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23 publications mentioning rno-mir-33

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-33. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 126
In the present study, we predicted the potential miRNAs which might target at the 3′UTR of CCL2, and further identified miR-33 as a suppressor of CCL2 expression. [score:7]
miR-33 is a regulator of CCL2 expressionTo observe the regulatory role of miR-33 in CCL2 expression, we performed gain- or loss-of-function studies on miR-33 in primary chondrocytes. [score:7]
Figure 3miR-33 suppresses CCL2 expression via targeting at the 3′UTR(A) The schematic diagram of potential binding sites (79–98) for miR-33 in the 3′UTR of mouse CCL2 gene. [score:7]
miR-33 suppresses CCL2 expression via targeting at the 3′UTR. [score:7]
In the present study, we are the first to report the expression of miR-33 in mouse chondrocytes and identify CCL2 as its direct target. [score:6]
miR-33 suppresses CCL2 expression via targeting at the 3′UTRTo investigate the precise regulatory mechanism between miR-33 and CCL2, we subcloned the 3′UTR of mouse CCL2 gene into a miRNA reporter gene vector (Figure 3A). [score:6]
Those results indicated that miR-33 suppressed mouse CCL2 expression via a binding element locating at 79/98 in the 3′UTR. [score:5]
Those findings confirmed the suppressive role of miR-33 in CCL2 expression. [score:5]
Figure 1Prediction of potential miRNAs targeting at the 3′UTR of CCL2 gene(A and B) The potential target sites of miR-124 (A) or miR-33 (B) in the 3′UTR of CCL2 gene were conserved in human, mouse and rat species. [score:5]
Here in chondrocytes, we identified miR-33 as a regulator of CCL2 expression and monocyte chemotaxis. [score:4]
Figure 2 miR-33 is a regulator of CCL2 expression(A) The relative mRNA levels of CCL2 in the primary mouse chondrocytes transfected with a scramble miRNA (100 nM) or an anti-miRNA of miR-33 (100 nM) (n=4, ** P<0.01). [score:4]
To observe the regulatory role of miR-33 in CCL2 expression, we performed gain- or loss-of-function studies on miR-33 in primary chondrocytes. [score:4]
miR-33 is a regulator of CCL2 expression. [score:4]
Inhibition of miR-33 was conducted by transfecting the chondrocytes with an anti-miRNA of miR-33 (AM12410, Thermo Fisher Scientific). [score:3]
We demonstrated that the treatment with an anti-miRNA of miR-33 could strikingly induce the expression of CCL2 in the mRNA (Figure 2A) and protein (Figure 2B) levels as well as the secretion of CCL2 in the supernatant of cultured chondrocytes (Figure 2C). [score:3]
However, the role of miR-33 in CCL2 expression was still not clear. [score:3]
Further, we overexpressed miR-33 in chondrocytes by treating the cells with a miR-33 mimic (Figure 2D). [score:3]
As shown in Figure 4, we found that the CM from miR-33 mimic -treated chondrocytes significantly inhibited the migration rate of the monocytes, whereas the CM from anti- miR-33 -treated chondrocytes notably stimulated the monocyte chemotaxis. [score:3]
We found that the potential binding sites for miR-124 (Figure 1A) and miR-33 (Figure 1B) were conserved in multiple species, indicating that those two miRNAs might be functional in CCL2 suppression. [score:3]
Overexpression of miR-33 was carried out by transfecting the chondrocytes with a miR-33 mimic (MC12410, Thermo Fisher Scientific). [score:3]
As expected, we found that anti- miR-33 treatment largely potentiated the reporter gene activity (Figure 3B), whereas miR-33 mimic could significantly suppress the luciferase activity (Figure 3C). [score:3]
The miR-33/CCL2 axis in chondrocytes regulates the monocyte chemotaxisCCL2 is a potent attractor of monocytes [12]. [score:2]
Those findings indicated that miR-33/CCL2 axis in chondrocytes was functional in regulating monocyte chemotaxis. [score:2]
The miR-33/CCL2 axis plays an important role in regulating monocyte chemotaxis. [score:2]
Noteworthily, the anti- miR-33-stimulated reporter gene activity was abolished with the mutation of the potential miR-33 binding sites (Figure 3E). [score:2]
