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21 publications mentioning mmu-mir-291b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-291b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 315
Other miRNAs from this paper: mmu-mir-290a, mmu-mir-291a, mmu-mir-219b, mmu-mir-290b
Notably, silencing of miR-291b-3p in the liver of HFD-fed mice reduced hepatic expression of PTEN protein (Fig. 5E), while hepatic overexpression of miR-291b-3p in C57BL/6 J mice up-regulated PTEN expression (Fig. 5F). [score:10]
Taken together, these data suggest that miR-291b-3p directly targets p65 to upregulate PTEN expression, thereby antagonizing AKT/GSK activation. [score:9]
How to cite this article: Guo, J. et al. Hepatic MiR-291b-3p Mediated Glucose Metabolism by Directly Targeting p65 to Upregulate PTEN Expression. [score:8]
MiR-291b-3p directly targets p65 to upregulate PTEN expression. [score:8]
In our previously study, we identified AMPK as a primary target of miR-291, and revealed that miR-291 inhibitors ameliorated hepatic TG accumulation, reduced FAS and SREBP-1 activity and this was attributed to the targeting of miR-291b-3p of AMPK 24. [score:7]
Strikingly, concomitant with increased PTEN expression, a converse decrease in p65 expression was observed in the NCTC1469 cells overexpressing miR-291b-3p (Fig. 6A). [score:7]
However, overexpression or inhibition of miR-291b-3p failed to affect the expression and activation of p38 MAPK, JNK and Smad2/3. [score:7]
Hepatic miR-291b-3p expression is upregulated in HFD-fed mice and induced by fasting in C57BL/6 J normal mice. [score:6]
To directly assess the pathological role of miR-291b-3p in glucose metabolism and insulin resistance, recombinant adenovirus expressing miR-291b-3p inhibitor (ad-miR-291i) was injected into HFD-fed mice through tail vein. [score:6]
Therefore, we further explored another possible target gene of miR-291b-3p that modulated the expression of PTEN, thereby regulating AKT/GSK/FoxO1 signaling pathway. [score:6]
Previously, we have shown that miR-291b-3p inhibitor ameliorated hepatic triglyceride (TG) accumulation, reduced fatty acid synthase (FAS) and Sterol-regulatory element binding protein (SREBP-1) activity, which was attributed to the targeting of AMPK by miR-291b-3p 24. [score:6]
As shown in Fig. 5B, the phosphorylation level of AMPK was significantly suppressed by compound c, and no significant difference was found between ad-NC group and ad-miR-291m group after injection of compound c. Importantly, after inhibition of AMPK, overexpression of miR-291b-3p still significantly reduced hepatic glycogen level compared that of Ad-NC mice (Fig. 5C). [score:6]
More importantly, we found that inhibition of miR-291b-3p could not abolish p65 silencing -induced PTEN upregulation as well as impaired AKT activation (Fig. 6F). [score:6]
Although we have demonstrated that AMPK was a direct target gene of miR-291b-3p, no direct interaction between PTEN and AMPK has been reported. [score:5]
More importantly, inhibition of miR-291b-3p partially restored the activation of AKT even in NCTC1469 cells transfected with the specific siRNA targeting p65. [score:5]
Taken together, these results demonstrate that miR-291b-3p contributed to hyperglycemia and hepatic insulin resistance through suppressing insulin-stimulated AKT/GSK signaling activation and increasing expression of gluconeogenic genes in hepatocytes. [score:5]
Taken together, our data suggest that hepatic inhibition miR-291b-3p expression ameliorated hyperglycemia and insulin resistance in vivo and in vitro. [score:5]
Accordingly, inhibition of miR-291b-3p resulted in a significant reduction of PTEN expression in NCTC1469 cells (Fig. 5G). [score:5]
As shown in Fig. 4A, hepatic inhibition miR-291b-3p expression in HFD-fed mice elevated the phosphorylation levels of AKT/glycogen synthase kinase (GSK)/Forkhead box protein O1(FoxO1), whereas reduced the mRNA levels of gluconeogenic genes including G6Pase, PGC-1α, and PEPCK (Fig. 4B). [score:5]
