sort by

37 publications mentioning rno-mir-15a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-15a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 276
Other miRNAs from this paper: rno-mir-15b, rno-mir-16, rno-mir-30d, rno-mir-20b
The finding that NOX and JNK inhibitors could largely prevent hyperosmolarity -induced upregulation of miR-15a, -15b and -16 expression (Figs 3 and 6) indicates that these miRNAs, either directly or indirectly, respond to ROS. [score:10]
In order to identify the footprint of miR-15a, -15b and -16 on gene expression in a genome wide scale, putative miR-15b and -16 targets obtained from the miRWalk algorithm (771 predicted targets) were compared with the downregulated genes at 180 minutes after hyperosmotic exposure (721 genes). [score:9]
The finding that both, apocynin and SP600125 were able to inhibit hyperosmolarity -induced upregulation of pre-miR-15a (Fig. 3d and Fig. 6d), strongly supports the hypothesis that expression of miR-15a is regulated by ROS at transcriptional level. [score:9]
Next, we examined whether the observed upregulation of miR-15a, -15b and -16 was sufficient to downregulate their targets at protein level. [score:9]
Overall, these findings implicate that signaling pathways activated by hyperosmotic hepatocyte shrinkage downregulate the expression of anti-apoptotic genes, which are either validated (Bcl2 and Ccnd1) or predicted (Mcl1) miR-15/16 targets. [score:8]
We found that the expression of miR-15a, miR-15b and miR-16 was significantly upregulated following perfusion of rat livers with hyperosmotic solution, whereas hypoosmotic perfusion had no significant effect on the expression level of these microRNAs (Fig. 1a-c). [score:8]
In order to identify additional putative targets of miR-15a, -15b and -16 that could be involved in regulation of cell death or survival we queried two different target prediction databases miRWalk and MicroCosm for miR-15b and miR-16 predicted targets. [score:8]
Altogether, these data show that Faim expression is inversely correlated to miR-15a/b and miR-16 expression, suggesting that Faim could be a novel functional target of miR-15a, -15b and -16. [score:7]
These findings suggest that NOX activity is required to mediate both the upregulation of miR-15a, -15b and -16 and the downregulation of Bcl2, Ccnd1, Mcl1 and Faim under hyperosmotic conditions. [score:7]
Upregulation of miR-15a/b and miR-16 by hyperosmolarity in perfused rat liver is blocked and downregulated by administration of apocynin. [score:7]
Notably, the levels of miR-15a (p = 0.0031 after 60 minutes, p = 0.0184 after 120 minutes, p = 0.0062 after 180 minutes) and miR-16 (p = 0.0245 after 60 minutes) were significantly upregulated by this treatment (Fig. 5a), while Bcl2 (p = 0.0421 after 30 minutes, p = 0.0131 after 180 minutes) and Faim (p = 0.022 after 180 minutes) were significantly downregulated (Fig. 5b). [score:7]
Hence, to gain an insight into the correlation between the observed upregulation of miR-15a, -15b and -16 and the downregulation of anti-apoptotic genes, extensive bioinformatics analyses of data sets were carried out. [score:7]
Specifically, expression of miR-15a, miR-15b and miR-16 was found to be significantly upregulated in the livers of hyperosmotically perfused rats. [score:6]
miR-15a, -15b and -16 upregulation could contribute to cell death through the inhibition of anti-apoptotic genes. [score:6]
Specifically, miR-15a was found to be significantly upregulated at both 60 minutes (5.3-folds, p = 0.0002) and 120 minutes (5.3-folds; p = 0.0001) compared to the preperfusion state (defined as T0), while miR-15b (1.7-folds; p = 0.006) and miR-16 (2.1-folds; p = 0.0078) were both found significantly upregulated at 60 minutes after perfusion of the livers with hyperosmotic solution. [score:6]
Altogether, these data indicate that the upregulation of miR-15a, -15b and -16 might repress the expression of several anti-apoptotic genes potentially impairing cell survival. [score:6]
