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60 publications mentioning mmu-mir-18b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-18b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 80
Other miRNAs from this paper: mmu-mir-18a
These results suggest that YKS reduces miR-18 expression and increases GR protein expression by downregulating the inhibitory effects of GR translation in the PVN of the hypothalamus after stress exposure. [score:12]
To obtain definitive evidence that this downregulation of miR-18 reduced inhibition of GR protein translation, we analyzed GR protein expression levels in the PVN of the hypothalamus. [score:10]
In conclusion, our findings suggest that YKS downregulates miR-18 expression and normalizes HPA axis activity by recovering GR protein expression in the hypothalamus of stress-exposed mice. [score:8]
In our stress mo del, miR-124a expression was unchanged in the hypothalamus and hippocampus, whereas miR-18 expression was only downregulated in the hypothalamus of stress-exposed mice with YKS pretreatment. [score:8]
In the present study, we provide the first evidence that YKS downregulates miR-18 expression in the hypothalamus after stress exposure and ultimately normalizes GR protein levels in the PVN, thus affecting HPA axis activity. [score:6]
Therefore, miR-18 expression may crucially control GR protein expression in the hypothalamus after stress exposure (Figures 3 and 4). [score:5]
In the brain, miR-18 and/or miR-124a posttranscriptionally regulate GR protein expression [22, 40, 41]. [score:4]
These findings indicate that YKS regulates miR-18 expression in the hypothalamus but has no effect on GR mRNA or miR-124a after stress exposure. [score:4]
The comparative CT method (ΔΔCt) was used to quantify the relative expression levels of miR-18 and 124a according to the manufacturer's instructions. [score:3]
We found that YKS pretreatment reduced miR-18 expression in the hypothalamus (Figure 3(a)). [score:3]
YKS Reduces miR-18 Expression in the Hypothalamus after Stress Exposure. [score:3]
In the present study, we demonstrate that YKS affects hypothalamic miR-18 expression levels in stress-exposed mice and investigate GR protein expression level in the paraventricular nucleus (PVN) of the hypothalamus in YKS-pretreated and stress-exposed mice. [score:3]
YKS pretreatment only reduced miR-18 expression in the hypothalamus (Figures 3(a) and 3(b)). [score:3]
Next, we determined if YKS is involved in the posttranscriptional regulation of GR protein levels by evaluating the effect of YKS on miR-18 and 124a expression in the hippocampus and the hypothalamus following stress exposure. [score:2]
Interestingly, miR-18 and/or miR-124a are candidate negative regulators of GRs in the brain [22]. [score:2]
Elucidating the functional roles of the YKS-miR-18-GR protein -regulating pathway in the PVN of the hypothalamus is a primary goal of future research. [score:2]
The finding of miR-18 reduction in the hypothalamus is in good agreement with a previous report [40]. [score:1]
Quantification of miR-18 and 124a. [score:1]
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2
[+] score: 63
Fig. 5. Atm expression is upregulated in Dgcr8 and Dicer c KOs and a target of germline-expressed miR-18, as well as miR-183 and miR-16. [score:10]
The target sites of two other miRNAs, miR-183 and miR-16, clustered in the same region of the Atm 3′UTR as the miR-18 target sites; moreover, the miR-183 and miR-16 target sites were predicted as the second and third strongest sites, respectively, within Atm (Fig.  5C). [score:7]
Taken together, these results indicate that miR-18, miR-183, and miR-16 target sites in Atm are functional and effective at eliciting downregulation in response to very low levels of miRNA. [score:6]
Many miRNAs are predicted to target the Atm 3′UTR, but only three are also expressed in spermatocytes and show depletion in Dgcr8 and Dicer c KOs: miR-18, miR-183 and miR-16. [score:5]
Therefore, miR-18, miR-183 and miR-16 are the strongest candidates for miRNA -mediated regulation of Atm expression in mammalian spermatogenesis. [score:4]
To investigate the efficacy of miR-18 target sites in the Atm 3′UTR, we designed a luciferase reporter construct containing 431 nucleotides of the endogenous Atm 3′UTR sequence encompassing the two predicted miR-18 target sites. [score:3]
It is worth noting that the miR-18 target sites are located close to each other, an arrangement previously observed to mediate synergistic enhancements to repression by miRNAs (Grimson et al., 2007; Saetrom et al., 2007). [score:3]
miR-18, a member of Oncomir-1, targets heat shock transcription factor 2 in spermatogenesis. [score:3]
We measured reporter activity in a cell line that does not express miR-18 by co-transfecting the reporter plasmids with either an siRNA corresponding to miR-18 or a control siRNA corresponding to a miRNA that does not target Atm. [score:3]
