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25 publications mentioning mmu-mir-299b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-299b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 142
Other miRNAs from this paper: mmu-mir-299a
Of these 3 miRs, only miR-299-5p downregulated the protein levels of LC3βII and upregulated the expression of p62 in primary hippocampal neurons from APPswe/PS1dE9 mice, indicating significant inhibition of autophagy (Fig. 1b and Supplementary Fig. S2). [score:11]
In this study, we demonstrate that miR-299-5p inhibits autophagy by downregulating Atg5, and that autophagy modulated by miR-299-5p is closely associated with caspase -mediated apoptosis in neurons. [score:6]
To further verify that miR-299-5p directly targets Atg5 within its 3′UTR, we co -transfected either Scr-miR or Ago299-5p with luciferase vectors bearing WT or MUT target sequences from the predicted site at position 489–498. [score:6]
Conventional online programs, including TargetScan 20 and miRBase 21 were used to predict the targets of miR-299-5p. [score:5]
To determine whether the anti-apoptotic effect of miR-299-5p on neurons is associated with the suppression of autophagy, we examined the effects of autophagy induction by EBSS and autophagy suppression by shLC3 on miR-299-5p function. [score:5]
To unravel the mechanisms of autophagy inhibition by miR-299-5p, we searched for autophagy-related targets. [score:5]
Taken together, these results suggest that the inhibition of autophagy by miR-299-5p reduces apoptosis by suppressing the activation of caspase-3 and caspase-8 in primary hippocampal neurons from AD mice. [score:5]
Nevertheless, the function of miR-299-5p in pathophysiological processes is likely to be determined by a wide variety of targets in a disease and tissue-specific manner 33. [score:5]
The miR-299-5p targeting sequence of the human miR (hsa-miR-299-5p) is identical to that of its mouse homolog (mmu-miR299-5p) and is predicted to target Atg5 at one binding site within its 3′UTR (Fig. 2a). [score:5]
Our analysis verified that miR-299-5p is downregulated in the hippocampi of 9-month-old APPswe/PS1dE9 mice (Transgenic mice, Tg) and under starvation conditions (Fig. 1c,d). [score:4]
The results demonstrate for the first time that miR -dependent dysregulation of Atg5 takes part in the autophagy of AD and, furthermore, that miR-299-5p may potentially be beneficial to the treatment of this disease. [score:4]
MiR-299-5p suppresses autophagy by targeting Atg5, which functions at the stage of elongation of membranes. [score:4]
These results confirm that mAtg5 is a direct target of miR-299-5p. [score:4]
There were no distinct changes in Bax, Bcl-2 and caspase-9 protein levels (Supplementary Fig. S9); however, a significant upregulation of caspase-3 and caspase-8 cleavage levels was observed 24 h after treatment with 40 nM miR-299-5p. [score:4]
To determine whether, as for APPswe/PS1dE9 AD mo del mice, miR-299-5p is downregulated for AD patients, we assessed the level of miR-299-5p in human CSF from 6 AD patients and from 6 non-AD controls with a similar range of age, sex and educational status (Supplementary Table S2). [score:4]
In the present study the downregulation of Atg5 by miR-299-5p may have potential impact on neuron survival (Fig. 8). [score:4]
To determine whether miR-299-5p regulates Atg5 expression, we examined the protein levels of Atg5 in primary hippocampal neurons from APPswe/PS1dE9 mice after treatment with agomiR-299-5p (Ago299-5p) or antagomiR-299-5p (AM299-5p). [score:4]
The miR-299-5p target, Atg5, conjugates with Atg12 and Atg16 and then participates in autophagosome closure (sequestration step) 41. [score:3]
Assessment of autophagy in miR-299-5p (Ago299-5p) or antagomiR-299-5p (AM299-5p) -overexpressing cells. [score:3]
In this study, we used of AVs and other methods to demonstrate that miR-299-5p inhibits neuronal autophagy both in vivo and vitro as verified by the change of LC3βII, Beclin1, Atg5 and p62. [score:3]