To further confirm the regulatory effect of miR-33 on CCL2 via the 3′UTR, the potential binding sites AAUGCA were mutated as ACCGAA (Figure 3D). [score:2]
The miR-33/CCL2 axis in chondrocytes regulates the monocyte chemotaxis. [score:2]
The miR-33/CCL2 axis might regulate monocyte chemotaxis in OA. [score:2]
To observe the regulatory role of miR-33/CCL2 axis in monocyte chemotaxis, transwell migration assays were carried out. [score:1]
To further correlate our in vitro findings to the physiopathological condition, we determined the levels of miR-33, CCL2, CD-68 and IL-1β in the cartilage of the patients with OA. [score:1]
These findings implied that the miR-33/CCL2 axis might not exist in macrophages or that the function of miR-33/CCL2 axis might be antagonized by other miR-33-initiated factors. [score:1]
In a previous study, miR-33 was reported to potentiate the pro-inflammatory activation of macrophages and aggravate the progression of atherosclerosis [31]. [score:1]
We presumed that the deficiency of miR-33 in the chondrocytes of OA patients would potentiate the production of CCL2, which then attracted the monocytes from peripheric blood to the articular tissues. [score:1]
Therefore, further studies on the role of miR-33/CCL2 axis in other cell types might be very interesting. [score:1]
Decreased miR-33 levels and elevated CCL2 levels in the cartilage of OA patientsTo further correlate our in vitro findings to the physiopathological condition, we determined the levels of miR-33, CCL2, CD-68 and IL-1β in the cartilage of the patients with OA. [score:1]
Therefore, our findings indicated a potential role of miR-33 in OA. [score:1]
miRNA-33 expression level was detected with the TaqMan microRNA assay real-time fluorescent quantitative PCR technology (TaqMan®MicroRNA Assays, Life Technologies). [score:1]
Then, the luciferase reporters (wt or mut) and miRNAs (miR-33 mimic, anti- miR-33 or scramble miRNA) were transfected using Lipofectamine 2000 according to the manufacturer's instructions (Invitrogen). [score:1]
The miR-33/CCL2 axis was identified in the primary mouse chondrocytes in the present study. [score:1]
Identical results were obtained in response to the treatment of miR-33 mimic (Figure 3F). [score:1]
Decreased miR-33 levels and elevated CCL2 levels in the cartilage of OA patients. [score:1]
Meanwhile, we demonstrated that the anti- miR-33 treatment -induced monocyte chemotaxis was prevented by supplementary CCL2 antibody. [score:1]
Figure 4The miR-33/CCL2 axis in chondrocytes regulates the monocyte chemotaxisThe primary chondrocytes were transfected with a scramble miRNA (100 nM), miR-33 mimic (100 nM) or anti- miR-33 (100 nM) for 36 h. Then, the supernatant was collected as CM for the chemotaxis test of monocytes in the transwell migration assays. [score:1]
We found that treatment of miR-33 mimic largely attenuated the mRNA (Figure 2E), protein (Figure 2F) and secretion (Figure 2G) levels of CCL2 in the chondrocytes. [score:1]
The previous and recent studies mainly focused the functions of miR-33 on the cholesterol homoeostasis [28, 29] and energy metabolism [30]. [score:1]
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2
[+] score: 53
up-regulated mRNAs (Fig.   7A), e. g., down-regulated miR-33-5p interacted with 34 up-regulated genes (Abi2, Ciita, Sult1c2, Vcan, etc. [score:10]
Among these DEMs, miR-33, miR-33-5p, miR-33-3p, miR-144-3p and miR-99a-3p were down-regulated in NAFLD, whereas miR-200b, miR-200b-3p, miR-200b-5p, miR-200c-3p and miR-349 were up-regulated. [score:7]
MiR-33 is a key regulator of lipid metabolism and transport that targets ATP -binding cassette A1 (ABCA1) and thus suppresses HDL synthesis by attenuation of cholesterol efflux to apolipoprotein A1 and nascent HDL [19]. [score:5]
Furthermore, miR-33-3p and miR-33-5p targeted 23 common genes such as Abi2, Apln, and Vcan (Figs  7C,D). [score:3]
