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42 publications mentioning rno-mir-19b-2

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-19b-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 177
Meanwhile, miR-19b overexpression led to increased expression of Bcl-2, decreased expression of Bax, and reduced cleaved-Caspase 3 to Caspase 3 ratio at protein levels, while miR-19b inhibition had inverse effects (Figure 3C). [score:9]
To overexpress or inhibit miR-19b expression, miR-19b mimic (50 nM), inhibitor (100 nM), or respective negative controls was transfected to H9C2 cardiomyocytes for 48 h using lipofectamine 2000 (Invitrogen, USA). [score:9]
Furthermore, our data demonstrated that miR-19b overexpression reduced H [2]O [2] -induced apoptosis and improved cell survival in H9C2 cardiomyocytes, accompanied with increased expression of Bcl-2 and decreased expression of Bax and cleaved-Caspase 3/Caspase 3 ratio, indicating that miR-19b overexpression might provide protective effects against oxidative stress-related cellular apoptosis. [score:9]
Meanwhile, miR-19b was also downregulated in H [2]O [2] -treated H9C2 cardiomyocytes, and miR-19b overexpression was sufficient to reduce H [2]O [2] -induced cardiomyocyte apoptosis. [score:6]
Besides the reduction of miR-19b expression in infarct area of heart samples from I-R mice, we also found that miR-19b was downregulated in H [2]O [2] -treated H9C2 cardiomyocytes. [score:6]
B. Flow cytometry analysis for necrosis, apoptosis, and survival of H [2]O [2] -treated H9C2 cardiomyocytes with miR-19b overexpression or inhibition (n = 4). [score:5]
C. Immunoblot analysis for Bcl-2, Bax, cleaved-Caspase 3 to Caspase 3 ratio in H [2]O [2] -treated H9C2 cardiomyocytes with miR-19b overexpression or inhibition (n = 3). [score:5]
miR-19b mimic was found to be sufficient to increase relative miR-19b level, while miR-19b inhibitor had inverse effect, confirming that miR-19b mimic and inhibitor took effects in H9C2 cardiomyocytes (Figure 3A). [score:5]
Figure 4PTEN is a target gene of miR-19b controlling H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes A. Immunoblot analysis for PTEN protein level in H9C2 cardiomyocytes transfected with miR-19b mimic, inhibitor, or respective negative controls (n = 3). [score:5]
Moreover, silencing PTEN alone led to reduced apoptosis and improved cell survival in H [2]O [2] -treated H9C2 cardiomyocytes, while co-transfection of PTEN-siRNA and miR-19b inhibitor could totally abolish the aggravated effect of miR-19b inhibitor on cell apoptosis in H9C2 cardiomyocytes treated with H [2]O [2] (Figure 4D–4E). [score:5]
The time-course change of miR-19b was determined and miR-19b was found to be downregulated in H [2]O [2] -treated H9C2 cardiomyocytes at 2 h but remained unchanged at 5 min, 15 min, 30 min and 60 min (Figure 2C). [score:4]
Using qRT-PCR, miR-19b was found to be the only one in the miR-17-92 cluster that was downregulated in infarct area of heart samples from a murine mo del of I-R injury (Figure 1B). [score:4]
Here, we found that miR-19b was markedly downregulated in infarct area heart samples from a murine mo del of I-R injury. [score:4]
PTEN is a well-known target gene of miR-19b, which mainly regulates cancer cell growth and proliferation [37– 40]. [score:4]
To the best of our knowledge, we firstly reported a downregulation of miR-19b in myocardial I-R injury, which promoted us to further determine the underlying mechanisms. [score:4]
Here we showed that miR-19b was the only member of the miR-17-92 cluster that was downregulated in infarct area of heart samples from a murine mo del of I-R injury. [score:4]
miR-19b is downregulated in the infarct area of myocardial ischemia-reperfusion mice. [score:4]
Therefore, miR-19b overexpression might be a novel therapy for myocardial I-R injury. [score:3]
miR-19b inhibitor. [score:3]
PTEN is a downstream target of miR-19b controlling H [2]O [2] -induced apoptosis in H9C2 cardiomyocytesHow miR-19b modulates H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes was examined. [score:3]
After transfected with miR-19b mimic, inhibitor, or respective controls for 48 h, cell apoptosis and necrosis were analyzed using Annexin V-FITC and propidium iodide (PI) kit (Dojindo, Japan) according to the manufacturer's instruction, followed by flow cytometry analysis (Beckman Coulter, USA). [score:3]
Importantly, silencing PTEN could abolish the aggravated apoptotic effect of miR-19b inhibitor in H [2]O [2] -treated H9C2 cardiomyocytes. [score:3]