Additionally, in a probe trial, APPswe/PS1dE9 mice treated with miR-299-5p at either 1 or 3 weeks spent a significant longer time than control mice in the target quadrant that formerly contained the platform (Fig. 7d), and the times of passing through the platform were also significantly increased (Fig. 7e,f). [score:3]
Levels of β-actin mRNA were used as an internal standard to normalize the individual gene expression level of Atg5, and U6 snRNA as a standard for miR-299-5p. [score:3]
To further reveal the mechanisms of inhibition of apoptosis in primary hippocampal neurons, the effect of miR-299-5p on the activation of apoptosis-related proteins was analyzed by western blotting. [score:3]
In SH-SY5Y cells, miR-299-5p also decreased Atg5 expression, and this effect was partially antagonized by AM299-5p (Fig. 2g and Supplementary Fig. S3c). [score:3]
In agreement with the mouse data, miR-299-5p was significantly downregulated in AD patients compared to the healthy controls (Fig. 1e). [score:3]
Nonetheless, the transfection with AM299-5p in SH-SY5Y cells did not increase the levels of Atg5 protein significantly (Supplementary Fig. S4a), potentially due to the low basal expression of miR-299-5p in SH-SY5Y cells (Supplementary Fig. S4b). [score:3]
These results indicate that autophagy inhibition by miR-299-5p attenuates apoptosis in primary hippocampal neurons from AD mice. [score:3]
Atg5 is an autophagy-related target of miR-299-5p. [score:3]
These results suggest that miR-299-5p suppresses autophagosome accumulation. [score:3]
Corresponding modulation of other autophagic proteins in Neuro-2a and SH-SY5Y cells is consistent with the physiological effects of miR-299-5p in regulating the autophagic pathway in these cells (Fig. 2f, g and Supplementary Fig. S3b,c). [score:2]
MiR-299-5p inhibits both autophagy and apoptosis in APPswe/PS1dE9 mice. [score:2]
Through microarray and western blotting analyses, we identified miR-299-5p as a potent autophagy regulator. [score:2]
These results verify the role of miR-299-5p in primary neurons. [score:1]
Decreased levels of miR-299-5p in autophagy and AD. [score:1]
MiR-299-5p is dysregulated in AD and is associated with autophagy. [score:1]
MiR-299-5p affects Atg5 levels directly and alters the levels of other autophagy-related proteins. [score:1]
These data suggest that miR-299-5p treatment had no significant effect on the levels of Aβ42 in APPswe/PS1dE9 mice. [score:1]
As shown in Fig. 7a, at both 1 and 3 weeks after injection, the freezing time for APPswe/PS1dE9 mice treated with Ago299-5p was higher than for mice treated with Scr-miR (Tg-ctr) or sham untreated mice (Tg-sham), demonstrating that miR-299-5p enhances hippocampal memory function. [score:1]
Mo del of miR-299-5p effect on autophagy and apoptosis in AD. [score:1]
Stem-loop real time PCR for miR-299-5p was performed using a commercial kit (GenePharma, Shanghai, China) according to the manufacturer’s protocol. [score:1]
MiR-299-5p regulates autophagy and apoptosis in primary hippocampal neurons. [score:1]
How to cite this article: Zhang, Y. et al. MiR-299-5p regulates apoptosis through autophagy in neurons and ameliorates cognitive capacity in APPswe/PS1dE9 mice. [score:1]
In the cortex of miR-299-5p treated mice, similar changes in protein levels were observed (Fig. 6b and Supplementary Fig. S11b). [score:1]
Effect of miR-299-5p on the cellular autophagy level. [score:1]
Our results show that miR-299-5p causes a significant decrease in AV formation in primary hippocampal neurons after 24 h transfection, while AM299-5p induces a significant increase in AVs (Fig. 3c). [score:1]
To further examine the effect of miR-299-5p on autophagy -associated apoptosis, caspase-3 and caspase-8 were analyzed using caspase activity kits. [score:1]
Intracerebral injection of miR-299-5p improves the cognitive performance of APPswe/PS1dE9 mice. [score:1]
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2
[+] score: 24