Moreover, to explore whether the nutritional status could affect the expression pattern of hepatic miR-291b-3p, the level of miR-291b-3p was determined in the liver of C57BL/6 J mice fasted for 16 h. As shown in Fig. 1B, hepatic miR-291b-3p expression level was also increased in the fasted states. [score:5]
Adenovirus vector expressing GFP or miR-291b-3p mimic or inhibitor was generated as previously described 24 37. [score:5]
In contrast, inhibition of miR-291b-3p resulted in enhanced protein level of p65, accompanied by decreased PTEN expression (Fig. 6B). [score:5]
Of note, inhibition of miR-291b-3p repressed expression of PTEN protein in the liver of HFD-fed mice and NCTC1469 hepatocytes. [score:5]
Next, we determined whether the glucose-lowering effects of miR-291b-3p inhibition is cell-autonomous, murine liver cell lines NCTC1469 was transfected with miR-291b-3p inhibitor. [score:5]
In comparison, forced expression of miR-291b-3p increased the expression of PTEN in C57BL/6 J mouse livers and NCTC1469 cells. [score:5]
However, overexpression of miR-291b-3p led to an increase in PTEN expression in NCTC1469 cells (Fig. 5H). [score:5]
MiR-291b-3p targets p65 to regulate PTEN expression, in turn mediated glycogen synthesis and gluconeogenesis in hepatocytes. [score:5]
Hepatic inhibition miR-291b-3p expression ameliorates hyperglycemia and insulin resistance in HFD-fed mice. [score:5]
MiR-291b-3p targeted p65 to regulate PTEN expression, in turn mediated glycogen synthesis and gluconeogenesis in hepatocytes. [score:5]
Notably, hepatic inhibition miR-291b-3p expression improved glucose tolerance, insulin tolerance and pyruvate tolerance. [score:5]
MiR-291b-3p suppresses insulin-stimulated AKT/GSK/FoxO1 signaling and increases the expression of gluconeogenic genes in hepatocytes. [score:4]
MiR-291b-3p suppresses insulin-stimulated AKT/GSK/FoxO1 signaling and increases expression of gluconeogenic genes in hepatocytes. [score:4]
Thus, miR-291b-3p impaired PI3K/AKT signaling mainly by positively regulating PTEN expression in the liver. [score:4]
We further identified the direct effector of miR-291b-3p -induced increased PTEN expression. [score:4]
In this study, we further profiled the expression of miR-291b-3p in different organs. [score:3]
Glucose tolerance was also significantly improved by hepatic inhibition miR-291b-3p expression, as measured by oral glucose tolerance test (Fig. 2A). [score:3]
Moreover, overexpression of miR-291b-3p caused an increase in mRNA and protein levels of G6Pase, PGC-1α and PEPCK (Fig. 4H). [score:3]
In contrast, overexpression of miR-291b-3p in the liver of C57BL/6 J mice impaired the activation of AKT/GSK/FoxO1 signaling (Fig. 4C) and increased the transcript levels of G6Pase, PGC-1α and PEPCK (Fig. 4D). [score:3]
The expression of miR-291b-3p was normalized to that of the U6 snRNA as previously described 38. [score:3]
In previous study, we demonstrated that the expression level of miR-291b-3p was increased in the liver of db/db mice and HFD-fed mice. [score:3]
In the present study, we found that short-term fasting led to increased level of miR-291b-3p (Fig. 1B) without reduced expression of AMPK (Fig. 5A), indicating a different mechanism for glucogenesis under fasting. [score:3]
Real-time PCR and showed that silencing of miR-291b-3p suppressed the mRNA and protein levels of gluconeogenic genes (Fig. 4F). [score:3]
MiR-291b-3p mimic, inhibitor, or miR negative control (NC) (Genepharma, Shanghai, China) were mixed with HiperFect transfection reagent (QIAGEN, Duesseldorf, German) and incubated at room temperature for 10 min according to the manufacturers’ instructions. [score:3]
Consistent with the results in vivo, silencing of miR-291b-3p in NCTC1469 cells enhanced glycogen synthesis and suppressed glucose production (Fig. 2G and H). [score:3]
Mice were injected intravenously through the tail vein with adenovirus encoding green fluorescent protein (Ad-NC), miR-291b-3p mimic (Ad-miR-291m) or inhibitor (Ad-miR-291i) at a dose of 1 × 10 [9] plaque-forming units (PFU) in 0.2 ml PBS (0.2 ml/25 g body weight). [score:3]