Moreover, hypoxia treatment (0% O [2]) was also conducted in H9C2 cardiomyocytes for 8 h. The miR-19b mimic, inhibitor, and their negative controls, as well as PTEN-siRNAs, were all purchased from RiboBio (Guangzhou, China). [score:3]
PTEN is a target gene of miR-19b, responsible for the anti-apoptosis effect of miR-19b. [score:3]
Figure 3miR-19b reduces H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes A. qRT-PCR analysis for miR-19b level in H9C2 cardiomyocytes transfected with miR-19b mimic, inhibitor, or respective negative controls (n = 4). [score:3]
Moreover, PTEN was identified as a target gene of miR-19b that was responsible for its anti-apoptosis effects. [score:3]
PTEN is a downstream target of miR-19b controlling H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes. [score:3]
Therefore, our data suggest that miR-19b might be a novel therapeutic target for reducing early cellular apoptosis during myocardial I-R injury. [score:3]
Overexpression of miR-19b led to decreased apoptosis and improved survival of H [2]O [2] -treated H9C2 cardiomyocytes. [score:3]
To further examine the functional effect of miR-19b in H [2]O [2] -treated H9C2 cardiomyocytes, transfection of miR-19b mimic, inhibitor, or their negative controls, were conducted. [score:3]
PTEN is a target gene of miR-19b controlling H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes. [score:3]
Furthermore, PTEN was identified as a downstream target of miR-19b controlling apoptosis in H [2]O [2] -treated cardiomyocytes. [score:3]
E. Flow cytometry analysis for necrosis, apoptosis, and survival of H [2]O [2] -treated H9C2 cardiomyocytes with miR-19b inhibition and/or PTEN silence (n = 4). [score:3]
PTEN is a well-known target gene of miR-19b [25– 27]. [score:3]
Flow cytometry showed that miR-19b mimic reduced H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes, while miR-19b inhibitor aggravated that (Figure 3B). [score:3]
A. qRT-PCR analysis for miR-19b level in H9C2 cardiomyocytes transfected with miR-19b mimic, inhibitor, or respective negative controls (n = 4). [score:3]
In conclusion, miR-19b overexpression is able to attenuate apoptosis in H [2]O [2] -treated H9C2 cardiomyocytes. [score:3]
Figure 5Proposed mechanisms by which miR-19b protects apoptosis induced by H [2]O [2] in H9C2 cardiomyocytes A. Immunoblot analysis for PTEN protein level in H9C2 cardiomyocytes transfected with miR-19b mimic, inhibitor, or respective negative controls (n = 3). [score:3]
As expected, PTEN was negatively regulated by miR-19b at the protein level in H9C2 cardiomyocytes. [score:2]
In the current study, immunoblot analysis showed that PTEN was inversely regulated by miR-19b in H9C2 cells (Figure 4A). [score:2]
miR-19b reduces H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes. [score:1]
As a key functional member of miR-17-92 cluster, miR-19b has emerging roles implicated in cardiac physiology and pathophysiology changes [15– 19]. [score:1]
Knowing that during the early stage (first 24 h after ischemia) of myocardial I-R injury, production of reactive oxidative species triggers and further enhances cardiomyocyte apoptosis, we continued to determine the functional roles of miR-19b on H [2]O [2] -induced apoptosis in rat H9C2 cardiomyocytes. [score:1]
Interestingly, hypoxia treatment for 8 h also decreased miR-19b (Figure 2D). [score:1]
These data provide evidence that increasing miR-19b might be a novel therapeutic strategy for reducing cellular apoptosis during myocardial IRI. [score:1]
Proposed mechanisms by which miR-19b protects apoptosis induced by H [2]O [2] in H9C2 cardiomyocytes. [score:1]
These data suggest that PTEN is a downstream effector of miR-19b controlling cardiomyocyte apoptosis -induced by H [2]O [2]. [score:1]
Figure 5Proposed mechanisms by which miR-19b protects apoptosis induced by H [2]O [2] in H9C2 cardiomyocytes Coronary artery ligation for 30 min followed by reperfusion until 24 h was conducted to induce I-R injury in mice. [score:1]
miR-19b is decreased in infarct area of myocardial ischemia-reperfusion mice. [score:1]
These data suggest that PTEN is responsbile for the effects of miR-19b in H2O2 -induced apoptosis in H9C2 cardiomyocytes (Figure 5). [score:1]
How miR-19b modulates H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes was examined. [score:1]
C. The time-course change of miR-19b as determined by qRT-PCRs in H [2]O [2] -treated H9C2 cardiomyocytes. [score:1]
miR-19b is decreased in H [2]O [2] -treated H9C2 cardiomyocytes. [score:1]