Like the miR-18 target sites, the single site for miR-183 (Fig.  5F) and combined miR-16 sites (Fig.  5H) were able to mediate an ∼2-fold repression of the reporter construct at high-to-moderate concentrations (25-nM–1-nM) of miR-183 and miR-16 mimetic. [score:3]
We also identified alterations in many small RNAs, including miR-18, miR-183 and miR-16, among whose targets is the mRNA encoding ATM. [score:3]
Strikingly, the miRNA predicted to mediate the strongest repression of Atm was miR-18, a miRNA known to exhibit meiosis-preferential expression (Björk et al., 2010). [score:3]
Fold regulation mediated by miR-18 was calculated by generating reporter constructs containing mutations disrupting both predicted target sites (purple bars) and normalizing luciferase activity to this construct. [score:3]
Reporter constructs were transfected into A549 cells along with varying levels of siRNA duplexes corresponding to miR-18 (using RNA oligonucleotides: 5′-UAAGGUGCAUCUAGUGCA-GAU-3′ and 5′-CUGCACUAGAUGCACCUUAAU-3′), miR-183 (5′-UA-UGGCACUGGUAGAAUUCACU-3′ and 5′-UGAAUUCUACCAGUG-CCAGAUA-3′), miR-16 (5′-UAGCAGCACGUAAAUAUUGGCG-3′ and 5′-CCAAUAUUUACGUGCUGUUAUU-3′), or, as a control, miR-124 (Lim et al., 2005). [score:1]
Importantly, miR-18 is not one of the most abundant miRNAs in the murine male germ line (compare supplementary material Fig.  S2J with supplementary material Fig.  S2K,L). [score:1]
Concentrations of miR-18 at which target sites contribute synergistically to repression are indicated with an asterisk and bracket above red and orange-striped bars; synergism was inferred when the observed repression of the Atm 3′UTR (red bar) significantly (P<0.01) exceeded that expected based on measurements of each site individually (orange-striped bar) (5 nM, P=0.0022; 1 nM, P=0.0029; 0.2 nM, P=0.0006; Bonferroni-corrected Wilcoxon-rank sum test). [score:1]
Sites were mutated as follows: the miR-18 site (GCACCUUA) was mutated to GCAggaUA for both miR-18 sites; the miR-183 site (GUGCCAUA) was mutated to GUGaCgUA, the miR-16 sites (GCUGCU) were mutated to either GCcGaU, GaUGgU, GCcGaU (corresponding to the order of the sites within the reporter construct). [score:1]
Luciferase reporter constructs containing a portion of the Atm 3′UTR (red bars) were transfected into A549 cells together with different concentrations (x-axis) of a miR-18 mimetic siRNA duplex (D) or miR-124, as a control (E). [score:1]
Our results underscore the significance of specific miRNAs in ensuring the fi delity of gametogenesis, and point to miR-18, miR-183 and miR-16 as miRNAs playing an important role in male fertility. [score:1]
Using this approach, we did not observe evidence of synergism at high concentrations (25 nM) of the miR-18 mimetic; at lower concentrations (5, 1 and 0.2 nM), however, we observed increasingly strong evidence for synergistic interactions between the sites (Fig.  5D). [score:1]
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3
[+] score: 35
For example, Hlf was targeted by mmu-miR-18b-5p, mmu-miR-429-3p and mmu-miR-291a-3p; Cnot6 and Zfp91 were targeted by mmu-miR-206-3p and mmu-miR-291a-3p; Rbfox2 was targeted by mmu-miR-429-3p and mmu-miR-449c-5p; Aebp2 was targeted by mmu-miR-125a-3p, mmu-miR-223-3p and mmu-miR-496-3p; Nfya was targeted by mmu-miR-199a-5p, mmu-miR-216b-5p and mmu-miR-671-5p; Nucks1 was targeted by mmu-miR-142-3p, mmu-miR-146a-5p and mmu-miR-223-3p; Notch2 was targeted by mmu-miR-146a-5p and indirectly via Ascl1 by mmu-miR-1903. [score:16]
For example, miR-200a, miR-429 and miR-141 were shown to play important roles in neurogenesis, epithelial-to-mesenchymal transition and Notch signaling [73, 75– 84], miR-214 was found to be overexpressed in fetal sclera versus adult sclera and shown to play important role in brain and retina development and function [36, 85– 89], miR-18b, miR-21, miR-101a, miR-200a and miR-429 were found to be involved in stem cell function and differentiation [90– 100], miR-1306 negatively regulated Alzheimer’s disease gene ADAM10 [101]. [score:7]
Seven of the up-regulated miRNAs (miR-465b, miR-466f, miR-669o, miR-18b, miR-291a, miR-696, miR-101a) were also much more (≥ 5 fold) expressed in the retina compared to the sclera suggesting that they might be involved in the regulation of retina-specific processes. [score:6]
miR-18b and miR-518b Target FOXN1 during epithelial lineage differentiation in pluripotent cells. [score:3]
Several miRNAs exhibited more than 10-fold change in expression in the myopic retina (Table 1), including mmu-miR-1947-5p (FC = 31.5, p = 1.47 × 10 [−04]), mmu-miR-200a-5p (FC = 18.8, p = 9.46 × 10 [−05]), mmu-miR-141-5p (FC = 13.9, p = 4.75 × 10 [−06]), mmu-miR-465b-5p (FC = 12.8, p = 5.93 × 10 [−04]), mmu-miR-214-5p (FC = 12.6, p = 8.27 × 10 [−03]), mmu-miR-1936 (FC = 12.3, p = 9.56 × 10 [−06]), mmu-miR-466f-5p (FC = 11.5, p = 3.85 × 10 [−03]), mmu-miR-669o-5p (FC = 10.9, p = 2.18 × 10 [−03]), mmu-miR-18b-5p (FC = 10.1, p = 1.79 × 10 [−03]), and mmu-miR-145-5p (FC = -10.5, p = 8.87 × 10 [−09]). [score:3]