As analyzed by real-time PCR, miR-291b-3p is wi dely expressed in main organs of C57BL/6 J mice including liver, muscle, fat, heart, kidney, pancreas, spleen, stomach, lung and testis. [score:3]
Of note, miR-291b-3p is abundantly expressed in the liver and the pancreas (Fig. 1A). [score:3]
A pyruvate tolerance test (PTT) clearly indicated that inhibition of miR-291b-3p repressed hepatic glucose production (Fig. 2C). [score:3]
Moreover, when we examined glycogen synthesis and glucose production in NCTC1469 cells, we found a significant reduction of glycogen content and a striking increase in glucose production by miR-291b-3p overexpression (Fig. 3G and H). [score:3]
Thus, we speculated that aberrant miR-291b-3p expression might lead to abnormal AKT/GSK/FoxO1 phosphorylation in diabetic mouse livers. [score:3]
Moreover, to assess whether the effect of miR-291 on insulin resistance is dependent on AMPK, compound c (Sigma), an AMPK inhibitor, was intravenously injected at a dose of 2 mg/kg for 3 days before sacrifice. [score:3]
Hepatic overexpression of miR-291b-3p results in hyperglycemia and insulin resistance in C57BL/6 J mice. [score:3]
Our findings indicate the therapeutic potential of miR-291b-3p inhibitor in hyperglycemia and insulin resistance. [score:3]
Similarly, overexpression of miR-291b-3p in the liver of C57BL/6 J mice significantly increased de novo hepatic glucose production (Fig. 3C). [score:3]
To gain further insights into the significance of miR-291b-3p in manipulating glucose metabolism and insulin resistance, recombinant adenovirus expressing miR-291b-3p mimic was injected into C57BL/6 J normal mice through tail vein. [score:3]
These data indicate that hepatic increased PTEN expression might be involved in miR-291b-3p-reduced AKT/GSK signaling activity. [score:3]
Adenovirus -mediated overexpression of miR-291b-3p in C57BL/6 J mice led to impaired glucose and insulin tolerance, as indicated by GTT and ITT experiments (Fig. 3A and B). [score:3]
In addition, inhibition of miR-291b-3p reduced glucose production in the medium of cultured NCTC1469 cells. [score:3]
The 3′untranslated region (UTR) of p65 containing the predicted binding site for miR-291b-3p was cloned into the pmirGLO (Promega, Madison, Wisconsin, USA) luciferase reporter vector. [score:3]
The NCTC1469 cells transfected with miR-291b-3p inhibitor exhibited increased AKT and GSK activity after insulin stimulation (Fig. 4E). [score:3]
That is, miR-291b-3p indirectly reduced AKT/GSK /FoxO1 phosphorylation via the p65/PTEN pathway, thereby contributing to the negative regulating role of miR-291b-3p in insulin signaling. [score:3]
More importantly, we also found that fasting increased the expression of miR-291b-3p in the liver of C57BL/6 J mice. [score:3]
To verify that p65 is a true target of miR-291b-3p, we generated dual luciferase reporter plasmids containing miR-291b-3p binding sites in the 3′UTRs of mouse p65. [score:3]
Conversely, overexpression of miR-291b-3p in C57BL/6 J mice caused remarkable impaired glucose tolerance, insulin sensitivity and glucose homeostasis. [score:3]
Therefore, we searched for another target of miR-291b-3p. [score:3]
And dual luciferase reporter assay revealed that p65 was a target gene of miR-291b-3p. [score:2]
Notably, we found that miR-291b-3p functions as a negative regulator of NF-κB subunit p65, but not p38MAPK, JNK, Smad2/3 and NF-κB subunit p50. [score:2]
MiR-291b-3p elevates the expression of PTEN. [score:2]
Next, we sought to determine how miR-291b-3p regulated AKT/GSK signaling activity. [score:2]
In addition, adenovirus -mediated knockdown of miR-291b-3p improved insulin-sensitive performance, as identified by steeper rate of reduced blood glucose levels in response to insulin (Fig. 2B). [score:2]
In conclusion, as indicated in Fig. 7, we proposed mechanisms by which hepatic miR-291b-3p regulates insulin signaling and glucose metabolism. [score:2]
Proposed mechanisms by which hepatic miR-291b-3p regulates insulin signaling and glucose metabolism. [score:2]