Intriguingly, we observed that the expression levels of miR-33, miR-33-5p and miR-33-3p were significantly decreased in high-fat-diet -induced NAFLD. [score:3]
In addition, we observed that miR-33-3p interacted with 53 mRNAs, while miR-33-5p targeted 32 genes. [score:3]
Altered expression of miR-33-5p was also reported in Western-diet -induced NAFLD rats and high-fructose-diet -induced chronic metabolic disorders mice 24, 25. [score:3]
Researchers observed that high-fat-diet feeding reduced miR-33 expression along with an increase in body weight, fasting blood glucose, triglyceride, cholesterol, AST and ALT in NAFLD mice [23]. [score:3]
Collectively, there is strong evidence indicating the potential roles of miR-33-3p and its target genes in NAFLD. [score:3]
A study reported that persistent inhibition of miR-33 in high-fat-diet-fed mice might cause deleterious effects such as moderate hepatic steatosis and hypertriglyceridemia [22]. [score:3]
Ghareghani, P. et al. Aerobic endurance training improves nonalcoholic fatty liver disease (NAFLD) features via miR-33 dependent autophagy induction in high fat diet fed mice. [score:3]
By integrated analysis, we observed 14 decreased miRNAs (such as miR-33, miR-33-5p, miR-33-3p, miR-144-3p, and miR-99a-3p) and constructed 459 miRNA and mRNA regulatory pairs in NAFLD rats. [score:2]
Moreover, the miRNA-mRNA regulatory networks revealed that 23 genes interacted with both miR-33-5p and miR-33-3p. [score:2]
Studies have reported that genetic ablation and antagonism of miR-33 attenuates the progression of atherosclerosis in mice 20, 21. [score:1]
All data suggested that miR-33, its guide strand miR-33-5p and passenger strand miR-33-3p might play pivotal roles in NAFLD. [score:1]
However, little is known about miR-33-3p in NAFLD. [score:1]
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3
[+] score: 47
Other miRNAs from this paper: rno-mir-122
Although the deregulation of miR-33 and miR-122 has been related to the development of risk factors associated to metabolic diseases, such as obesity and metabolic syndrome, most of the studies on the regulation of lipid metabolism by these two miRNAs have been performed using knockout or antisense mo dels [9]– [12], [17]– [19], [40]. [score:7]
Specifically, miR-33 and miR-122 are known as major regulators of lipid metabolism in the liver, and their deregulation may contribute to the development of metabolic diseases such as obesity and metabolic syndrome [5], [6]. [score:6]
Additionally, miR-33 plays an important role in the regulation of cholesterol homeostasis in the liver, regulating the ATP -binding cassette transporters (ABC transporters) ABCA1 and ABCG1 in addition to its role in FA β-oxidation by targeting the carnitine palmitoyltransferase 1a (CPT1a) [13]. [score:5]
Moreover, the inhibition of miR-33 in African green monkeys increased hepatic abca1 expression and the HDL-C plasma levels and decreased plasma very low density lipoprotein (VLDL) levels [19]. [score:5]
In contrast to our results, a downregulation of miR-33 has been described in mice fed a high fat diet (HFD) [38]. [score:4]
Thus, it seems that the type of diet conditions an over- or down-regulation of srebp2 and consequently miR-33 levels. [score:4]
Thus, further studies of liver miR-122 and miR-33 expression using different types of diets are warranted. [score:3]
Furthermore, the silencing of miR-33 by knockout or antisense techniques in mice results in an improvement in the plasma lipid profile, increasing plasma high density lipoprotein-cholesterol (HDL-C) levels [15], [17], [18]. [score:2]
Additionally, miR-33 plays a crucial role in the regulation of cholesterol metabolism [15], [18], [38], [39]. [score:2]
However, to our knowledge, there is not any study showing the influence of ω-3 PUFAs on lipid regulator miRNAs such as miR-33 and miR-122. [score:2]
Specific Taqman probes were used for each gene: microRNA-122a (miR-122a: hsa-mir-122a), 5′UGGAGUGUGACAAUGGUGUUUG-3′ and microRNA-33 (miR-33: hsa-mir-33), 5′- GUGCAUUGUAGUUGCAUUG-3′. [score:1]