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4
[+] score: 25
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-27b, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-182, mmu-mir-199a-1, mmu-mir-122, mmu-mir-143, mmu-mir-298, mmu-let-7d, 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-27a, mmu-mir-31, mmu-mir-98, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-181b-1, mmu-mir-379, mmu-mir-181b-2, mmu-mir-449a, mmu-mir-451a, mmu-mir-466a, mmu-mir-486a, mmu-mir-671, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-491, mmu-mir-700, mmu-mir-500, 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-466d, mmu-mir-466l, mmu-mir-669k, mmu-mir-669g, mmu-mir-669d, mmu-mir-466i, mmu-mir-669j, mmu-mir-669f, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-669e, mmu-mir-669l, mmu-mir-669m-1, mmu-mir-669m-2, mmu-mir-669o, mmu-mir-669n, mmu-mir-466m, mmu-mir-669d-2, mmu-mir-466o, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-466b-7, mmu-mir-669p-2, mmu-mir-669a-10, mmu-mir-669a-11, mmu-mir-669a-12, mmu-mir-466p, mmu-mir-466n, mmu-mir-486b, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-145b, mmu-let-7j, mmu-mir-451b, mmu-let-7k, mmu-mir-126b, mmu-mir-466c-3
To validate the miR array data, we studied several differentially expressed miRs (upregulated miRs: miR-122 and miR-181a and downregulated miRs: miR-23a, miR-18b, miR-31, and miR-182). [score:9]
Similarly, we observed downregulated (>1.5-fold) expression of mmu-let (mmu-let-7b, 7c and 7e), miR-18b and miR-98 in fetal thymocytes post TCDD exposure and these miRs possess highly complemantary sequence with FasL 3′-UTR (Table 2) demonstrating that these miRs may be involved in FasL expression. [score:8]
Similarly, the expression of miRs, miR-31, miR-23a, and miR-18b which regulate CYP1A1, Fas, and FasL respectively, were decreased following TCDD treatment. [score:4]
Similarly, we observed downregulation of miR-23a, miR-18b, miR-31 and miR-182 in TCDD -treated thymocytes when compared to vehicle controls (Fig 2A–B). [score:3]
miR-23a and miR-23b possessed highly omplementary sequence with Fas 3′UTR region (Table 2) whereas, miR-18b and miR-98 showed highly complementary sequence with FasL 3′UTR region (Table 2). [score:1]
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5
[+] score: 22
All members of miR-17-92 cluster, except miR-18, are also known to downregulate expression of the tumor suppressor PTEN [52]. [score:8]
It is suggested that SMAD2/4 is regulated by miR-18 in neuroblastoma cells [66] and that SMAD4 is targeted by miR-19a/b in thyroid follicular cells [68]. [score:4]
One possible relevant difference between these two clusters is that miR-17-92, but not miR-106b-25, expresses members of the miR-19 and miR-18 families. [score:3]
Furthermore, the antiangiogenic proteins TSP11 and CTGF are both negatively regulated by miR-18 and miR-19 [58]. [score:2]
The six miRNAs can be grouped into four miRNA families based on their seed-sequence: the miR-17 family (miR-17 and miR-20a), the miR-18 family (miR-18a), the miR-19 family (miR-19a and miR-19b-1), and miR-92 family (miR-92a-1) [31, 34, 39]. [score:1]
It is tempting to speculate that loss of miR-19a, miR-19b, and miR-18 is significantly responsible for the phenotype caused by deletion of miR-17-92. [score:1]
In addition, it has been demonstrated that miR-18 and miR-19 repress the antiangiogenic factors TSP-1 and CTGF [51]. [score:1]
Both the evolutionary sequence analysis and the seed-sequence -based grouping partition these miRNAs into four families: the miR-106 family (miR-17, miR-20a/b, miR-106a/b, and miR-93), the miR-18 family (miR-18a/b), the miR-19 family (miR-19a/b-1/2), and the miR-92 family (miR-25, miR-92a-1/2, and miR-363). [score:1]
This cluster encodes six miRNAs: miR-106a, miR-18b, miR-19b-2, miR-20b, miR-92a-2, and miR-363 [42]. [score:1]
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6
[+] score: 17
Evidence of the concerted interplay of miRNAs regulated by CpG-ODN and their potential target mRNAs was observed (Fig. 4) for 2 miRNAs upregulated (hsa-miR-302b and hsa-miR-374b) and for 13 miRNAs downregulated in CpG-ODN -treated mice (hsa-miR-135a, hsa-miR-136, hsa-miR-340, hsa-miR-445-5p, hsa-miR-424, hsa-miR-96, hsa-miR-142-3p, hsa-miR-140-5p, hsa-miR-542-3p, hsa-miR-18a, hsa-miR-18b, hsa-miR-101, and hsa-miR-99a). [score:10]
Comparison of hsa-miR-18a, hsa-miR-18b, hsa-miR-140-5p, hsa-miR-101, hsa-miR-556-3p, hsa-miR-424, hsa-miR-136, hsa-miR-340, hsa-miR-302b expression obtained by miRNA expression profile and qRT-PCR on tumors collected from human IGROV-1 ovarian tumor-bearing mice treated daily i. p. with CpG-ODN or saline (control group). [score:5]