Hyperinsulinemic euglycemic clamp assay demonstrated that inhibition of miR-291b-3p significantly improved the global insulin sensitivity of HFD-fed mice, as assessed by increased glucose infusion rates (Fig. 2D). [score:2]
In line with the metabolic changes, inhibition of hepatic miR-291b-3p substantially activated the AKT/GSK/FoxO1 signaling pathway and ad-miR-291m -treated C57BL/6 J mice exhibited decreased phosphorylation level of AKT/GSK/FoxO1 compared with ad-NC. [score:2]
In contrast, following transfection with miR-291b-3p mimic in NCTC1469 cells, the activation of AKT/GSK/FoxO1 signaling was significantly lowered (Fig. 4G). [score:1]
Based on these observations, we proposed that miR-291b-3p, as a liver-enriched miRNA, could prompt hepatic insulin resistance in mice. [score:1]
Firstly, we analyzed the effect of miR-291b-3p on these transcription factors and pathways. [score:1]
Furthermore, silencing of miR-291b-3p in the liver of HFD-fed mice elevated glycogen level and reduced glucose production (Fig. 2E and F). [score:1]
We then determined the effect of miR-291b-3p on HFD -induced hyperinsulinemia and hyperglycemia. [score:1]
However, in the present study, we did not investigate the mechanism that controls the hepatic expression/induction of miR-291b-3p. [score:1]
We further assessed the effect of miR-291b-3p on insulin-stimulated AKT/GSK/FoxO1 activation in cultured NCTC1469 hepatocytes. [score:1]
These results imply that miR-291b-3p may be involved in hepatic insulin resistance. [score:1]
We previously identified that the hepatic levels of miR-291b-3p were decreased by ~40%, accompanied by a significant reduction in the liver weight and the liver weight-to-body weight ratio, and a significant decrease in hepatic lipid deposition 24. [score:1]
However, short-term fasting did not change the mRNA level of AMPK in the livers of C57 mice, indicating miR-291b-3p may control glucose production through a different mechanism. [score:1]
Then, we aligned the 3′UTR of p65 with miR-291b-3p and identified a conserved binding site (Fig. 6C). [score:1]
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2
[+] score: 26
Along the same lines, DRGs from mice injected intrathecally with miRNA mimics showed a strong expression of targeted miRNAs in comparison to corresponding non -targeting mimics (examples with overexpression of miR-370-3p and miRNA-291b-5p with their respective mimics in comparison with non -targeting-controls is shown in Fig 2, panel D; p < 0.05 two tailed t-test). [score:11]
Finally, we observed that reversing the down-regulation of miRNA-291b-5p, another candidate deregulated miRNA from profiling analyses, resulted in no significant change in the magnitude of tumour -associated mechanical hyperalgesia when compared to corresponding controls (Fig 4, panels E, F and Supporting Information Fig 3, panel C, p > 0.05). [score:4]
Change in frequency of paw withdrawal to plantar application of a von Frey filament force of 0.07 g following induction of tumor growth in the calcaneous bone of the heel in mice receiving intrathecally delivered miR-291b-5p mimic (red symbols) or non -targeting mimic (green) or vehicle (grey symbols). [score:3]
* denotes p < 0.0001 from PID-3 through PID-14 in vehicle, non -targeting -mimic and miR-291b-5p -mimic groups. [score:3]
In panel (C), * denotes p = 0.02 for miR-1a-3p, 0.04 for miR-34c-3p as compared to corresponding mismatch inhibitor and in panel (D), * denotes p = 0.001 for miR-370-3p and <0.0001 for miR-291b-5p as compared to non -targeting mimic, ANOVA followed by post hoc Fischer's test, n = 3 per group. [score:3]
miRIDIAN microRNA mimics for mmu-miR-370-3p (C-310619-07), miR-483* (C-310641-07) and miR-291b-5p (C-310666-03) were further custom -modified with 3′-cholesterol conjugation on passenger strand and 3′-FITC conjugation on guide strand to facilitate the in vivo uptake and facilitate visualization, respectively. [score:1]