Analyzing the percentage of decrease of srebp2 and miR-33 levels it seems that the mechanisms repressing miR-33 by DHA-OR or GSPE are not exactly the same for each treatment. [score:1]
Interestingly, miR-33 has two isoforms:miR-33b, which is present in a subset of species, such as dogs, pigs, non-human primates and humans, but not in rodents and miR-33a, which is highly conserved from humans to Drosophila. [score:1]
Hence, the PBMCs could be used as a non-invasive diagnostic or therapeutic biomarker for the levels of liver miR-33. [score:1]
Specifically, miR-122 and miR-33 play key roles in lipid metabolism. [score:1]
Regardless of the well-defined roles of miR-33 and miR-122 in controlling lipid metabolism in genetic mo dels, the association of these miRNAs with lipemia in pathophysiological conditions is not well understood. [score:1]
In order to elucidate the mechanism by which GSPE and DHA-OR treatments can repress miR-33a in the liver, the expression of the host gene of miR-33, srebp2, was also evaluated. [score:1]
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4
[+] score: 30
We found that the expression levels of other two miRNAs (i. e., miR-150 and miR-155) were up-regulated only in the vesicular-fraction, while the expression of both miR-21 and miR-33 was found to be up-regulated in RNA isolated from vesicles enriched pellets and down-regulated in the RNA isolated from vesicles -depleted sera. [score:14]
The expression of miRNA associated to regeneration [i. e., miR-21 (P = 0.03) and miR-33 (P = 0.04)] is up-regulated over the analyzed time points reaching the highest-level 6 days after PHx (Fig. 6, middle row). [score:6]
On the other hand, miR-150 and miR-155 were found up-regulated only in the VEP fractions, while miR-21 and miR-33 were found differentially regulated across the two populations. [score:5]
However, the expression of miRNAs associated to infection and inflammation (i. e., miR-150 and miR-155) is unchanged in the VDS fraction (Fig. 7, middle row), while the expression of regeneration -associated miRNAs [i. e., miR-21 (P = 0.01) and miR-33 (P = 0.02)] is significantly reduced in the VDS RNAs. [score:5]
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5
[+] score: 27
Other miRNAs from this paper: hsa-mir-33a, hsa-mir-33b
Regarding mitochondrial β-oxidation, the expression of CPT1A was changed following BDL and CP-MSC transplantation via miR-33, which is known as a posttranscriptional regulator of CPT1A, independent of PPAR α. Decreased cellular ATP production after BDL, which reflects mitochondrial dysfunction, was increased by CP-MSC transplantation via regulation of HO-1 and HO-2. Stem cell therapy with MSCs has been tried for the treatment of various liver diseases, including cirrhosis and hepatic failure, as an alternative to liver transplantation. [score:7]
The expression of miR-33 was normalized to U6 snRNA expression. [score:5]
Therefore, we explored the possibility of posttranscriptional regulation of CPT1A and verified that CPT1A is changed via alternative expression of miR-33 [23]. [score:4]
As expected, we determined that miR-33 expression was reduced in BDL rats and was restored by transplantation of CP-MSCs (Figure 3(e)). [score:3]
Taken together, these results suggest that CPT1A may be regulated posttranscriptionally by miR-33 in a PPAR α-independent manner. [score:2]
MiR-33 represses its target genes, which are involved in free fatty acid oxidation, such as CPT1A [23]. [score:2]
To evaluate whether miR-33 is a posttranscriptional regulator of CPT1A in BDL rat liver, we analyzed the expression levels of miR-33. [score:2]
CPT1A Expression Is Changed via MiR-33 in BDL Rats. [score:2]
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6
[+] score: 22
We performed a comprehensive study of miR-33 expression in a rat cardiac fibrosis mo del in vivo, Ang-II -treated primary cardiac fibroblasts in vitro, and miR-33 target genes. [score:5]