Analysis of global profiles of miRNA expression in skeletal muscle with microarray shows that expression of 4 miRNAs (miR-29a, miR-29b, miR-29c and miR-150) are up-regulated [23], whereas expression of 11 miRNAs (miR-379, miR-127, miR299-5p, miR-434-3p, miR-335, miR130a, miR-19b, miR-451, miR-148a, miR-199a and miR-152) are down-regulated in skeletal muscle of type 2 diabetic rats [23]. [score:13]
For example, it has been shown that expression of 4 miRNAs (miR-29a, miR-29b, miR-29c and miR-150) is up-regulated [23], whereas expression of 11 miRNAs (miR-379, miR-127, miR299-5p, miR-434-3p, miR-335, miR130a, miR-19b, miR-451, miR-148a, miR-199a and miR-152) is down-regulated in skeletal muscle of type 2 diabetic rats [23]. [score:11]
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3
[+] score: 24
The double-stranded oligonucleotides encoding the pre-miRNA sequences of miR-376a, miR-299, miR-382 or irrelevant miRNA (a miR -negative control, predicted not to target any known vertebrate gene) were cloned into the pcDNA6.2-GW/EmGFP-miR expression vector such that the pre-miRNA insertion site was in the 3′ untranslated (3′UTR) region of the green fluorescent protein (GFP) gene as per the instruction manual (Invitrogen, Carlsbad, CA). [score:7]
0014416.g004 Figure 4 (A) of stably expressing miR-376a, miR376abc (a polycistronic cluster of miR-376a, miR-376b and miR-376c), miR-299-5p or miR -negative and 10-87 LP cells; (B) with stably expressing miR-376a, miR-376abc, miR-299-5p or miR -negative 10-87 HP cells. [score:5]
No change in migration and invasion phenotypes was observed in cells expressing miR-382 or miR-299-5p. [score:3]
To determine whether the overexpression of the identified signature miRNAs could confer phenotypic changes, stable cell lines were created by cloning the pre-miRNA sequences of miR-376a, miR-376abc, miR-299, or miR-382 into the pcDNA6.2-GW/EmGFP-miR vector, which contains a green fluorescent protein (GFP) cassette, and introducing them into the non-tumorigenic 10-87 LP cells. [score:3]
However, little or no migration was observed for cells expressing miR-299 or miR-382. [score:3]
In agreement with the wound-healing assay, over -expression of miR-376a or miR-376abc also resulted in more than a four-fold increase in invasiveness, whereas miR-299 or miR-382 had no effect (Fig. 4B). [score:2]
miR-299-5p sense, 5′- tgctGAAGAAATGGTTTACCGTCCCACATACATTTTGAATATGTATGTGGGATGGTAAACCGCTTCTT-3′ and miR-299-5p anti-sense 5′-cctgAAGAAGCGGTTTACCATCCCACATACATATTCAAAATGTATGTGGGACGGTAAACCATTTCTTC-3′, miR-382 sense 5′- tgctGTACTTGAAGAGAAGTTGTTCGTGGTGGATTCGCTTTACTTATGACGAATCATTCACGGACAACACTTTTTTCAGTA-3′ and miR-382 anti-sense 5′-cctgTACTGAAAAAAGTGTTGTCCGTGAATGATTCGTCATAAGTAAAGCGAATCCACCACGAACAACTTCTCTTCAAGTAC-3′. [score:1]
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4
[+] score: 17
Our study also identified miR-107 and miR-299-3p as being responsible for an up-regulation in the expression of human GP Ibα mRNA. [score:6]
Furthermore, by performing a literature review, we found that miR-10a, miR-10b and miR-107 were previously reported to be involved in the regulation of hematopoietic gene expression [15, 19], and miR-299-3p is predicted to target the 3′-UTRs of both human and mouse GP1BA gene. [score:6]
Therefore, we chose to assess four miRNAs (miR-10a, miR-10b, miR-107, and miR-299-3p) and investigate if they can target the 3′-UTR and regulate the expression of human GP Ibα (Figure 1A). [score:4]
Of these two miRNAs, interestingly, miR-299-3p is predicted to bind the 3′-UTRs of both human and mouse GP1BA gene and thus is potentially able to play important roles in GP Ibα expression and megakaryopoiesis in both human and mouse, a speculation worthy of further investigations. [score:1]
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5
[+] score: 10
Among the up regulated miRNAs in STHdh [Q111]/Hdh [Q111] cells, expressions of miR-214, miR-299 and miR-335 were also up regulated in three of the four cell mo dels and expression of miR-199a was increased in two cell mo dels. [score:7]
Other miRNAs which showed a consistent expression pattern across the mo dels were miR-100, miR-214, miR-299, miR-335, miR-34a and miR-148a. [score:3]
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6