*, P < 0.05. miR-19b is decreased in H [2]O [2] -treated H9C2 cardiomyocytesAs a common reactive oxygen species, H [2]O [2] is usually used to mimic I-R injury in in vitro experiments. [score:1]
In addition, to determine the time-course of miR-19b changes, H9C2 cardiomyocytes were also treated with 600 μM H [2]O [2] from 0 min to 120 min. [score:1]
In the present study, we found that miR-19b was the only one among the miR-17-92 cluster that was decreased in infarct area of heart samples from a murine mo del of I-R injury. [score:1]
These data indicate a protective effect of miR-19b against H [2]O [2] -induced apoptosis in H9C2 cardiomyocytes. [score:1]
Meanwhile, decreased miR-19b was also detected in H9C2 cardiomyocytes treated with hydrogen peroxide (H [2]O [2]) mimicking myocardial IRI in vitro. [score:1]
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2
[+] score: 69
Finally, we showed that miR-19b suppression can phenocopy the morphological effects of inhibiting mTOR signaling by over -expressing TSC1 and 2, two proteins known to regulate of mTOR [45]. [score:8]
To confirm that fear conditioning induced miRNAs that regulate mTOR signaling, we reduced the level of mature miR-19b expression in hippocampal neurons using a complementary sequence -based modified oligonucleotide inhibitor (locked nucleic acid, LNA) of miR-19b. [score:6]
Therefore, their induction should lead to increases in mTOR signaling activity and, in fact, when one of them (miR-19b) was suppressed, its known target PTEN was increased and mTOR activity decreased. [score:5]
We confirmed that we could reduce expression of miR-19b to less than 0.1%, and inhibition lasted more than 4 days in culture (Figure 8B). [score:5]
For example, miR-106b, miR-21, miR- 22, miR-19b and miR-25 are known to regulate PTEN and miR-27 and miR-139 repress FoxO1 translation through direct binding to the 3′-UTR [31], [32], [33], [34], [35], [36], [37], [38]. [score:5]
Among the up-regulated miRNAs, miR-106b, miR-25 and miR-19b share the same primary transcripts, and miR-24 and miR-27 share primary transcripts. [score:4]
Reducing miR-19b expression increased level of PTEN protein as reported previously [37] and down regulated phosphorylation of the S6 ribosomal subunit, which is thought to reflect mTORC1 activity (Figure 8A and C). [score:4]
In contrast, reducing miR-19b expression did not change the phosphorylation of PKCa, which reflects mTORC2 activity (Figure 8C). [score:3]
Inhibition of miR-19b didn’t change phospho-PKCa/PKCa ratio, representing mTORC2 activity. [score:3]
Suppression of miR-19b also reduced neurite outgrowth in DIV5 hippocampal neurons consistent with decreased mTOR activity. [score:3]
Inhibition of miR-19b reduced phospho-S6/S6 ratio representing mTORC1 activity. [score:3]
0024682.g008 Figure 8 Cultured hippocampal neurons were transiently transfected with either complementary sequence based locked nucleic acid inhibitors of miR-19b or a scrambled control in DIV1 (50 nM). [score:3]
Cultured hippocampal neurons were transiently transfected with either complementary sequence based locked nucleic acid inhibitors of miR-19b or a scrambled control in DIV1 (50 nM). [score:3]
We transiently transfected LNA inhibitors to DIV1 neurons and inhibition of miR-19b was measured using real time PCR. [score:3]
Rat hippocampal neurons at DIV5 have extended a set of neuritis; however, miR-19b was knocked down, early neurite outgrowth was significantly impaired (Figure 8D). [score:2]
Longest and total neurite lengths were reduced in miR-19b knock down neurons. [score:2]
miR-19b regulates mTORC1 activity in neurons. [score:2]
About 30% of protein is increased in miR-19b knock down neurons. [score:2]
We measured inhibition of miR-19b using real time PCR. [score:1]
miR-19b changes mTOR activity in hippocampal neurons. [score:1]
PTEN (#9559, 1∶500 dilution, Cell Signaling), Phospho-S6 (#2211, 1∶1000 dilution, Cell Signaling), S6 (#2317, 1∶1000 dilution, Cell Signaling), phospho-PKCa (06-822, 1∶1000 dilution, Millipore), PKCa (#2056, 1∶1000 dilution, Cell Signaling) antibodies were used to measure miR-19b target and mTOR activity. [score:1]
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3
[+] score: 66
Of the two miRNAs predicted to target EGR2, miR-19b was downregulated, which in accordance with the increased expression of EGR2, while miR-137 was downregulated only at T1 followed by upregulation from T2 to T4. [score:14]
Rno-miR-19a, rno-miR-19b-2 and rno-miR-214 were downregulated at all four time-points, while rno-miR-137 was downregulated at T1 followed by upregulation from T2 to T4 (Fig.   6). [score:10]