Furthermore, reversing pathophysiological decrease of miR-483-3p, but not of miR-291b-5p, attenuated tumour -mediated hyperalgesia. [score:1]
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3
[+] score: 24
Regarding these observations, we performed qRT-PCR for 8 target genes of commonly regulated miRNA; 4 target genes (ATG5, ITGA6, NCKAP1, SARBS1) of the 2 up-regulated miRNA (mmu-miR-291b-5p, mmu-miR-296-5p) and 4 target genes (AKT1, APC, LMO7, MSN) of the 3 down-regulated miRNA (mmu-miR-30c-1*, mmu-miR-467b* and mmu-miR-374*). [score:14]
Interestingly, in cluster A, 3 miRNAs (mmu-miR-30c-1*, mmu-miR-374* and mmu-miR-497b*) were identified as being down-regulated by all nine polyphenols tested, while in cluster 2, 2 miRNAs (mmu-miR-291b-5p and mmu-miR-296-5p) were observed as up-regulated by all nine polyphenols (Table 2). [score:7]
Moreover, changes in miRNA expression were observed after polyphenol supplementation, and five miRNAs (mmu-miR-291b-5p, mmu-miR-296-5p, mmu-miR-30c-1*, mmu-miR-467b* and mmu-miR-374*) were identified as being commonly modulated by these polyphenols. [score:3]
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4
[+] score: 13
We chose to profile the ubiquitously expressed miR-16, five ESC-specific miRNAs (miR-290, miR-291-3p, miR-292-3p, miR-294, and miR-295) [23], [24], and two miRNAs that are upregulated in ESCs undergoing differentiation (miR-21 and miR-22) [23], [24]. [score:6]
RNU6b is significantly less abundant than all miRNAs tested except for miR-22, miR-290, and miR-291. [score:1]
The miRNAs tested include miR-16 (lane 1), miR-21 (lane 2), miR-22 (lane 3), miR-290 (lane 4), miR-291-3p (lane 5), miR-292-3p (lane 6), miR-294 (lane 7), miR-295 (lane 8), and the small nuclear RNA, RNU6b (lane 9). [score:1]
Thus, based on the 95 [th] percentile confidence interval, it appears that RNU6b is significantly less abundant than several of the miRNAs tested except miR-22, miR-290, and miR-291. [score:1]
The difference in Ct values between the negative control (MEFs alone) and each experimental group (miR-290, miR-291-3p, miR-292-3p, miR-294, miR-295, miR-16, and RNU6b) is shown. [score:1]
The relative abundance of all tested miRNAs overlaps except for that of miR-295, which is significantly more abundant than miR-290 and miR-291 (Figure 5B). [score:1]
The abundance of several miRNAs (miR-290, miR-291-3p, miR-292-3p, miR-294, and miR-295) increased in MEFs as early as 1 hour after incubation, suggesting transfer. [score:1]
The majority of miRNAs tested do not differ significantly from one another except for miR-295, which is significantly more abundant than miR-290 and miR-291. [score:1]
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5
[+] score: 11
Thus, similarly to its interaction with the mouse miR-291-3p0, miR-294-3p0 and/or miR-295-3p0, the 2-7C-S target appears to interact via G:U wobble base pairing with miR-372-3p0 and/or miR-373-3p0 which also have a 2-7U seed. [score:3]
Finally, we note that neither the miR-291b-5p nor the miR-291b-3p reporters were silenced in any of the above experiments, which is consistent with the fact that pre-miR-291b sequences represent about 0.1% of all reads that map to the entire miR-290–295 locus in the various sequencing datasets (Figure S1, note that the 5′- end distributions are different in the different libraries and, thus, indicative of noise due to non-specific pri -RNA degradation). [score:1]
Normalized frequencies of the 5′-end positions of RNA species that map to pre-miR-291b in various sequencing datasets. [score:1]
Of these reporters, only 2-7C-S and 2-7U-S were silenced in mouse J1 ES cells, consistent with the predicted absence of isomiRs with 2-7A and 2-7G seeds (Figure 4A, no 3p0 miRNAs within miR-290-295 have a G at position 8 and the 2-7A seed is only present in miR-291b-3p0, which is inactive according to the sequencing and luciferase data). [score:1]
Figure S1 Short RNA 5′-end distributions for pre-miR-291b. [score:1]