[+] score: 9
Our findings also demonstrate that miR-299, miR-499, miR-302, and miRNA-200 were upregulated in EPO-MVs (Fig.   8c). [score:4]
The miRNA profiles of the MVs revealed that EPO-MVs changed 212 miRNAs (fold-change ≥ 1.5), including miR-299, miR-499, miR-302, and miRNA-200, and that 70.28 % of these changes involved upregulation. [score:4]
miR-299 may delay or protect against replicative senescence via improvements in the metabolic activity of senesced cells, but it does not stimulate growth in the remaining senescent cells [46]. [score:1]
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7
[+] score: 8
Other miRNAs from this paper: mmu-mir-154, mmu-mir-299a, mmu-mir-495
Expression of miR-495 and miR-299-5p, both localized to the chromosome 14q32 cluster, were also upregulated in a setting of MI and inversely correlated to cardiac function (Supplementary Fig. S5B,C) 4. Thus, further improvements in cardiac function and pathology may be observed if multiple members of the 14q32 cluster are inhibited. [score:8]
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8
[+] score: 8
12 microRNAs passed the threshold of mean fold change > 1.3 and p-value < 0.05 between the lean and obese groups, with one microRNA significantly downregulated (miR-299-3p) and nine significantly upregulated (miR-202-3p, -15b-5p, -451, -24-2-5p, 1184, -187-5p, -486-5p, -10b-5p, and -223-3p). [score:7]
miR-187, miR-202, and miR-299-3p were not significantly correlated with any of the four markers. [score:1]
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9
[+] score: 7
Our newly identified ES/iPS cell-specific miRNAs, miR-299, -499-5p, -628-5p, and -888, were included in the list, further confirming that these miRNAs are more highly expressed in immature cells than in differentiating or differentiated cells. [score:3]
However, the involvement of miR-187, miR-299-3p, and miR-628-5p in some aspects of biology, including cancer, has been reported [43]– [46]; thus these miRNAs may play roles in regulating the proliferation of iPS/ES cells. [score:2]
However, a previous microarray study did not detect miR-299-3p in ES or iPS cells, perhaps because of the insensitivity of the microarray technique used [13]. [score:1]
miR-299-3p was described in ESCs [31], but not in iPSCs. [score:1]
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10
[+] score: 6
Four additional miRNAs, miR-299, miR-182, miR-23a and miR-125b, representing varying degrees of differential expression were validated using. [score:3]
miR-299, miR-182, miR-23a and miR-125b are representative of varying degrees of differential expression in the array. [score:3]
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11
[+] score: 5
The array uncovered the induction of 117 miRNAs with the signal intensity ≥500 (the fluorescence amount of each miRNA probe is measured by a photo multiplier tube or charge-coupled device and signal scaled across the range of detection for the platform) in GA muscle (Table 1, Fig. 1A and 1B), including the highly downregulated miRNAs (≥1.5-fold) miR-194-5p, miR-101b-3p, miR-148a-3p, miR-199b-5p, miR-335-5p, miR-127-3p, miR-379-5p, miR-541-5p, miR-382-5p, miR-329-3p, miR-299-5p and miR-434-3p, and the highly up-regulated miRNAs (≥1.5 fold), miR-146b-5p and miR-146a-5p (Fig. 1C). [score:5]
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12
[+] score: 4
Impressively, of the 17 upregulated miRNAs in MRL- lpr mice, 11 miRNAs (miR-154, miR-127, miR-379, miR-382, miR-433, miR-300, miR-376b, miR-394, miR-299, miR-495, and miR-329) are located at a genomic imprinted DLK1-Dio3 region. [score:4]
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13
[+] score: 4
044hsa-miR-18b2.20.014hsa-miR-423-5p1.70.048hsa-miR-932.10.014hsa-miR-1911.50.049hsa-miR-548b-5p2.30.015Downregulated miRNAs  hsa-miR-252.10.015hsa-miR-885-5p-4.20.00011hsa-miR-324-3p2.30.017hsa-miR-874-5.80.00018hsa-miR-3262.60.017hsa-miR-486-3p-4.60.00040hsa-miR-18a3.10.017hsa-miR-299-5p-4.20.0020hsa-miR-20b2.00.017hsa-miR-488-3.90.0063hsa-miR-1942.80. [score:4]