The results of the present study indicate that propofol may have the ability to regulate the expression of rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214 and their target genes, ARC and EGR2. [score:6]
Rno-miR-19a (Rno, Rattus Norvegicus) and rno-miR-137, and their target gene EGR2, as well as rno-miR-19b-2 and rno-miR-214 and their target gene ARC were found to be closely related to neural developmental processes, including proliferation, differentiation, and maturation of NSCs. [score:6]
The expression of four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) and their target genes (EGR2 and ARC) were shown to be regulated by propofol in primary cultured embryonic NSCs. [score:6]
MiR-19 of the miR-17–92 cluster promotes NSC proliferation [15] and targets FoxO1 to regulate NSC differentiation through cooperation with the Notch signaling pathway [16]. [score:4]
The expression patterns obtained in the present study combined with the results of these previous reports indicate that miR-19b and miR-137 interact with EGR2 to promote proliferation and repress the differentiation of NSCs. [score:3]
The fold-change in the mean expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 ranged from -2.56 to -12.15, -2.02 to 4.61, -2.33 to -6.68 and -2.16 to -4.63, respectively (Table  5). [score:3]
In this way, we confirmed two genes (EGR2 and ARC) and four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) that exhibited at least a 2-fold change in the mean expression level following propofol treatment at all four time-points. [score:3]
Fig. 6Quantitative RT-PCR analysis of relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214. [score:3]
Relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 at all four time-points (immediately (T1), Day 1 (T2), Day 3 (T3) and Day 7 (T4) after treatment with propofol or DMSO). [score:3]
However, the potential relationship between EGR2 and miR-19b/miR-137 on the development of NSCs remains to be fully elucidated. [score:2]
MiR-19b is a member of miR-19 family located in the miR-106–25 cluster, which has been reported to be involved in regulating NSC proliferation and differentiation through a network related to the insulin/IGF-FoxO pathway [37]. [score:2]
The miRNAs predicted by all four databases (rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214, (Rno, Rattus Norvegicus)) were selected for validation (Table  4 and Fig.   5). [score:1]
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4
[+] score: 35
Relative quantification of miR-19b expression was found to be upregulated along with downregulated expression of Bcl2 (Fig. 2). [score:11]
miR-208a, miR-133b and miR-30e showed more than 2.5-fold upregulation during physiological cardiac hypertrophy, while miR-19b showcased an upregulation of 1.5 fold only. [score:7]
To be specifically mentioned (fold change >2.5), miR-208, miR-19b, miR-133b and miR-30e were significantly upregulated and miR-99b, miR-100, miR-191a, miR-22 andmiR-181a-1 were significantly downregulated. [score:7]
miR-19b positively regulates cardiomyocyte hypertrophy by targeting atrogin-1 and MuRF-1 and negatively regulates apoptosis through CN/NFAT–αCryB and Bim signaling under endoplasmic reticulum stress conditions [27]. [score:5]
We found the upregulation of miR-19b during physiological cardiac hypertrophy. [score:4]
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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5
[+] score: 33
The relative expression of miRNAs in DCM samples and healthy control samples is shown in Figure 9. We found a 2.6-fold increase in hsa-miR-340 expression (P < 0.001), a 2.4-fold increase in hsa-mir-19b expression (P < 0.01) and a twofold increase in hsa-miR-302 expression (P < 0.05) in DCM samples. [score:9]
The hsa-miR-19b and hsa-miR-302 were down-regulated in the profile analysis, but up-regulated in the quantitative RT-PCR assay. [score:6]
Van Almen et al. [29] reported that decreased hsa-miR-19 expression leads to increased expression of CTGF and TSP-1 in aged failure-prone hearts. [score:5]
The miRNAs hsa-miR-19a (12 degrees) and hsa-miR-19b (12 degrees) were significantly down-regulated in the DCM samples. [score:4]
Importantly, our study identified miRNAs, hsa-miR-19b, hsa-miR-302d and hsa-miR-340 (Fig. 9) which were significantly up-regulated in human DCM and may play a critical role in the pathophysiology of heart failure. [score:4]