Of the 9 miRNAs, hsa-miR-18a and hsa-miR-18b were selected based on their reported role in the pathogenesis of ovarian cancer [25]; [26], and hsa-miR-101 and hsa-miR-302b for their described involvement in DNA repair processes and sensitivity to chemotherapy [20]; the remaining 5 miRNAs were randomly selected. [score:1]
RT-qPCR using the RNA profiled in microarray analysis validated all 9 miRNAs (Fig. S1), whereas RT-qPCR using the RNA of the replica confirmed 6 of 9 miRNAs (p<0.05), with a trend observed for hsa-miR-18b and hsa-miR-101 but not for hsa-miR-136 (Fig. 2). [score:1]
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7
[+] score: 17
The pro-oncogenic activity of miR-17–92 partially involves the regulation of the ECM proteins CTGF and thrombospondin-1 (TSP-1) by the cluster members miR-18 and miR-19, through sequence-specific targeting within the 3′-untranslated region (3′-UTR) of these gene transcripts (Supporting information Fig. S1) (Dews et al., 2006). [score:6]
This, together with miR-18 and miR-19 targeting CTGF and TSP-1 and the fact that ECM proteins are crucial for healthy cardiac aging, has led us to hypothesize that these miRNAs play a role in age-related cardiac remo deling. [score:3]
The miR-18/19 – CTGF/TSP-1 axis is regulated in aged cardiomyocytes in vitroTo gain further insight into the role of the miR-17–92 cluster in aging of cardiomyocytes, neonatal rat cardiomyocytes (NRCMs) were aged in vitro, and miRNA levels were determined. [score:2]
The miR-18/19 – CTGF/TSP-1 axis is regulated in aged cardiomyocytes in vitro. [score:2]
Cardiomyocyte CTGF and TSP-1 and collagen production are regulated by miR-18/19. [score:2]
The miR-18/19 – CTGF/TSP-1 axis is regulated in human age -associated heart failure. [score:2]
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8
[+] score: 12
Several down-regulated (i. e. miR-1, miR-7, miR-34a, miR-122, miR-125b, miR-200) or up-regulated (i. e. miR-17, miR-18, miR-19, miR-155, miR-93, miR-221/222) miRNAs have been identified as tumor suppressor or oncomirs, respectively, by targeting and regulating genes involved in cell proliferation, apoptosis, angiogenesis and metastasis [13]. [score:12]
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9
[+] score: 11
In HepG2 cells, miR-192, miR-204, miR-18, miR-19 and miR-211 could down-regulate HOTTIP expression (all P<0.05). [score:6]
All miRNA mimics (miR-138, miR-18, miR-192, miR-215, miR-19, miR-204 and miR-211), miRNA inhibitors(miR-192 and miR-204) and small interfering RNA (siRNA) duplexes (siHOTTIP-1 and siHOTTIP-2) were products of Genepharma (Shanghai, China). [score:3]
20 nmol/L mimics of miR-138, miR-18, miR-192, miR-215, miR-19, miR-204, and miR-211, two HOTTIP siRNAs (siHOTTIP-1 and siHOTTIP-2)or NC RNA were transfected into SMMC7721,HepG2 and Hep3B HCC cells. [score:1]
* MicroRNAs Seed position Conservation Primates Mammals Other Vertebrates miR-138 chr7:27245289 89% 30% 0% miR-18 chr7:27238346 89% 30% 0% miR-192/215 chr7:27241747 89% 91% 77% miR-19 chr7:27245115 100% 0% 0% miR-204/211 chr7:27245995 89% 43% 0%*Data from miRcode (http://www. [score:1]
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10
[+] score: 10
However, there was no further increase in miR-18 levels in tumors with Xpcl1 integrations, so this likely represents expression from the miR-17∼92 paralog. [score:3]
Thus, the increased miR-18 levels noted in tumors (Figure 1B), may be due to expression from paralogous miR-17∼92 cluster. [score:3]
We observed increased expression of miR-18 in lymphomas, compared to normal thymic tissue. [score:2]
Mir-18, in contrast, is also encoded by the paralogous miR-17∼92 cluster. [score:1]
Sequence of a sixth microRNA, miR-18b, also lies in the cluster but it was not increased in Xpcl1+ tumors relative to Xpc1- tumors. [score:1]
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11
[+] score: 10
While miR-18 is expressed in multiple tissues, miR-124 is particularly enriched in the brain [21] and has been shown to inhibit Nr3c1 expression in cultured cells and in vivo [22]. [score:7]
The 3′ untranslated region of the Nr3c1 gene contains multiple microRNAs’ seed regions, including miR-124 and miR-18 [20]. [score:3]
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12
[+] score: 10
Similar BMI and CYCLIN D1 expression was observed in the C666-1 cells stably expressing miR-96 and miR-18 and the vector control. [score:5]
C666-1 cells stably overexpressing miRNA were generated by lentiviral transfection with a vector expressing miR-96 or miR-18 and a miR -negative control vector according to the manufacturer’s protocol (Lenti-miR™ microRNA precursor clones, SBI System Biosciences, Palo Alto, CA, USA). [score:5]
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13
[+] score: 10
Although some miRNA candidates, such as miR-18b and miR-518b, were reported to lead to downregulation of FOXN1 in stem cells [11], herein, we add one more candidate miR-125a-5p leading to downregulation of FoxN1 in the aged thymus. [score:7]
