, β-Oxidation and Insulin Signaling-Related Genes and the MicroRNA-194 Expression in the Soleus Muscle. [score:2]
MicroRNA-194 modulates glucose metabolism and its skeletal muscle expression is reduced in diabetes. [score:2]
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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, mmu-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-194-2, 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: 14
Analysis of cellular miRNAs identified that administration of FGF2, FGF4 or INF-β significantly regulated the expression of several miRNAs (Fig. 7a) including the liver-enriched miR-194 31. miR-194 expression is regulated by hepatocyte nuclear factor 1α (HNF1-α 45) and its down-regulation may have an effect on cellular mobility 46. [score:10]
Microarray analysis identified a panel of miRNAs, which are either highly expressed in the heart (miR-1, miR-133a and miR-16) or in the liver (miR-122, miR-192 and miR-194) or invariant (miR-21; Supplementary Figure 1a). [score:3]
Total RNA from heart or liver were reverse transcribed according to the miQPCR and TaqMan protocols and the expression of 7 miRNAs (miR-1, miR-133b, miR-16, miR-122, miR-194 and miR-21) and a small nuclear RNA (RNU6) was measured by qPCR with respectively SYBR-Green (top panel) or TaqMan probes (lower panel). [score:1]
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[+] score: 13
In agreement, we showed that the expression of rno-miR-192, rno-miR-194, and rno-miR-499 was higher in the stone-forming group while their potential target gene chemokine receptor 2 (CCR2) was lower. [score:5]
Among these differentially expressed miRNAs, rno-miR-130b-3p, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, rno-miR-351-5p, and rno-miR-21-3p had the largest positive fold changes, while rno-miR-335, rno-miR-192-3p, rno-miR-194-5p, rno-miR-192-5p, rno-miR-499-5p, and rno-miR-210-3p had the largest negative fold changes (Table 1). [score:3]
Therefore, we proposed that, in the process of kidney stone formation, the overexpression of CCR2 mediated by relevant miRNAs, such as rno-miR-192, rno-miR-194, and rno-miR-499, would induce the inflammation and damage to the renal tubular epithelial cells and promote nephrolithiasis. [score:3]
Relative expression levels of the selected miRNAs and mRNAs were depicted in Figure 3. Consistent with the microarray data, real-time PCR confirmed that, compared with controls, rno-miR-132-3p, rno-miR-181a-1-3p, rno-miR-222-3p, and rno-miR-351-5p were significantly increased, while rno-miR-192-3p, rno-miR-194-5p, rno-miR-29c-3p, rno-miR-185-5p, and rno-miR-30c-5p were significantly decreased in stone-forming rat kidneys. [score:2]
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[+] score: 13
Of the nine miRNAs in this IRI-specific expression signature, six showed differential expression in our study (four of which exhibited increasing expression with age, including miR-21, miR-146a, miR-192, and miR-194) (Figure  6). [score:7]
The miRNAs that showed highest expression during middle or young adult ages (15 and 21 weeks) were miR-192 and miR-194 (Figure  6B,H), both of which show steady increase in expression at early ages, that peak at 15 and 21 weeks of age, before decreasing at older ages. [score:5]
For example, nine miRNAs (miR-21, miR-20a, miR-146a, miR-199a-3p, miR-214, miR-192, miR-187, miR-805, and miR-194) have been identified in C57BL/6 mice as promising biomarkers of kidney injury after renal ischemia reperfusion injury (IRI) [15]. [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
Finally, through GO and pathway analysis of putative targets of individual miRNA, it was identified that certain miRNAs, including let-7f, regulated target genes associated with drug metabolism; certain miRNAs, including miR-150, regulated target genes associated with the response to glucose stimulation; numerous miRNAs, including miR-145, regulated genes associated with cell proliferation and apoptosis; and numerous other miRNAs, including miR-194, regulated genes associated with the inflammatory response. [score:11]
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[+] score: 8
Specifically, miR-194 was found significantly up-regulated only in the VDS fractions. [score:4]
It was found that the expression of miR-122 (P = 0.0001), miR-192 (P = 0.004), miR-194 (P = 0.03)] and Let-7a (P = 0.006) followed the same pattern as observed for vesicles -associated miRNAs (top rows in Figs 6 and 7), suggesting that these miRNAs do undergo comparable modulation in both fractions. [score:3]
Specifically, we found that the cytokines used in this study significantly increased levels of miR-122, miR-150, miR-21, miR-192 and miR-194 associated to EVs secreted from PCs. [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-194-2, 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-194-2, 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: 7
The expression of tissue specific miRNAs is often regulated at the transcription level by tissue specific transcription factors (for examples, miR-122a by HNF4, miR-192 and miR-194 by HNF1 [8], [9]. [score:4]
Similarly, genes encoding for miR-192 and miR-194 are clustered on chromosome 1, and could explain their coordinated increase in expression (Table 2). [score:3]
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[+] score: 6
Six of them, namely, rno-miR-107-5p, rno-miR-383-5p, rno-miR-24-1-5p, rno-mir-191b, rno-miR-196b-5p, and rno-miR-3552, were upregulated, while only rno-mir-194-1 was downregulated in the MCAO group compared with the sham group. [score:6]
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[+] score: 5
For instance, we observed a decrease in the levels of 5 miRNA with predicted target sites in the Foxa1 3′UTR (miR-106b, miR-194, miR-30c, miR-30b-5p and miR-20a) along with increased Foxa1 mRNA expression on methamphetamine exposure. [score:5]
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[+] score: 4
In this study, several altered hippocampal miRNA, including miR-133b, miR-152, miR-194, miR-22, miR-30a*, miR-347, and miR-874, have potential ability to regulate the expression of Gnai3. [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, mmu-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-194-2, 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
A recent study demonstrates that AA treatment altered a number of miRNAs in proximal tubular epithelial cells such as up-regulation of miR-192, miR-194, miR-450a, and miR-542. [score:4]
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[+] score: 2
Furthermore, miR-194 and miR-150 regulated ECM synthesis and HSCs activation by reducing Ras-related C3 botulinum toxin substrate 1 and c-myb gene [13]. [score:2]
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[+] score: 1
Other miRNAs from this paper: rno-mir-143, rno-mir-194-2
For example, miR-194 or miR-143 strongly influences adipocyte differentiation [60– 62]. [score:1]
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[+] score: 1
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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[+] 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-194-2, 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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