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14
[+] score: 4
Moreover, latest studies reported that H [2]S participated in regulating the expression of microRNAs (miR-129, miR-299b, and miR-369) in Ang II -induced hypertensive kidney (Weber et al., 2017). [score:4]
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15
[+] score: 4
Our results showed that the expression patterns of miR-1, miR-133a, miR-133b, miR-144, miR-206, miR-299, miR-331 and miR-4286 (Additional file 3: Figure S3) were significantly different in the three stages (p < 0.01), indicating that they may participate in the regulation of follicular transition. [score:4]
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16
[+] score: 4
Particularly, among the down-regulated miRNAs the set of miR-124a, miR-189, miR-299-5p and miR-379, was previously reported associated with autoimmune disorders [17]. [score:4]
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17
[+] score: 3
Among those, let-7i, miR-146b, miR-152, miR-155, miR-214*, miR-299 and miR-411 are similarly regulated in differentiating MSCs, whereas miR-421, miR-702 and miR-703 were oppositely regulated in MSCs. [score:3]
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18
[+] score: 3
miR-299-3p was completely identical across all primates except for a single change (C10T) in humans. [score:1]
The secondary structure of miR-299 was entirely conserved (SCI = 1) and was the most thermodynamically stable hairpin of all the miRNA in this study (z = -10.33). [score:1]
miR-299-3p. [score:1]
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19
[+] score: 3
Cahill and colleagues have shown that human derived BRAFT1799A- and RET/PTC-bearing thyroid tumor cells, KAT10 and TPC-1 respectively, express lower levels of 14q32-encoded miRNAs miR-323-3p, miR-370-5p, miR-127-3p, miR-299 and miR-154 [22, 23]. [score:3]
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20
[+] 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-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, 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-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The 3′ UTR of mouse Xbp1 mRNA contains several putative target sites for miR-199, miR-299, miR-433, miR-221, and miR-490. [score:3]
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21
[+] score: 3
However, the expression of the remaining 9 miRNAs (miR-411, miR-434-3p, miR-299*, miR-193, miR-146b, miR-379, miR-193b, miR-22, and miR-223) has not been verified. [score:3]
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22
[+] score: 1
Several of these miRNAs (mir-299, mir-431, mir-467c, mir-222, mir-32, mir-330, mir-384, mir-665, and mir-671) have previously been identified as sex-biased in the neonatal mouse whole brain and/or rat cortex [23, 48]. [score:1]
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23
[+] score: 1
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-mir-208a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-328, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, mmu-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-744, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, mmu-mir-208b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
On contrary, four of liver-specific miRNAs reported here were reported in Kim et al. [9] as muscle (eca-miR-299, eca-miR-32, eca-miR-656) or colon-specific miRNAs (eca-miR-429). [score:1]
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24
[+] score: 1
The results revealed potentially conserved sites for approximately nine miRNA family candidates (miR-30c, miR-34a/c, miR-449b, miR-181, miR-301a, miR-421, miR-299-5p, miR-609 and miR-99a) in the PAI-1 mRNA 3′ UTR. [score:1]
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Formosa A. Markert E. K. Lena A. M. Italiano D. Finazzi-Agro E. Levine A. J. Bernardini S. Garabadgiu A. V. Melino G. Candi E. MicroRNAs, miR-154, miR-299-5p, miR-376a, miR-376c, miR-377, miR-381, miR-487b, miR-485-3p, miR-495 and miR-654-3p, mapped to the 14q32. [score:1]
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