miR-18b and miR-518b Target FOXN1 during epithelial lineage differentiation in pluripotent cells. [score:3]
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14
[+] score: 10
Most of the 15 guide strands were upregulated in the aging heart, where 11 guide strands were expressed in the same direction, but four guide strands (miR-18a-5p, miR-18b-5p, miR-20b-5p, and miR-363-5p) were increased in some old mice while decreased in other old mice (Figure 3(a)). [score:7]
The SRF gene is a target of miR-18a and miR-18b. [score:3]
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15
[+] score: 9
Upon activation, both miR-17~92 miRNAs and their target mRNAs are up-regulated (Fig 3C and 3D), but the fold increase of the latter outpaces the former, thereby increasing the ratios between conserved binding sites and miRNA molecules to 2.8 (miR-92 family) and 8.7 (miR-18 family) in 25.5h activated B cells (Fig 3E). [score:6]
Our calculation showed that each naïve B cell expresses 900–1,800 molecules of miR-17, miR-19, and miR-92 subfamily miRNAs, and 80 molecules of miR-18 subfamily miRNAs (Fig 3B and 3C and S7 Table). [score:1]
They fall into four miRNA subfamilies (miR-17, miR-18, miR-19, and miR-92 subfamilies), with members in each subfamily sharing the same seed sequence. [score:1]
The ratios between conserved miR-17~92 binding sites and miRNA molecules range from 0.5 (miR-92 subfamily) to 4.6 (miR-18 subfamily) in naïve B cells (Fig 3E). [score:1]
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16
[+] score: 9
To address this issue, we first screened the miRNAs whose expressions are modulated in 4T1 cells by miRNA microarray analysis using both total cellular miRNA and exosomal miRNA after treatment with 100 μM of EGCG for 24 h. In brief, a set of miRNAs including let-7, miR-16, miR-18b, miR-20a, miR-25, miR-92, miR-93, miR-221, and miR-320 were up-regulated, and dozens of miRNAs including miR-10a, miR-18a, miR-19a, miR-26b, miR-29b, miR-34b, miR-98, miR-129, miR-181d were down-regulated in both total cellular and exosomal fraction by EGCG treatment (data not shown). [score:9]
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17
[+] score: 8
Bjork JK Sandqvist A Elsing AN miR-18, a member of Oncomir-1, targets heat shock transcription factor 2 in spermatogenesis. [score:3]
[19] miR-18 displays a cell-type-specific expression, with highest intensity in the spermatocytes. [score:3]
The miR-17-92 gene cluster encodes 6 miRNAs of 4 miRNA families: the miR-17 family including miR-17-5p and miR-20a, the miR-18 family (miR-18a), the miR-19 family (miR-19a and miR-19b-1), and the miR-92 family. [score:1]
[4] The miR-17-92 gene cluster encodes 6 miRNAs of 4 miRNA families: the miR-17 family including miR-17 and miR-20a, the miR-18 family (miR-18a), the miR-19 family (miR-19a and miR-19b-1), and the miR-92 family. [score:1]
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18
[+] score: 8
Interestingly, downregulation of HDAC9 by si-HDAC9 in P-PDLSCs restored the expression of pri-miR-17-92a as well as the mature miR17-92a, though, miR-18 was not affected, suggesting that HDAC9 inhibited miR17-92a (Fig.   3a, b). [score:8]
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19
[+] score: 8
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]
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]
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20
[+] score: 7
In Dicer c KO mutants, miR-18, -19, and- 92a were downregulated, whereas miR-17 and -20a were upregulated. [score:7]
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21
[+] score: 6
The circulating miRNA targets that were up-regulated following CLP belong not only to the miR-17∼92 cluster but also to its evolutionary paralogs, miR-106a∼363 (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2, and miR-363) and miR-106b∼93 (miR-106b, miR-93, miR-25). [score:6]
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22
[+] 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-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-194-1, 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-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
Similarly, we found all members of the miR-15, miR-16, miR-18 and miR-133 families in our sequences, suggesting that all members belonging to these miRNA families are expressed in these three (heart, liver and thymus) tissues. [score:3]
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]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-199a-1, mmu-mir-18a, mmu-mir-199a-2, mmu-mir-199b
Recent association studies between miRNA markers and lung cancer development have demonstrated that the miRNAs miR-18, miR-199, and miR-519c can suppress HIF-1α expression for the purpose of assessing cancer prognosis [39– 41]. [score:6]