Anti-miR33 therapy inhibits mitochondrial respiration and ATP production, which in conjunction with increased ABCA1 expression, works to promote macrophage cholesterol efflux and reduce atherosclerosis [5]. [score:5]
Cardiac fibrosis can be ameliorated in miR-33 knockout hearts, and cardiac fibroblasts (CFs) are mainly responsible for miR-33 expression in the heart [5]. [score:4]
Long-term therapeutic silencing of miR-33 increases circulating triglyceride levels and hepatic lipid accumulation in mice [20], and genetic permanent miR-33 inhibition may cause cardiac dysfunction [5]. [score:3]
We used online prediction programs to predict all target genes of miR-33, and MMP16 was screened for further research because MMPs are a group of proteolytic enzymes that are responsible for the maintenance of the ECM [21]. [score:3]
Considering these harmful side effects, we adopted the tentative silencing of miR-33 approach by antagomiR-33a. [score:1]
We assessed miR-33’s function in heart fibrosis. [score:1]
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7
[+] score: 19
As seen in Figure 3, the expression levels of miR-146a, miR-210 and miR-27a were up-regulated, while the expression levels of miR-135b and miR-33 were down-regulated (* p < 0.05). [score:11]
To validate the altered expression of miRNAs as detected by miRNA microarray, miR-146a, miR-210, miR-27a, miR-135b and miR-33 were selected for confirmation by quantitative real-time PCR. [score:3]
The five differentially expressed miRNAs (miR-146a, miR-210, miR-27a, miR-135b and miR-33) in the TLE rat hippocampus as detected by the Rat miRNA microarray were confirmed using qPCR (Data are presented as the mean ± SEM, * p <0.05; n = 6/TLE rats, n = 6/control). [score:3]
Some of the deregulated miRNAs (miR-146a, miR-210, miR-27a, miR-135b and miR-33) were confirmed using qPCR. [score:2]
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8
[+] score: 11
Other miRNAs from this paper: hsa-mir-33a, hsa-mir-145, rno-mir-145, hsa-mir-33b
As shown in Fig. 2c, miR-33-3p expression was increased (x1.4-fold, p < 0.05), whereas the expression of miR-145-3p and 7-1-5p was reduced (x0.65-0.68-fold, p < 0.0001). [score:5]
Besides observing that same increment in mTOR activity within this study, we show an increase in miR-33-3p as a new mechanism contributing to fructose reduction of hepatic IRS2 expression 40. [score:3]
To our knowledge, this is the first report on the modulation of miRNA-33 by fructose ingestion, although dietary glycaemic load, and specifically diet supplementation with liquid fructose, can alter the miRNA liver expression profile 41 42. [score:3]
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9
[+] score: 11
Rno-miR-33-5p is involved in the SREBP2 signaling pathway and plays an important role in cholesterol metabolic homeostasis, likely through target repressing the expression of ATP binding cassette transporter subfamily A, member 1 (ABCA1) [55]. [score:5]
In our study, fish oil feeding diminished the elevated rno-miR-33-5p and rno-miR-34a-5p expression levels in Western-style diet -induced NAFLD rats, indicating that these two miRNAs may contribute to the protective effects of fish oil on hepatic triglyceride and cholesterol metabolic disorder. [score:3]
Among these DEMs, the expression of rno-miR-33-5p and rno-miR-34a-5p was reduced in FOH compared with WD group. [score:2]
The functional roles of miR-33 and miR-34a in metabolic syndrome have been well reviewed [23]. [score:1]
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10
[+] score: 8
Other miRNAs from this paper: rno-mir-21
The top 10 most significantly differentially expressed miRNAs are listed in Table I. The rno-miR-21-5p and rno-miR-33-5p were the most significantly up- and downregulated differentially expressed miRNAs, respectively (Fig. 1). [score:8]
[1 to 20 of 1 sentences]
11
[+] score: 7
Other miRNAs from this paper: mmu-mir-33
Zhao G-J, Tang S-L, Lv Y-C, Ouyang X-P, He P-P, Yao F, et al. Antagonism of betulinic acid on LPS -mediated inhibition of ABCA1 and cholesterol efflux through inhibiting nuclear factor-kappaB signaling pathway and miR-33 expression. [score:7]