Interestingly, miR-15a, -15b and -16 are known as tumor-suppressor miRNAs as their activity directly represses the expression of anti-apoptotic genes such as Bcl2 (validated in human, mouse and rat 23 24), Ccnd1 (validated in human, mouse and rat 25) and protein carboxyl-O-methyltransferase (Pcmt1; validated in human 26). [score:6]
The expression of members of the miR-15 family is upregulated in response to hyperosmotic stimulation. [score:6]
How to cite this article: Santosa, D. et al. Hyperosmotic stress activates the expression of members of the miR-15/107 family and induces downregulation of anti-apoptotic genes in rat liver. [score:6]
qPCR validation of the 18 putative targets of miR-15a, miR-15b and miR-16 detected as significantly downregulated by Affymetrix arrays in hyperosmotically perfused livers. [score:6]
Specifically, statistical analysis with unpaired student’s t-test indicates that miR-15a and miR-16 were significantly downregulated, while miR-15b expression was unchanged after addition of apocynin (Fig. 3). [score:6]
Our data indicate that different types of regulation might be active, as a significant upregulation was observed for the pre-miR-15a (Supplementary Figure 3a) under hyperosmotic stimulation, whereas levels of pre-miR-16 were unchanged (Supplementary Figure 3b). [score:5]
ROS formation activates JNK 4 which may directly or indirectly regulate transcription factors being required for the regulation of apoptotic genes and the biogenesis of the miR-15/107 family. [score:5]
Fas apoptotic inhibitory molecule is a novel potential target of the miR-15 family. [score:5]
Mcl1 is indicated in the literature as validated miR-15a target in humans, however to the best of our knowledge, this interaction has never been experimentally validated and, for the purpose of this study, Mcl1 is included as miR-15a predicted target 27. [score:5]
analyses further revealed that the seed sequences of the miR-15 family are around 2,2 kb downstream of the 3′UTR of Bcl2, potentially targeting this miRNA which leads to inhibition. [score:5]
Noticeably, miR-15a, -15b and -16 are tumor suppressor miRNAs, as reduction in their expression either caused by the deletion of the genomic locus containing the miR15a/16 cluster or epigenetic silencing is frequently detected in B-cell chronic lymphocytic leukemia (CLL). [score:5]
Upregulation of miR-15a/b and miR-16 by hyperosmolarity in perfused rat liver. [score:4]
Above all, miR-15a, -15b and -16 are thought to regulate apoptosis through the inhibition of anti-apoptotic genes including Bcl2 and Ccnd1 23 25. [score:4]
Upregulation of miR-15a/b and miR-16 by hyperosmolarity in perfused rat liver is blocked by administration of SP600125. [score:4]
Further studies are required to substantiate the link between hyperosmotic Egr1/Foxo3 regulation and miR-15/16 expression. [score:4]
These data point to a transcriptional regulation of miR-15a expression. [score:4]
Benzylamine upregulates miR-15a/16 in a NAC-sensitive manner. [score:4]
Our analysis identified that pre-miR-15a was significantly upregulated under hyperosmotic conditions (Supplementary Figure 3a), while this effect was blocked by administration of apocynin (Fig. 3d). [score:4]
Apocynin leads to downregulation of the miR-15a and miR-16 in rat livers perfused with hyperosmotic solution. [score:4]
Next, we evaluated the effect of SP600125 on the expression levels of miR-15a, -15b and -16 target genes. [score:3]
Importantly, our analysis suggests that the transcription factors Foxo3 and Egr1 could be possible drivers of the hyperosmotic-specific activation of miR-15/16 expression. [score:3]
qPCR validation of potential target genes of the miR-15a/b and miR-16. [score:3]
Through this analysis, Faim, Aatf, Bfar and Ikbkb were identified as novel putative targets of miR-15a, -15b and -16 in the rat (Supplementary Figure 5). [score:3]
Importantly, Bcl2 was selected as it was recently shown that miR-15a, -15b and -16 directly regulate the 3′UTR of rat Bcl2 24. [score:3]
Moreover, these miRNAs, which are all members of the miR-15/107 family, serve key functions as they are known for repressing the expression of genes involved in cell division and metabolism 47. [score:3]