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24
[+] score: 5
Leivonen reported that five ERα -regulating miRNAs (e. g. miR-18a, miR-18b, miR-193b, miR-302c, and miR-206) directly targeted ERα in the 3′UTR [29]. [score:5]
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[+] score: 5
Sprague-Dawley rats treated with 2-AAF for 12 or 24 weeks exhibited disrupted regulation of the miR-34a-p53 feed-back loop and substantial deregulation of expression of miR-18, miR-21, miR-182, and miR-200 family miRNAs [11]. [score:5]
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[+] score: 5
2013.125 24212931 42. van Almen GC Verhesen W van Leeuwen RE van de Vrie M Eurlings C Schellings MW MicroRNA-18 and microRNA-19 regulate CTGF and TSP-1 expression in age-related heart failureAging Cell. [score:4]
Our findings do not add value to its involvement in aging process (not present in consensus modules) and its synergy impact was not substantial (miR-18b/-22 pair appeared on the 552 [th] rank). [score:1]
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[+] score: 5
Based on the partial residual expression of the miR-17 and miR-92 families (Figure 7B, 7C), and the generally very low expression of the miR-18 family (Figure 7D, note y axis units), we hypothesized that loss of the miR-19 family was responsible for the defective invasion of 17KPC cell lines. [score:5]
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[+] score: 4
A recent report has linked silencing of microRNAs (miR-18b and miR-518b) with the upregulation of FoxN1 in embryonic stem cells. [score:4]
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29
[+] score: 4
Except for miR-18, the oncogenic contributions of miR-17/20a, miR-19a/b and miR-92 have all been demonstrated and several functional targets identified, including E2F1, PTEN and BIM1 [26]. [score:3]
Figure S4 Comparison of miR-17, miR18, miR-19a, miR19b and miR92 levels between NN10#5, 745A#44 and K16 erythroleukemic cells. [score:1]
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[+] score: 4
In conclusion, chronic exposure to a mixture of five EDCs induces changes in the expression profiles of specific miRNAs (such as miR-34b-5p, miR-7686-5p and miR-1291), along with alterations in the miRNAs/isomiRs association (in particular for miR-15b-5p, miR-18b-5p, miR-20b-5p, and miR-1981-5p) regulating mRNAs implicated in key biological process in the testes (Table  3). [score:4]
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[+] score: 4
We further confirmed this by a complementary approach using lentiviral overexpression of antagomirs against miR-17, miR-18 and miR-20a in the human BCR-ABL -positive BV173 cell line. [score:3]
[19] It is interesting to note that while this effect, in MYC -driven lymphoma at least, is primarily mediated by miR-19 family members (miR-19a/b), we have identified principally a miR-17 family- (miR-17, miR-20a/b, miR-106a/b and miR-93) and miR-18 family(miR-18a/b) -driven effect in BCR-ABL -positive ALL on BCL2, indicating differences in pro- and anti-apoptotic functions of miR-17∼92 between the various cellular contexts. [score:1]
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[+] score: 4
In addition, the miR-17-19 cluster, which comprises seven miRNAs (miR-17-5p, miR-17-3p, miR-18, miR-19a, miR-20, miR-19b, and miR-92-1) and promotes cell proliferation in various cancers, has been demonstrated to be significantly upregulated at the clonal expansion stage of adipocyte differentiation. [score:4]
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33
[+] score: 3
Murakami et al. [48] showed a correlation between miR-222, miR-106a, miR-92, miR-17-5p, miR-20 and miR-18 and the degree of differentiation suggesting an involvement of specific miRNAs in the progression of the disease. [score:3]
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[+] score: 3
In one of the first studies performed on peripheral blood leukocytes from MS patients, Otaegui et al. reported an association between miR-18b and miR-599 with disease relapses and miR-96 with remissions [6]. [score:3]
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[+] score: 3
In the past few years, a number of studies of miRNAs in AD have emerged to support that deregulated miRNAs, such as miR-18b, miR-34c, miR-615, miR-211, miR-216 and miR-325, play important roles in the development and prognosis of AD [16]. [score:3]
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[+] score: 3
For example, miR-18b, miR-20a, and miR-30d have been reported to be highly expressed in the serum of relapsing TNBC patients [88]. [score:3]
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[+] score: 3
Several miRNAs from the MYCN -induced miR-17–92 cluster (miR-17-5p, miR-18-5p, miR-20a-5p and miR-92a-3p) were significantly upregulated in LSL- MYCN;Dbh-iCre tumors compared with normal adrenals from wild-type mice (Supplementary Figure 8b). [score:3]