In the miR-290-295 cluster the specialized pre-miR-371 co-orthologs are interspaced by pre-miRNAs, which are processed, or in the case of pre-miR-291b could potentially be processed, into isomiRs that contain (3p)2-7U seeds. [score:1]
The data for pre-miR-291b, which yields very few reads in all datasets and is, thus, noisy is given in Figure S1. [score:1]
Therefore, pre-miR-291a, pre-miR-291b and pre-miR294 are likely co-orthologs of pre-miR-372 and pre-miR-295 is an ortholog of the promoter distal pre-miR-373. [score:1]
All of the 3p-reporters except miR-290-3p and miR-291b-3p were robustly silenced in wild type ES cells. [score:1]
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6
[+] score: 11
In addition, Luningschror and his co-workers [29] have demonstrated that two members of this cluster, namely miR-291b-5p and miR-293, inhibit NF-κB signaling pathway through inhibition of p65. [score:5]
The other miRNAs of the miR-290-295 cluster (miR-290-5p, miR-291a-5p, miR-291b-5p, miR-292-5p, miR-293, miR-293 [*], miR-294 [*], and miR-295 [*]) differing in their seed sequences, are still highly expressed in ESCs with the exception of the hardly detectable [22] minor forms of miR-293, miR-294, and miR-295 (miR-293 [*], miR-294 [*], and miR-295 [*]). [score:3]
More interestingly, Ash1l is a target of miR-291, which was validated by using reporter assays [65]. [score:2]
Within the miR-290-295 cluster, the seed sequences of ‘AAGUGC’ hexamer are found in miR-290-3p, miR-291a-3p, miR-291b-3p, miR-292-3p, miR-294, and miR-295. [score:1]
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7
[+] score: 9
Expression levels of these miRNAs were maintained in both male and female germ cells at E12.5 and E13.5, except miR-291-5p and miR-292-3p both of which were slightly down-regulated in E13.5 female PGCs (Figure 1A). [score:6]
MiRNAs belonging to miR-17-92 and miR-290-295 clusters were still highly expressed in neonatal spermatogonia and at almost the same levels as those in E13.5 PGCs (Figure 4E), although miR-290 and miR-291-3p were not detectable. [score:3]
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8
[+] score: 8
qPCR analysis of miR291-5p, miR290-3p, and miR292-3p expression levels in RNA purified from primary wild-type pro-B (B220+, CD43+, IgM−) or pre-B (B220+, CD43−, IgM−) cells. [score:3]
However, aside from miR291-5p, we could not detect their expression in sorted pre-B cells of wild-type mice. [score:3]
A third member of the miR290 polycistronic cluster with a similar seed sequence as miR290-5p/292-5p, miR291-5p, is also induced; however other members of the miR290 cluster with an alternate seed sequence did not increase upon STI571 treatment (Figure S1). [score:1]
miR290-5p/292-5p share the seed sequence CUCAAA similar to miR291-5p (100049715, 100124471), AUCAAA. [score:1]
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9
[+] score: 7
Briefly, 1500 ng of biotinylated cRNA was hybridised to Illumina expression BeadChips (Mouse-6 v1.1 for mmu-miR-291-3p and mmu-miR-25 mimics and cell line expression profiles, and Mouse-6 v2 for mmu-miR-302, mmu-miR-292-5p, mmu-miR-106a, mmu-miR-21 and mmu-miR-298 mimics. [score:5]
miRIDIAN Negative Control #2 (Dharmacon CN-002000-01-05) miRIDIAN mmu-miR-291-3p mimic (Dharmacon C-310470-01-0005) miRIDIAN mmu-miR-25 mimic (Dharmacon C-310564-01-0005) miRIDIAN mmu-miR-302 mimic (Dharmacon C-310483-05-0005) miRIDIAN mmu-miR-292-5p mimic (Dharmacon C-310471-03-0005) miRIDIAN mmu-miR-106a mimic (Dharmacon C-310488-07-0005) miRIDIAN mmu-miR-21 mimic (Dharmacon C-310515-05-0005) miRIDIAN mmu-miR-298 mimic (Dharmacon C-310479-07-0005) Trizol purified RNA was cleaned up with an RNeasy MiniElute Cleanup Kit (Qiagen). [score:1]
miRIDIAN Negative Control #2 (Dharmacon CN-002000-01-05) miRIDIAN mmu-miR-291-3p mimic (Dharmacon C-310470-01-0005) miRIDIAN mmu-miR-25 mimic (Dharmacon C-310564-01-0005) miRIDIAN mmu-miR-302 mimic (Dharmacon C-310483-05-0005) miRIDIAN mmu-miR-292-5p mimic (Dharmacon C-310471-03-0005) miRIDIAN mmu-miR-106a mimic (Dharmacon C-310488-07-0005) miRIDIAN mmu-miR-21 mimic (Dharmacon C-310515-05-0005) miRIDIAN mmu-miR-298 mimic (Dharmacon C-310479-07-0005) Trizol purified RNA was cleaned up with an RNeasy MiniElute Cleanup Kit (Qiagen). [score:1]