Next, qPCR was used to evaluate whether Faim expression levels are inversely correlated with miR-15a, -15b and -16 expression in hyperosmotically perfused livers (Fig. 2d). [score:3]
mRNA analysis of target genes of the miR-15 family under hyper- and normoosmotic conditions in perfused rat liver. [score:3]
Altogether, these findings indicate that the expression levels of miR-15a, -15b and -16 are rapidly modulated in response to hyperosmotic stress. [score:3]
Interestingly, literature search indicates the anti-apoptotic gene Mcl1 as a miR-15a target 47. [score:3]
ROS -mediated activation of JNK is required to activate the expression of miR-15a, miR-15b and miR-16. [score:3]
However, this report could not be validated and, to the best of our knowledge, Mcl1 has been reported only as miR-15a predicted target in human 27. [score:3]
Applying this approach, two putative binding sites for miR-15b and -16 were identified in the 3′UTR of Faim at positions 493/513 (rno-miR-16) and 292/313 (rno-miR-15b and rno-miR-16), suggesting that Faim could be a novel target for miR-15/16. [score:3]
Reason for miR-15a exclusion from the query is that rno-miR-15a was only recently added to the miRNA repository database miRbase (miRbase v21, release June 2014), hence, to date no pre-compiled target predictions for miR-15a are available for the rat transcriptome. [score:3]
We found that SP600125 largely counteracted the hyperosmotic activation of miR-15a, -15b, -16 and pre-miR-15a expression (Fig. 6). [score:3]
Importantly, correlation among the 57 genes included in this GO term with literature mining suggests that the transcription factors Foxo3 and Egr1 are potential candidates for mediating the transcriptional regulation of miR-15a, -15b and -16 39 40. [score:2]
In order to evaluate whether miRNA expression was regulated at the transcriptional level, expression of miR-15a precursor (pre-miR-15a) was measured by using miQPCR. [score:2]
Overall, these data confirm that the observed regulation of miR-15a, -15b and -16 by hyperosmolarity is down-stream to NOX and requires JNK activity. [score:2]
In order to investigate whether ROS formation is involved in the regulation of miR-15a,-15b and -16, a new set of hyper- and normoosmotic perfusion experiments using the NOX inhibitor apocynin was performed. [score:2]
miR-15a, miR-15b and miR-16 are conserved between human, mouse and rat genome. [score:1]
Notably, these miRNAs belong to the miR-15/107 family, which comprises 10 paralogous miRNAs sharing the same seed sequence AGCAGC 22. [score:1]
qPCR was carried out in 5 independent experiments for miR-15a/b and miR-16 in hyper-, hypo- and normoosmotically treated samples. [score:1]
miR-15a levels are stable in the normoosmotic controls. [score:1]
Altogether, these data indicate that NOX activation is required to modulate the activation of miR-15a, -15b and -16. [score:1]
Transcription factors Foxo3a and Egr1 are potential candidates in the modulation of the miR-15 family. [score:1]
The analysis identified that apocynin was able to block the hyperosmotic activation of miR-15a, -15b and -16 (Fig. 3). [score:1]
Taken together, these findings strengthen the view that ROS is required to mediate the observed response and that miR-15a, -15b and -16 are redoximiRs. [score:1]
Overall, these findings support the hypothesis that miR-15a, -15b and -16 are redoximiRs. [score:1]
of the miR-15a/b and miR-16 was carried out by using the miRWalk algorithm. [score:1]
Following, the expression of miR-15 family members was measured by miQPCR. [score:1]
[1 to 20 of 65 sentences]
2
[+] score: 44
It was reported that miR-15 family members were upregulated in infarct region of pigs [15] but downregulated in both border and infarct zone of mice [17] in response to myocardial infarction, while they were found to be up-regulated in the overloaded heart in multiple species [19]. [score:10]
We noted that miR-15 family members may be upregulated, downregulated or unchanged in response to various cardiac stresses (Supplementary Material, Figure S1). [score:7]