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[+] score: 3
These results show that miR-17 and miR-18 levels were reduced by PMIS-miR-17-18 and this is consistent with other studies demonstrating miR degradation by inhibitors. [score:3]
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39
[+] score: 3
This cluster is located on chromosome 13q31.3 in the third intron of the C13orf25 gene, and contains 6 miRNAs (miR-17, miR-18, miR-19a, miR-20a, miR-19b-1, miR-92-1). [score:1]
Together these three miRNA clusters contain a total of 15 miRNAs constituting four “seed” families: the miR-17, the miR-18, the miR-19 and the miR-92 family. [score:1]
The human genome contains two paralogues of the miR-17-92 cluster: 1) the miR-106b/25 cluster (miR-106b, miR-93, miR-25) is located on chromosome 7 (7q22.1) in the 13th intron of the Mini-Chromosome Maintenance gene MCM7); 2) the miR-106a/363 cluster (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92-2, miR-363) is located on chromosome X (Xq26.2). [score:1]
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[+] score: 3
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-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-98, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-150, mmu-mir-155, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-217, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-150, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-21a, mmu-mir-23a, mmu-mir-34a, mmu-mir-98, mmu-mir-322, mmu-mir-338, hsa-mir-155, mmu-mir-17, mmu-mir-19a, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-217, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-338, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-18b, hsa-mir-503, mmu-mir-541, mmu-mir-503, mmu-mir-744, hsa-mir-541, hsa-mir-744, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Among this group, miR-18 has been reported to control ctgf/ccn2 gene expression in chondrocytic cells [64]. [score:3]
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[+] score: 3
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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[+] score: 3
Moreover, Bar and colleagues [33] found that the most overexpressed miRNAs in undifferentiated human ES cells are miR-302b, miR-302c, miR-302d, miR-92b, miR-20b, miR-519d, miR-302a, miR-324-3p, miR-187, and miR-18b. [score:3]
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[+] score: 2
For example, miR-182, miR-141, miR-18b, miR-200a, miR-17 and, especially, miR-421 appear recurrently along PyMT cancer progression regulating genes involved in ABC transporters (DNAH8, ABCC5, ABCA8A, ABCB4, and ABCA8B), which are significant in cancer research due to their impact in treatment resistance [47]. [score:2]
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[+] score: 2
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-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-495, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
In the miR-17-92 cluster, ssc-miR-17 and ssc- miR-18 had higher expression in mpiPSCs compared with the pEFs. [score:2]
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45
[+] score: 2
Protein levels and function of p53 have been shown to be regulated by miRNAs including miR-125 [43], miR-18 [23], and miR-504 [28]. [score:2]
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46
[+] score: 2
showed that expression levels of miR-335, miR-10b, miR-944, miR-301a, miR-18b, miR-204, miR-130b, and miR-188-5p were similar in both assays (Fig. 1B). [score:2]
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47
[+] score: 1
The first cluster “mir-17-92” is composed with 5 microRNAs; mir17, mir18, mir19a, mir20a and mirhg, all located closed one to each other’s on the chromosome 14. [score:1]
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48
[+] score: 1
was performed by transfecting PTEN-WT vector into A549 cells together with miR-18 mimics or miR-18a mimics + pcDNA-TP53TG1 (c), and anti-miR-18a or anti-miR-18a + si-TP53TG1#1 (d). [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-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-191, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-196a-2, hsa-mir-181a-1, mmu-mir-296, mmu-mir-298, mmu-mir-34c, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-148a, mmu-mir-196a-1, mmu-mir-196a-2, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-93, mmu-mir-34a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-330, mmu-mir-346, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-107, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34c, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-375, hsa-mir-381, mmu-mir-375, mmu-mir-381, hsa-mir-330, mmu-mir-133a-2, hsa-mir-346, hsa-mir-196b, mmu-mir-196b, hsa-mir-18b, hsa-mir-20b, hsa-mir-146b, hsa-mir-519d, hsa-mir-501, hsa-mir-503, mmu-mir-20b, mmu-mir-503, hsa-mir-92b, mmu-mir-146b, mmu-mir-669c, mmu-mir-501, mmu-mir-718, mmu-mir-92b, hsa-mir-298, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