Real-time PCR demonstrated that hsa-miR-19b, hsa-miR-302d and hsa-miR-340 were significantly increased (P < 0.05), which validate the results from the and implied an important role of miR-340. [score:1]
In the network, the performance differences in the most critical miRNAs (hsa-miR-340, hsa-miR-19a, hsa-miR-19b, etc. ) [score:1]
The miRNAs hsa-miR-200b (16 degrees), hsa-miR-181c (14 degrees), hsa-miR-340 (13 degrees), hsa-miR-557 (13 degrees), hsa-miR-19a (12 degrees), hsa-miR-19b (12 degrees) and hsa-miR-548f (12 degrees) were significantly differentially regulated in DCM samples compared with non-failing control samples. [score:1]
Selected miRNAs (hsa-miR-10a, miR-19b, miR-181c, miR-302d and miR-340) were further quantified with TaqMan qRT-PCR. [score:1]
The key miRNAs identified included hsa-miR-181c, hsa-miR-19a and hsa-miR-19b, which all have higher degrees in the network diagram. [score:1]
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6
[+] score: 22
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-183, rno-mir-146b
Our results showed that rno-miR-19b-3p, -146b-5p and -183-5p are significantly downregulated, and an increased level of omega-3 PUFAs can suppress inflammation in vivo by regulating the transcription of these three miRNAs, which in turn specifically suppress the expression of a set of inflammation-related genes. [score:11]
In particular, miR-19b-3p in PBMCs showed a notable downregulation trend in the AA rats and an increase in the AP rats compared to the Ct rats, and was not differentially expressed in a significant manner in the other tissues. [score:5]
Based on the results of the RT-qPCR validation, we obtained 53 experimentally verified (16) MTGs from rno-miR-19b-3p, -146b-5p and -183-5p using the miRWalk Validated Targets tool. [score:3]
These findings indicated that rno-miR-19b-3p, -146b-5p and -183-5p are regulated by the PUFA diets in the visceral fat, PBMCs, and liver tissues. [score:2]
According to these filtering criteria, certain miRNAs were excluded, and rno-miR-19b-3p, -29c, -146b-5p, -183-5p and -292-3p were selected as candidate miRNAs for RT-qPCR validation. [score:1]
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7
[+] score: 21
Analysis at P21 revealed 74 mature miRNAs with differential expression between LPD -induced IUGR rat lungs and control lungs (Fig 1): 10 showed more than twofold differential expression: miR-184, miR-127-3p, miR-378a-5p and miR541-5p were downregulated, and miR-30e-5p, miR-23b-5p, miR-451-5p, miR-1839-5p, miR-449a-5p, and miR-19b-3p were upregulated in LPD -induced IUGR versus control lungs. [score:11]
Furthermore, five deregulated miRNAs (miR-128-3p and miR-34c-5p, both downregulated at P10; miR-19b-3p, miR-449a-5p and miR-30e-5p, these three being upregulated at P21) have E2F3 in common as a target gene. [score:10]
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8
[+] score: 20
Significant mechanical allodynia was observed in rats overexpressing miR-18a, miR-19a, miR-19b or miR-92a, but not in those overexpressing miR-17 or miR-20a (Fig. 2e). [score:5]
The number of putative target genes for miR-18a, miR-19a/b (miR-19a and miR-19b have the same seed sequence) and miR-92a were 695, 1,448 and 1,138, respectively (a total of 2,834 genes). [score:3]
L5 DRGs were obtained 28 days after SNL from rats injected with mixture of AAV vectors expressing antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a 7 days after SNL. [score:3]
Only the cluster members whose overexpression reduced the mechanical paw withdrawal threshold (miR-18a, miR-19a, miR-19b and miR-92a) were examined. [score:3]
AAV vectors expressing either a control AAV vector or mixture of AAV vectors encoding TuD antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a were administered 7 days after SNL. [score:3]
Clone IDs of TuD were as follows: NC000001 (negative control), RH000611 (miR-17), RH000323 (miR-18a), RH000643 (miR-19a), RH000352 (miR-19b), RH000277 (miR-20a) and RH000184 (miR-92a). [score:1]
Furthermore, the established mechanical allodynia was reversed by injection of a mixture of AAV vectors encoding antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a 7 days after SNL (Fig. 3b). [score:1]
Error bars are s. e. m. * P<0.05, ** P<0.01 and *** P<0.001 (K [V]1.1, P=0.014 for miR-17-92 and P=0.034 for miR-18a; K [V]1.4, P<0.001 for miR-17-92; K [V]3.4, P<0.001 for miR-17-92, P=0.047 for miR-19b and P=0.009 for miR-92a; K [V]4.3, P=0.031 for miR-17-92; K [V]7.5, P=0.002 for miR-17-92, P=0.048 for miR-19a and P=0.013 for miR-19b; DPP10, P=0.003 for miR-17-92 and P=0.043 for miR-92a; Na [V]β1, P=0.002 for miR-17-92 and P=0.030 for miR-19b), Dunnett’s test. [score:1]