Although miR-15 family members share similar structure and some common targets, they can also exert distinct role in the pathogenesis of cardiovascular disease. [score:5]
Anti-miR chemistries suppressing miR-15 in mice were reported to reduce myocardial infarct size [15], while inhibition of either miR-15a or miR-16 enhanced post-ischemic neovascularization [19]. [score:5]
MiR-15 and miR-16 were reported to induce apoptosis by inhibiting Bcl-2 [18]. [score:3]
The miR-15 family members including miR-15a, miR-15b, miR-16, miR-195, miR-424, and miR-497, show 5′-end sequence similarity and many common targets [16, 17]. [score:3]
Similar to our findings on miR-497, Hullinger et al has demonstrated that miR-15b, also a member of miR-15 family, aggravates myocardial IR injury by targeting Bcl-2 [15]. [score:3]
The expression heterogeneity of miR-15 family members was also supported by previous studies. [score:3]
The regulation of miR-15 family is spatial, temporal and dynamic [15, 17]. [score:2]
It was reported miR-195 increases cardiac hypertrophy [27] and worsens systolic dysfunction in mice with MI [17], while miR-15b, another member of the same miR-15 family, was found to attenuate myocardial fibrosis and hypertrophy in pressure-overloaded mice [19]. [score:1]
Recent studies have shown that the miR-15 family can worsen or alleviate myocardial ischemia and heart failure [13– 15]. [score:1]
The expressions of other members of miR-15 family in cardiomyocytes or heart subjected to AR or MI or pressure overload induced by transverse aortic constriction were also investigated. [score:1]
[1 to 20 of 12 sentences]
3
[+] score: 23
miR-15a overexpression leads to a decrease in the number, but an increase in the size, of murine adipocytes by inhibiting Delta-like 1 homolog expression [29]. [score:7]
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]
Some of the circulating miRNAs identified in this study have also been reported in the adipose tissue of DIO mice or implicated in adipogenic processes [11– 13], including Let-7, miR-103, miR-15, the miR-17-92 cluster (miR-17, miR-20a, and miR-92a), miR-21, miR-221, and miR-30b. [score:1]
In a study of miRNA libraries reconstructed from pre- and post-differentiated 3T3-L1 cells, it was noted that miR-15a may not be related to the actual differentiation process, but it may induce growth arrest and/or hormonal stimulation [30]. [score:1]
[1 to 20 of 5 sentences]
4
[+] score: 20
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-193b
Among them are two polycistronic transcripts (miR-15a~16-1 and miR-193b~365-1), and two expressing single miRNAs (miR-148a and miR-155). [score:3]
The predicted genomic coordinates of pri-miRNAs are provided in Additional file 1. Here, we describe in detail the annotation of the pri-miRNA containing miR-15a and miR-16-1. The structure of a polycistronic transcript expressing miR-15a and miR-16-1 is strongly supported by all seven types of transcriptional features. [score:3]
The predicted genomic coordinates of pri-miRNAs are provided in Additional file 1. Here, we describe in detail the annotation of the pri-miRNA containing miR-15a and miR-16-1. The structure of a polycistronic transcript expressing miR-15a and miR-16-1 is strongly supported by all seven types of transcriptional features. [score:3]
The structure of a polycistronic transcript expressing miR-15a and miR-16-1 is strongly supported by all seven types of transcriptional features. [score:3]
These data agree with previous annotation by the VEGA project of non-protein-coding transcripts (accessions: OTTHUMT00000044959 and OTTHUMT00000044961) expressing miR-15a and miR-16-1 in human, called DLEU2 [39]. [score:3]
In human, we predict 8 TSSs with an average distance of 32,242 bp upstream of miR-15a. [score:1]
miR-15a~16-1. Species-specific (Group III and IV) pri-miRNAs. [score:1]
Taking all these features together, we annotate the 5' end of the human pri-miRNA at ~33 kb upstream of miR-15a. [score:1]
The features mapped to the flanking regions surrounding the hsa-mir-15a~16-1 are shown (Figure 6). [score:1]