One example of miRNAs that can be actively involved in cell proliferation is the miR-17-92 cluster, which comprises seven miRNAs (miR-17-5p, miR-17-3p, miR-18, miR-19a, miR-20, miR-19b, and miR-92-1). [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-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-23b, mmu-mir-27b, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-140, mmu-mir-24-1, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, hsa-mir-30c-2, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-200b, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, 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-18a, mmu-mir-20a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-92a-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-17, mmu-mir-19a, mmu-mir-200c, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-92a-1, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-301a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-196b, mmu-mir-196b, dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, hsa-mir-18b, 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-1-2, dre-mir-1-1, dre-mir-15a-1, dre-mir-15a-2, dre-mir-15b, dre-mir-17a-1, dre-mir-17a-2, dre-mir-18a, dre-mir-18b, dre-mir-18c, dre-mir-19a, dre-mir-20a, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30c, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-130a, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-140, dre-mir-196a-2, dre-mir-196b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-301a, dre-let-7j, hsa-mir-92b, mmu-mir-666, mmu-mir-92b, mmu-mir-1b, dre-mir-196c, dre-mir-196d, mmu-mir-3074-1, mmu-mir-3074-2, hsa-mir-3074, mmu-mir-133c, mmu-let-7j, mmu-let-7k, dre-mir-24b
Similarly, Mir92a which is in the Mirc1 cluster on mouse chromosome 14 containing Mir17, Mir18, Mir19a, Mir20a, Mir19b-1, and Mir92a-1, is required to promote proliferation of orofacial development (Ning et al., 2013). [score:1]
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d KON049.01 [11] T cell Gpc5 HeLa Follicular lymphoma mir-18* B5_12171B1 [16] B cell HeLa, BM mir-19a* Lnz25-3 [14] T cell HeLa, Colon mir-20a HeLa, BM mir-19b-1 HeLa, Colon mir-92-1 BM a Not all RISs are shown. [score:1]
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miR-17∼92 [flox/ flox] mice (Jax mice stock 8458 – on a mixed C57BL/6 and 129S4 background) harbouring loxP sites on each side of the miR-17∼92 cluster (Mir17, Mir18, Mir19a, Mir20a, Mir19b-1, Mir92–1) (23), were bred to LysMCre mice (kind gift from Dr. [score:1]
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Elr-type proteins protect Xenopus Dead end mRNA from miR-18 -mediated clearance in the soma. [score:1]
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Other miRNAs from this paper: mmu-mir-18a, mmu-mir-337
To a lesser extent some miRNAs including the X-linked Mir-18, -19 [51] and Mir-337 [52] also showed a small increase. [score:1]
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The miR-17 family consists of three paralogous polycistronic clusters on different chromosomes: miR-17~92 (miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1), miR-106b~25 (miR-106b, miR-93, and miR-25), and miR-106a~363 (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2, and miR-363). [score:1]
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Real time PCR was done on all of the following mature microRNAs of the miR-17-92 Cluster: miR-17, miR-18, miR-19a, miR-19b, miR-20 and miR-92. [score:1]
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The miR-106a-363 cluster contains miR-106a, miR-18b, miR-20b, miR-19b, miR-92a and miR-363. [score:1]
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For example, the probe mixture for the miR-17 subfamily contains probes for miR-17, miR-20a, miR-106a, miR-20b, miR-106b, and miR-93, the probe mixture for the miR-18 subfamily contains probes for miR-18a and miR-18b, the probe mixture for the miR-19 subfamily contains probes for miR-19a and miR-19b, and the probe mixture for the miR-92 subfamily contains probes for miR-92, miR-363, and miR-25. [score:1]
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The human cluster contains six miRNAs (MIR363, MIR19A2, MIR19B2, MIR20B, MIR18B and MIR106A), all six of which were predicted from Meug_1.0 (ENSMEUG000000: 16895, 17431, 17730, 17261, 17356, and 17668 respectively). [score:1]
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In human and mouse, two paralog clusters exist, i. e. the miR-106a-363 cluster comprising 6 miRNAS (miR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2 and miR-363) and the miR-106b-25 one with 3 members (miR-106b, miR-93 and miR-25). [score:1]
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