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9
[+] score: 18
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
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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10
[+] score: 14
In addition, only miR-19b was overexpressed in HUVECs treated with EEP (Figure 5(c)). [score:3]
In silico and in vitro analyses have suggested that miR-19b targets mRNA corresponding to the proangiogenic proteins FGFR2 and MAPK1 (ERK2). [score:3]
In addition, previous work showed that miR-19b blocks the cell cycle from the S phase to the G(2)/M phase transition by controlling the expression of cyclin D1c [35]. [score:3]
Among them, only miR-19b was overexpressed in cells treated with EEP. [score:3]
On the other hand, both EEP and Pn significantly inhibited in a dose -dependent manner the activation of HIF1 α. Finally, VEGF mRNA and microRNAs associated with angiogenesis in previous studies (miR-126, miR-19b, miR-221, miR-222, miR-27b, and miR-17) were evaluated by real-time PCR. [score:1]
In summary, the findings in the current study demonstrate that a nonapoptotic/toxic concentration of polyphenol-rich extract of Chilean propolis can modulate in vitro angiogenesis in part by modulating HIF1 α and ERK1/2 signaling pathway and mechanism involving miR-19b. [score:1]
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11
[+] score: 11
MiR-148-3p, mir-17-5p, miR-181a-5p, miR-19b-3p and miR-24-3p were predicted to control the expression of the following target genes: Interleukin 6 signal transducer IL6ST (gp130). [score:5]
Amongst the 5 miRNAs (miR148-3p, miR17-5p, miR181a-5p, miR19b-3p and miR24-3p) targeting multiple genes from our 70 genes list, mir17-5p, which is increased with stress was confirmed by qRT-PCR. [score:3]
In contrast, there was no change in the expression of mir148-3p or mir19b-3p (Fig 5). [score:3]
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12
[+] score: 9
Inhibition of FGF signaling through SU5402 -treated primitive streak regions of chick embryos identified up-regulation of let-7b, miR-9, miR-19b, miR-107, miR-130b, miR-148a, miR-203, and miR-218 and down-regulation of miR-29a and miR-489 (Bobbs et al. 2012). [score:9]
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13
[+] score: 9
In contrast, Arc -regulating miR-34a, miR-326, miR-19 and miR-193a were not significantly regulated, although there was trend for miR-34a upregulation at 30 minutes post-BDNF (p = 0.07). [score:6]
Interestingly miR-19, miR-34 and miR-326 are all dysregulated in multiple sclerosis patients [62]. [score:2]
Three nucleotides in the seed -binding region of miR-34, -193, -326, -378 and -512_5p were mutated in the Arc 3′UTR and the whole seed binding region was removed for miR-19. [score:1]
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14
[+] score: 9
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-26b, rno-mir-203a, rno-mir-203b
Fish oil/pectin treatment up-regulated miR-19b, miR-26b and miR-203 expression as compared to corn oil plus cellulose (CCA) specifically in Lgr5 (high) cells. [score:5]
They further demonstrated that only miR-19b and its indirect target PTK2B were modulated by the fish oil/pectin diet in Lgr5 (negative) cells. [score:4]
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15
[+] score: 9
Cells were divided into six groups: control group (normal cardiomyocytes), PE + NC group (PE mo del transfected with negative control), PE + miR19 mimics group (PE mo del transfected with miR-19a-3p mimics), PE + miR19 inhibitor group (PE mo del transfected with miR-19a-3p inhibitor), PE + miR19 mimics + SFI group (PE mo del transfected with miR-19a-3p mimics, and treated with SFI 10 um/ml) and PE + miR19 inhibitor + SFI group (PE mo del transfected with miR-19a-3p inhibitor, and treated with SFI 10 um/ml). [score:9]
[1 to 20 of 1 sentences]
16
[+] score: 7
[67] On the other hand, MECP2, a transcriptional regulator targeted by miR-19, miR-30e and miR-365, binds to methylated DNA and has been shown to contribute to early life stress -dependent epigenetic programming of HPA axis -associated genes. [score:4]
[63] A large number of cyclic AMP-specific PDEs are also targets of multiple miRNAs (miR-101a, miR-124, miR-721, miR-137, miR-19b, miR-30e, miR-365). [score:3]
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[+] score: 7