Figure 6 Transcription features mapped in the flanking regions surrounding the cluster mir-15a~16-1 in human. [score:1]
[1 to 20 of 10 sentences]
5
[+] score: 19
Other miRNAs from this paper: hsa-mir-15a
miR15a overexpression in PCK cholangiocytes decreases Cdc25A levels, inhibits cell proliferation, and reduces cyst growth, indicating a potential therapeutic strategy for the disease. [score:7]
In addition, PCK cholangiocyte hyperproliferation is accompanied by the overexpression of Cdc25A protein and the downregulation of miR15a [26, 57]. [score:6]
The biliary epithelium of CHF overexpresses Cdc25A protein (an isoform of Cdc25), which is accompanied by the downregulation of a microRNA (miR15a) [26]. [score:6]
[1 to 20 of 3 sentences]
6
[+] score: 15
Furthermore, our findings that the expression of miR-21 and miR-15 was significantly lower in MSC-Exo compared to MSC, which are in line with previous reports that downregulation of miR-21 prevents hypertrophy [39] and inhibition of miR-15 prevents cardiac ischemic injury [40]. [score:7]
To further characterize the difference of miRNA expression between MSC-Exo and MSCs, the hierarchical cluster of miRNA expression was made, which indicated that the expression of several miRNAs (including miR-15) derived from MSC-Exo was significantly different from that of MSCs (Figure 3(b)). [score:5]
For example, the expression of miR-21 and miR-15, which regulate cardiac functions, was significantly lower in MSC-Exo compared to that in MSCs (Figure 4(a)). [score:3]
[1 to 20 of 3 sentences]
7
[+] score: 14
Other miRNAs from this paper: rno-mir-140, rno-mir-16, rno-mir-23b, rno-mir-203a, rno-mir-203b
MyD88, a key adaptor protein for IL-1R and Toll-like receptors that was recently found to modulate myoblast fusion [33], is targeted by miR-203, and this results in the downregulation of MyD88 expression [34]; miR-15a and miR-16 were shown to repress the expression of Wnt3a [35]; and the miRNA-23b cluster was reported to inhibit the expression of Smad4 [36]. [score:14]
[1 to 20 of 1 sentences]
8
[+] score: 12
So we paid more attention to miR-15a, miR-15b, miR-16, miR-195, miR-424 and miR-497, which are the targeted results for CX3CL1 in the Targetscan Database. [score:5]
In order to investigate whether some micro -RNA contained in the MVs played a role, we searched CX3CL1 in the TargetScan database (version 6.2) and identified six putative micro -RNA (miR-15a, miR-15b, miR-16, miR-195, miR-424 and miR-497) targets to CX3CL1 mRNA by matching the seed regions of each. [score:3]
Interestingly, the miR-16, miR-15b and miR-15a were profiled successfully both in hWJMSCs and hWJMSC-MVs by the real-time quantitative PCR method with a high concentration, and we think that these micro -RNAs contained in MVs may involve the modulation of CX3CL1 expression. [score:3]
The real-time quantitative PCR analysis indicated that there were relatively high levels of miR-15a, miR-15b and miR-16 contained in hWJMSC-MVs, but none or low levels of miR-195, miR-424 and miR-497 (Figure  7B). [score:1]
[1 to 20 of 4 sentences]
9
[+] score: 9
The deletion of the miR15/16 family is causally linked to chronic lymphocytic leukemia, suggesting that miR-15b has a tumor suppressor/pro-apoptotic function [21]. [score:3]
Hullinger TG Inhibition of miR-15 protects against cardiac ischemic injuryCirc. [score:3]
Yue J Tigyi G Conservation of miR-15a/16-1 and miR-15b/16-2 clustersMamm. [score:1]
Indeed, in animal mo dels of myocardial infarction, antagomirs to miR-15 reduced infarct size and enhanced cardiac function [31]. [score:1]
The high conservation of the miR-15/16 clusters among 44 vertebrate species, including humans and primates, suggests conservation of function [22] with implications for human TBI. [score:1]
[1 to 20 of 5 sentences]
10
[+] score: 8
For example, it has been shown that miR-21 expression is downregulated in early diabetic nephropathy [41], while miRNA-15a is closely associated with polycystic kidney disease [42]. [score:8]
[1 to 20 of 1 sentences]
11
[+] score: 8