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12
[+] score: 5
Emerging evidence indicates that miRNAs act as key modulators of target gene expression, and some, such as miR-21, miR-126, miR-33, miR-125, and miR-222, have been shown to be involved in the pathogenesis of stroke [5, 6]. [score:5]
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13
[+] score: 4
and 24 miRNAs were significantly downregulated (rno-miR-192-3p, rno-miR-192-5p, rno-miR-33-5p, rno-miR-196c-3p, etc. ) [score:4]
[1 to 20 of 1 sentences]
14
[+] score: 4
Other miRNAs from this paper: mmu-mir-33
miR33 has been reported to depress PTHrP expression and may be a candidate that triggers this effects 29. [score:3]
A link between NO/cGMP and miR33, however, is still missing. [score:1]
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15
[+] score: 3
Eleven miRNAs, including miR-145-5p, miR-34c-5p, miR-365-3p, miR-214-3p, miR-151, miR-27a, miR-153-5p, miR-365-3p, miR-33-5p, miR-217-5p and miR-129-5p, were differentially and significantly expressed (P < 0.05; Figure 2B). [score:3]
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16
[+] score: 3
There are 6 common miRNAs (miR-138, miR-301a, miR-33, miR-34a, miR-146a, and miR-23a) between our data set and work of Hu et al. who studied miRNA expression profiles in a pilocarpine -induced mo del of epilepsy [23]. [score:3]
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17
[+] score: 2
Namely, pregnant rats fed SO and FO diets during the first 12 days of pregnancy showed significant lower expression of miR-449c-5p, miR-134–5p, miR-188, miR-32, miR130a, miR-144–3p, miR-431, miR-142–5p, miR-33, miR-340–5p, miR-301a, miR-30a, miR-106b, and miR-136–5p, as compared with OO, LO, and PO diets. [score:2]
[1 to 20 of 1 sentences]
18
[+] score: 2
Other miRNAs from this paper: hsa-mir-33a, hsa-mir-33b
Macrophage mitochondrial energy status regulates cholesterol efflux and is enhanced by anti‐miR33 in atherosclerosis. [score:2]
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19
[+] score: 2
Cholesterol regulation of receptor-interacting protein 140 via microRNA-33 in inflammatory cytokine production. [score:2]
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20
[+] score: 2
Previous studies have reported the regulatory role of miRNAs in lipid and cholesterol metabolism, particularly miR-33 (33, 34). [score:2]
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21
[+] 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-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-326-5p MIMAT0017028 3 8mer 7mer-m8 imperfect −0.442 −0.242 431 −65.97 TRUE rno-miR-485-5p MIMAT0003203 2 7mer-m8 −0.343 −0.372 290 −34.96 TRUE rno-miR-300-5p MIMAT0004743 1 8mer −0.338 −0.421 156 −15.16 TRUE rno-miR-702-5p MIMAT0017884 1 8mer −0.317 −0.274 142 −13.86 TRUE rno-miR-203b-3p MIMAT0017800 2 7mer-m8 −0.298 −0.421 295 −29.93 TRUE rno-miR-33-3p MIMAT0017104 2 8mer 7mer-m8 −0.297 −0.813 305 −22.7 TRUE rno-miR-466b-3p MIMAT0017285 1 8mer −0.295 −0.47 159 −15.26 TRUE rno-miR-532-5p MIMAT0005322 1 7mer-m8 −0.268 −0.302 151 −10.71 TRUE rno-miR-511-5p MIMAT0012829 1 7mer-m8 −0.268 −0.302 152 −10.37 TRUE rno-miR-343 MIMAT0000591 1 7mer-m8 −0.262 −0.24 140 −13.75 TRUE rno-miR-203a-3p MIMAT0000876 1 8mer −0.245 −0. [score:1]
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[+] score: 1
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-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
For instance, miR-32 and miR-33 were found to be restricted to the caput epididymis of the mouse, while being absent in all regions of the rat epididymis, and present in the caput, corpus, and cauda of the human epididymis (S4 Table). [score:1]
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[+] score: 1
Other miRNAs from this paper: rno-mir-122
miR-33 has also been recently identified as a key modulator of cholesterol homeostasis in hepatic tissue [37]. [score:1]
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