Of these, miR-500-3p, miR-23b-3p, miR-200a-3p, miR-19b-3p, miR-92a-1-5p, miR-21-5p, miR-21-3p, miR-1843-3p, miR-223-3p, miR-3473, and miR-129-2-3p were found to be upregulated, whereas miR-92b-3p, miR-3102, and miR-3577 were found to be downregulated in the rat brain. [score:7]
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18
[+] score: 7
miR-19b was found to inhibit TGF-β signaling, and its expression decreased in patients with advanced fibrosis, suggesting the potential of miR-19b as a therapeutic target for hepatic fibrosis [17]. [score:7]
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19
[+] score: 6
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-19a, rno-mir-27a, rno-mir-217
org/)] were used, and four miRs (i. e., miR-19a, miR-19b, miR-27a, and miR-217) were predicted to target the 3′-untranslated region (3′ UTR) of GRK6 according to the score (the sequence comparison is shown in Supplementary Fig. S3a). [score:5]
The sequences of the rno-miR-27a mimics were: 5′-UUC ACA GUG GCU AAG UUC CGC-3′ and 5′-GGA ACU UAG CCA CUG UGA AUU-3′; rno-miR-19a mimics were: 5′-UGU GCA AAU CUA UGC AAA ACU GA-3′ and 5′-AGU UUU GCA UAG AUU UGC ACA UU-3′; rno-miR-19b mimics were: 5′-UGU GCA AAU CCA UGC AAA ACU GA-3′ and 5′-AGU UUU GCA UGG AUU UGC ACA UU-3′; rno-miR-217 mimics were: 5′-UAC UGC AUC AGG AAC UGA CUG-3′ and 5′-AGU CAG UUC CUG AUG CAG UAU U-3′. [score:1]
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20
[+] score: 5
We found clear upregulation of miR-146a and miR-155, but not of miR-29a, miR-29b, miR-19b, or miR-20a in skin (Figure 4A and data not shown). [score:4]
Both miR-17 and miR-19, as representatives of the miR-17-92 cluster, were tested in all tissues, but no changes were observed between controls and aGvHD rats (data not shown). [score:1]
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[+] score: 5
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-143, rno-mir-145, rno-mir-146a
It has reported that miR-19b decreased COL-I expression 32, while miR-146a induced α-SMA expression 33. [score:5]
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[+] score: 5
Other miRNAs from this paper: 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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
First, a subgroup of miRNAs (miR-15b-5p, miR-17-5p, miR-18a-5p, miR-19a-3p, miR19b-3p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23b-5p, miR-24-3p, miR-27a-3p, miR-92a-3p, miR-93-5p, miR-142-3p, miR-344b-2-3p, miR-431, miR-466b-5p and miR-674-3p) displayed increased expression levels during latency (4 and 8 days after SE), decreased their expression levels at the time of the first spontaneous seizure and returned to control levels in the chronic phase (Fig. 2, Supplementary Fig. S1). [score:5]
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[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
For instance, among the 66 uniformly expressed miRNAs for which IPA assigned functions, we identified 12 candidates that have been implicated in androgen regulation, including: let-7a-5p, miR-15a-5p, miR-17-5p, miR-19b-3p, miR-23a-3p, miR-24-3p, miR-27b-3p, miR-30a-5p, miR-34a-5p, miR-140-5p, miR-193a-3p, miR-205-5p (S1 Fig). [score:4]
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24
[+] score: 4
Ventral combined with dorsal root avulsion resulted in a sustained upregulation of 10 miRNAs, including miR-19b-3p, miR-20b-5p, miR-21-5p, miR-27a-3p, miR-29b-3p, miR-106b-3p, miR-142-3p, miR-322-5p, miR-352, and let-7a-5p (Figure  2E). [score:4]
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25
[+] score: 4
Note relatively higher expression of 3′ members of the cluster, miR-20a, miR-19b, and miR-92. [score:3]
D. Age -dependent decline in miR-19b and -92. [score:1]
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[+] score: 4
Recent studies revealed that miR-19b, miR-30a, miR-301a promoted the progression of periodontitis [4] and miR-146a, miR-98 were upregulated to contribute to the progression of OA [10]. [score:4]
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[+] score: 3
Other miRNAs from this paper: rno-mir-19b-1, rno-mir-181b-1, rno-mir-181b-2, rno-mir-185
For example, miR-181b in serum may be a potential diagnostic biomarker for cirrhosis 24, and miR-19b was found to be up-regulated 4.3-fold in the serum of individuals with cirrhotic livers, compared with normal controls 18. [score:3]
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[+] score: 3
In hippocampus, a total of 475 targets of rno-miR-101b-3p, rno-miR-217-5p, rno-miR-375-3p, rno-miR-20a-5p, rno-miR-19b-3p, and rno-miR-182 were predicted. [score:3]