For example, miR-145 and miR-15a are down-regulated in GH and pituitary adenomas, respectively [23, 24]. [score:4]
miR-15a and miR-16-1 down-regulation in pituitary adenomas. [score:4]
[1 to 20 of 2 sentences]
12
[+] score: 7
It has been shown that miR-29, miR-15 and miR-107 are upregulated; while miR-124, miR-34 and miR-153 are downregulated in patients with AD (Delay et al., 2012; Lau et al., 2013). [score:7]
[1 to 20 of 1 sentences]
13
[+] score: 7
Conversely, changes in microRNA expression may reduce the activation of the inflammatory NF-κB Ρpathway; for example, this may have occurred via the decreased expression of miR-124 and miR-181b at 3 and 7 days after injury and the increased expression of miR-15, miR-223 and miR-146a (Table 8). [score:7]
[1 to 20 of 1 sentences]
14
[+] score: 7
Taxol down-regulated miR-192, miR-217 and miR-377 in remnant kidney, while it up-regulated miR-15a by microarray (Figure 5B, C) and real-time PCR analyses (Figure 5D). [score:7]
[1 to 20 of 1 sentences]
15
[+] score: 6
Knocking-down other stroke -induced miRNAs miR-497 and miR-15a was also reported to be beneficial by increasing the expression of their common target Bcl2 which is an important anti-apoptotic protein [10], [11]. [score:6]
[1 to 20 of 1 sentences]
16
[+] score: 6
There were no significant changes in the expression of miR-15, miR-30, and miR-133a between healthy subjects and patients with burn injury. [score:3]
MiR-15, miR-133a, and miR-30 also had P [CT] > 0.75. [score:1]
We assessed the levels of let-7b, let-7e, miR-194, miR-15, miR-133a, miR-15, and miR-195 (as a non-specific control) by real-time PCR. [score:1]
MiR-195, let-7e, miR-15, miR-133a, and miR-30 did not show any significant difference between burn rats and sham rats (Figure 1A) (P>0.05). [score:1]
[1 to 20 of 4 sentences]
17
[+] score: 5
The losartan treatment had no significant effect on the expression of miR-15a-5p, -24, -214, and -320 in the heart. [score:3]
In addition, miR-1, miR-15 and miR-21 can directly influence the survival of cardiomyocytes. [score:2]
[1 to 20 of 2 sentences]
18
[+] score: 5
A second a group of miRNAs whose expression is higher in the vesicles-enriched pellets (i. e., Let-7a, miR-15b, -142-3p and -98, Fig. 5, right column) and a third group of miRNAs which presents comparable expressions in both groups (i. e., miR-15a, -16, -155, -21, -18a and RNU6, Fig. 5, middle column). [score:5]
[1 to 20 of 1 sentences]
19
[+] score: 4
In contrast, proapoptotic miRNAs are usually downregulated in cancer, and include miR-15, miR-16, the let-7 family and members of the miR-34 family. [score:4]
[1 to 20 of 1 sentences]
20
[+] score: 4
miR-15a and miR-16 regulate serotonin transporter expression in human placental and rat brain raphe cells. [score:4]
[1 to 20 of 1 sentences]
21
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, 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-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]
[1 to 20 of 1 sentences]
22
[+] score: 4
The first documentation of a miRNA abnormality in cancer was reported by Croce and colleagues in 2002, who found that two miRNAs, miR-15 and miR-16, were lost or down-regulated in most patients with chronic lymphocytic leukaemia (CLL) [18]. [score:4]
[1 to 20 of 1 sentences]
23
[+] score: 4
In comparison with lung recipients without BOS, clear dysregulation of miR-34a, miR-193b, miR-9 and miR-15a, likewise present in the VTM list in Fig 5, was also detected in peripheral mononuclear cells obtained from BOS patients in a RT-PCR evaluation of miRNA expression by Xu at al. [3]. [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]
[1 to 20 of 2 sentences]
24
[+] score: 3
GRN expression is also under the post-transcriptional control of miR-107 (a member of a miRNA group also including miR-15, miR-16, miR-103, miR-195, miR-424, miR-497, miR-503, and miR-646), with implications for brain disorders (Wang et al., 2010). [score:3]
[1 to 20 of 1 sentences]
25