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10
[+] score: 5
For example, stem cell specific miRNAs of the miR-290 family (miR-291–295, [24]) were detected to be about 25-fold overexpressed in mouse embryonic stem cells, while brain-specific miR-124 and miR-9 were about 14-fold overexpressed in mouse brain (Supplementary Table  2). [score:5]
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11
[+] score: 5
Members of the miR-290-295 cluster (miR-290, miR-291a, miR-292, miR-291b, miR-293, miR-294 and miR-295-1) were the most abundant among known miRNAs that were upregulated in rat PSCs. [score:4]
Some miRNAs, such as miR-291, miR-294 and miR-295, can enhance reprogramming that is induced by OSK factors [22]. [score:1]
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12
[+] score: 4
By contrast, some miRNAs that are significantly up-regulated were also observed, including miR-290 cluster members, miR-291a and miR-291b, miR-129-1-3p, miR-129-2-3p, miR-23a-3p, miR-434-3p, miR-145-5p, and miR-203-3p. [score:4]
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13
[+] score: 4
miRNAs belonging to the 290 cluster (mir-291b-5p, -292, -294, and -295), the miRNA cluster involved in the maintenance of ESC pluripotency [42], were up-regulated and remained increased over 48 hours post-ESMV exposure. [score:4]
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14
[+] score: 4
These miRNAs, which include miR-291-3p, miR-294 and miR-295, are thus named ES cell-specific cell cycle -regulating (ESCC) miRNAs based on their ability to regulate G1-S transition [39]. [score:3]
Although miR-290 itself was not known to promote reprogramming, several members of the miR-290 family, miR-291-3p, miR-294 and miR-295, enhance reprogramming of MEFs in the absence of c-Myc [41]. [score:1]
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15
[+] score: 4
In addition, after subcutaneous injection of S. aureus, no up-regulated miRNAs were detected in the whole blood at 4 h and 8 h. At 24 h after S. aureus injection, the levels of 7 miRNAs (miR-133b, miR-133a, miR-122, miR-205, miR-1899, miR-714, and miR-291b) increased significantly (Table 3). [score:4]
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16
[+] score: 3
In contrast, control miRNAs derived from the mir-291 cluster were strongly expressed in the RNA derived from ES cells, as expected. [score:3]
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17
[+] score: 3
A closer look at those 5 miRNA revealed that the expression of 4 miRNA including mmu-miR-291a-5p, mmu-miR-291b-5p, mmu-miR-664-3p, and mmu-miR-1306-3p increased in tumor tissues following cigarette smoke exposure, yet they decreased in the parenchyma of exposed mice, whereas mmu-miR-378-3p displayed the same behavior in both tissues following MS exposure. [score:3]
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[+] score: 2
More specifically, they include “miR-291b-3p/519a/519b-3p/519c-3p”, “miR-290-3p/292-3p/467a”, “miR-467cd”, “miR-106/302”, and “miR-467b”. [score:1]
Within the mir-290-295 cluster, the ‘AAGUGC’ seed is found in miR-290-3p, miR-291a-3p, miR-291b-3p, miR-292-3p, miR-294, and miR-295. [score:1]
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[+] score: 1
HEK-293 cells were transiently transfected with psiCHECK-Arid4b together with miR-302d, miR-291-3p, or a control siRNA, using lipofectamine 2000 (Invitrogen). [score:1]
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Only miR-291-3p, miR-294 and miR-295 can promote the G1-S transition of the cell cycle and the induction of pluripotency [13], [14]. [score:1]
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Additionally, seven miRNAs exhibited a consistent pattern of no amplification in TEC from infected animals (miR-144, miR-208b, miR-291b-3p, miR-295, miR-302a, miR-488, and miR-654-3p, Figure S4 in). [score:1]
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