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[+] score: 3
Other miRNAs from this paper: rno-mir-10b, rno-mir-19b-1
Although this could suggest that such differences are due to the changes to somatic cells as a result of the nutritional exposure, Grandjean et al. went on to show that microinjection of miRNA mir-19b, which had increased expression in the testis and epididymal sperm of HFD fed mice, into one-cell embryos resulted in an altered metabolic phenotype mirroring that of offspring of HFD exposed fathers 14. [score:3]
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[+] score: 3
In our previous study [12], we found that miR-17, miR-19a, miR-20a, miR-19b and miR-92a, but not miR-18a, were highly expressed in the heart of C57BL/6 mice. [score:3]
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[+] score: 3
At neonatal stage (around P0), when the majority of pyramid neurons have already migrated to their destinations and are extending axons and dendrites [31], we found high expression of several miRNAs at this stage, i. e. rno-miR-137 and rno-miR-19b. [score:3]
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32
[+] score: 3
miR-19b, -106a, and -629 have been confirmed differentially expressed in colon tissues of endoscopic pinch biopsies between UC and CD patients [15]. [score:3]
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33
[+] score: 2
For example, Pparα (regulates metabolic pathways) was found to harbor putative binding sites for miR-19b/351 (5 algorithms), miR-17-5p (3 algorithms), miR-214 and -503 (2 algorithms). [score:2]
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34
[+] score: 2
MiR-17-5p belongs to the miR-17~92 cluster, located on the human chromosome 13q31, and is a prototypical example of a polycistronic miRNA gene encoding six miRNAs (miR-17-5p, miR-18, miR-19a, miR-19b, miR-20 and miR-92). [score:1]
This cluster has two paralogs, miR-106a~363 (miR-106a, miR-18b, miR-19b-2, miR-20b, miR-92a-2 and miR-363, located on the X chromosome) and miR-106b~25 (miR-106b, miR-93, and miR-25, located on human chromosome 7), which are located on different chromosomes but contain individual miRNAs that are highly similar to those encoded by the miR-17~92 cluster [36, 37]. [score:1]
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[+] score: 2
The following miRNAs, also present in the VTMs list of Fig 5, were found by RT-PCR to be dysregulated in mouse lung tissue: miR-21, miR-146, miR-20, miR-302, miR-19, miR-98, let-7a, miR-15a. [score:2]
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36
[+] score: 1
Among the spleen-specific miRNAs identified, five of them belong to the mir17 miRNA cluster, which comprise miR-17, miR-18, miR-19a, miR-19b, miR-20, miR-25, miR-92, miR-93, miR-106a, and miR-106b [59]. [score:1]
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37
[+] score: 1
Further, miR-19 appears to affect the level of proapoptotic protein Bim, thereby preventing apoptosis and promoting cell survival. [score:1]
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38
[+] score: 1
33rno-miR-19b−1.590.33rno-miR-451−4.370.05rno-miR-196c*−1.660.32Tissue/LungLog2(infected/control)Fold changemmu-miR-32*−2.170.22rno-miR-2062.234.69mmu-miR-328*−2.630.16rno-miR-2231.823.53rno-miR-32*−2.850.14rno-miR-981.22.3mmu-miR-468−3.490.09mmu-miR-4681.192.28mmu-miR-691−4.040.06mmu-miR-669d1.112.16mmu-miR-297a−4.620.04rno-miR-328a*1.12.14mmu-miR-467h−4.960. [score:1]
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[+] score: 1
Therefore, ten miRNAs (miR-19b-3p, miR-21-5p, miR-25-3p, miR-30a-5p, miR-133b-3p, miR-140-5p, miR-150-5p, miR-199a-3p, miR-342-5p, miR-3473) were chosen as candidate reference genes. [score:1]
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40
[+] score: 1
In the order of genome location, the cluster then reads: mir-106a, HN-14/MP-56/RP-100, mir-19b-2, mir-92-2, and HP-85/MN-8/RP-99. [score:1]
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[+] score: 1
In addition, the neural progenitor cells isolated by LCM exhibited increases in miR-146a, miR-146b, miR-210, miR-19b and miR-378 and decreases in miR-128, miR-291a-3p, and miR-139-5p (Fig. 3A to 3C), which are consistent with the array data findings. [score:1]
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[+] score: 1
Most changes were modest in magnitude, with two–thirds showing a fold change less than ±0.40 and only four miRNA (miR-181c-5p, miR-19b-3p, miR-218a-5p, miR-9a-5p) showing more than a twofold change. [score:1]
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