[+] 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-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, 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-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, 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-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, 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-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
These miRNAs (miR-15a, miR-30, miR-182, and miR-804) are involved in cell proliferation, apoptosis, inflammation, epithelial-mesenchymal transition, invasion, oncogene inhibition, and intercellular adhesion. [score:3]
[1 to 20 of 1 sentences]
26
[+] score: 3
However, there is no experimental evidence on the effect of miR-16 on cardiac ischemia, although a member of the miR-15 family miR-15a has been proven to participate in the regulation of myocyte proliferation and apoptosis [3, 31]. [score:2]
miR-16 located at 13q14, which is identified as miR-15 miRNA cluster that includes miR-15a, miR-15b, miR-16, miR-195, and miR-497 [25]. [score:1]
[1 to 20 of 2 sentences]
27
[+] 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-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-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, 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]
[1 to 20 of 1 sentences]
28
[+] score: 3
Hullinger TG Inhibition of miR-15 protects against cardiac ischemic injuryCirc. [score:3]
[1 to 20 of 1 sentences]
29
[+] score: 3
We found that miRNAs with higher expression in WBCs includes different miRNA families: mir-15, mir-17, mir-181, mir-23, mir-27 and mir-29 families. [score:3]
[1 to 20 of 1 sentences]
30
[+] score: 2
MiR-195, an important member of the miR-15 family, plays a crucial role in regulating cell cycle progression and cell apoptosis [15]. [score:2]
[1 to 20 of 1 sentences]
31
[+] score: 2
In type 2 diabetes, plasma levels of miR-15a decreased in patients [33]. [score:1]
5 mmu-miR-214 -1.7 -6.1 -10.9 mmu-miR-137 -31.7 -6.8 -144.8 mmu-miR-29c -1.8 -10.5 -10.7 rno-miR-532–5p -2.0 -59.1 -126.9 mmu-miR-466d-3p -2.7 -4.2 -9.9 mmu-miR-466d-5p -23.2 -64.7 -105.7 mmu-miR-22 -1.6 -4.6 -9.9 mmu-miR-582–5p -21.3 -59.4 -97.1 mmu-miR-690 -1.9 -2.1 -9.7 rno-miR-421 -21.3 -59.3 -97.0 mmu-miR-193 -4.9 -3. 5 -8.1 mmu-miR-369–5p -20.9 -58.3 -95.3 mmu-miR-27b* -2.1 -2.9 -8.0 mmu-miR-684 -20.8 -58.1 -94.9 mmu-miR-378 -1.6 -4.6 -7.7 mmu-miR-375 -20.6 -57.6 -94.2 mmu-miR-9* -1.9 -18.4 -7.7 mmu-miR-337–5p -20.5 -57.4 -93.8 mmu-miR-204 -2.5 -5.3 -7.5 mmu-miR-15a* -20.3 -56.8 -92.8 mmu-miR-28* -1.9 -3.2 -6.5 mmu-miR-532–5p -19. [score:1]
[1 to 20 of 2 sentences]
32
[+] score: 1
Other miRNAs from this paper: hsa-mir-15a, hsa-mir-16-1, hsa-mir-16-2, rno-mir-16
Aqeilan R. I. Calin G. A. Croce C. M. miR-15a and miR-16-1 in cancer: Discovery, function and future perspectives Cell. [score:1]
[1 to 20 of 1 sentences]
33
[+] score: 1
Other miRNAs from this paper: rno-mir-210
They showed that injected ds miR-15a, which induces cell apoptosis, was detected in the liver, but no apoptosis in the liver was observed. [score:1]
[1 to 20 of 1 sentences]
34
[+] score: 1
Several recent reports have highlighted the post-transcriptional repression of HMGA proteins by non-coding RNAs and, in particular, numerous miRNAs with this activity have been identified (let-7a, miR-15, miR-16, miR-26a, miR-34b, miR-196a2, miR-326, miR-432, miR-548c-3p, miR-570, miR-603) (53, 54). [score:1]
[1 to 20 of 1 sentences]
35
[+] score: 1
Three miRNAs of this initial cardiovascular reference list, however, are not 100% conserved between human and rat (miR-1, miR-211 and miR-424) and six miRNAs have not yet been registered for rats (miR-7g, miR-149, miR-15a, miR-199b, miR-372 and miR-486). [score:1]
[1 to 20 of 1 sentences]
36
[+] score: 1
Int J Cancer In press 70 Aqeilan RI Calin GA Croce CM 2010 miR-15a and miR-16-1 in cancer: discovery, function and future perspectives. [score:1]
[1 to 20 of 1 sentences]
37
[+] score: 1
For example, miR-105, miR-125b and miR-140 are involved in the inflammatory phase; miR-15a, miR-15b and miR-16 participate in the granulation phase; and miR-29 and miR-192 function in the remo deling phase [10]. [score:1]
[1 to 20 of 1 sentences]