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19 publications mentioning mmu-mir-409

Open access articles that are associated with the species Mus musculus and mention the gene name mir-409. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 224
Other miRNAs from this paper: hsa-mir-409
miR-409-3p functions as a tumor suppressor by inhibiting the development and metastasis of CRC, suggesting that miR-409-3p is expected to become a novel diagnostic marker and a new target of the treatment of CRC. [score:8]
Our results suggest that miR-409-3p functions as a tumor suppressor by inhibiting the development and metastasis of CRC, suggesting that miR-409-3p is expected to become a new diagnostic marker and a new target of the treatment of CRC. [score:8]
It has been reported that miR-409-3p targets PHF10, radixin and c-Met [8, 9, 11, 19] Here, we found that NLK could be a potential target of miR-409-3p since NLK would be the potential target in the CRC scenario. [score:7]
In this study, we analyzed the down-regulation expression of miR-409-3p in CRC tissues compared with patient-matched normal tissues, and determined that the expression level of miR-409-3p was closely correlated with the clinicopathologic variables of CRC. [score:7]
The expression of miR-409-3p is down-regulated in CRC and correlated with tumor size, and local invasion. [score:6]
In these studies, the expression levels of miR-409-3p was significantly lower in cancer tissues compared with corresponding non-tumor tissues, and it inhibits proliferation, invasion and tumorigenesis in vitro or in vivo, suggesting that it may serve as a tumor suppressor. [score:6]
We also show that miR-409-3p may function as an tumor suppressor by directly targeting NLK. [score:6]
Ectopic expression of miR-409-3p inhibits proliferation, invasion and metastasis of CRC cells, reduces the tumorigenic ability of CRC cells in nude mice. [score:5]
Ectopic expression of miRNA mimics suggested that miR-409-3p could inhibits the abilities of proliferation, wound healing, metastasis and invasion in CRC cells. [score:5]
We searched miR-409-3p’s putative targets using online search tools (e. g. TargetScan, Microrna. [score:5]
Given that miR-409-3p inhibits metastasis of CRC cells in vitro, we next tested whether ectopic expression of miR-409-3p could influence the tumor growth and metastasis of CRC cells in vivo. [score:5]
The results showed that overexpression of miR-409-3p led to significantly inhibited migration and invasion of CRC cells. [score:5]
Ectopic expression of miR-409-3p mimics suggested that miR-409-3p could inhibits the abilities of proliferation, wound healing, metastasis and invasion in CRC cells. [score:5]
The results showed that the average expression level of miR-409-3p was significantly down-regulated in tumor tissues compared to the adjacent non-tumor tissues (Figure  1a, b). [score:5]
The results are mean ± SD, * P < 0.05. miR-409-3p targets the 3′-UTR of NLKTo identify how miR-409-3p functions in CRC cells, computational prediction of miR-409-3p targets was performed. [score:5]
The transcriptional regulation of miR-409-3p has been implicated in some diseases [32, 33]. [score:4]
In conclusion, our data showed that miR-409-3p was frequently down-regulated in CRC. [score:4]
d miR-409-3p mimics down-regulated luciferase activities controlled by wild-type NLK 3′UTR (* P < 0.01), but did not affect luciferase activity controlled by mutant NLK 3′UTR. [score:4]
miR-409-3p inhibits peritoneal spreading CRC cells in nude mice in vivo. [score:3]
This result is consistent with the expression profile of miR-409-3p in our study. [score:3]
These findings indicate that miR-409-3p inhibits the proliferation and colony forming ability of CRC cells. [score:3]
miR-409-3p inhibits migration and invasion of CRC cells in vitro. [score:3]
miR-409-3p inhibits CRC cells proliferation and clonogenicity of CRC cells in vitro. [score:3]
of clinical cases revealed that low miR-409-3p expression had inclinations towards lager tumor size and local invasion. [score:3]
In the present study, statistical analysis of clinical cases revealed that low miR-409-3p expression had inclinations towards lager tumor size and local invasion. [score:3]
showed that the low expression of miR-409-3p was significantly correlated with tumor size and local invasion (* P < 0.05). [score:3]
The results supported that miR-409-3p could be a potential therapeutic target. [score:3]
b Expression levels of miR-409-3p in 45 CRC patients were analyzed by qRT-PCR. [score:3]
To identify how miR-409-3p functions in CRC cells, computational prediction of miR-409-3p targets was performed. [score:3]
Aberrant miR-409-3p expression has been reported in several cancers. [score:3]
The peritoneal spreading nude mice assay confirmed that miR-409-3p could inhibits the ability of metastasis in CRC cells in vivo, which is an important aspect of tumor development. [score:3]
Thus, these results indicate that miR-409-3p could suppress metastasis of CRC cells in vivo. [score:3]
Notably, we found the NLK could be a potential target of miR-409-3p. [score:3]
To explore the expression levels of miR-409-3p in CRC tissues and adjacent non-tumor tissues, qRT-PCR analysis was performed. [score:3]
miR-409-3p expression levels were determined in 45 pairs of primary CRC and their corresponding adjacent non-tumor tissues by qPCR. [score:3]
miR-409-3p inhibits scratch wound healing ability of CRC cells. [score:3]
Table 1 Relationship between miR-409-3p expression levels and clinicopathological variables in 62 CRC patients Clinicopathologic parameters No. [score:3]
Thus, our results suggest that miR-409-3p is a potential diagnostic marker and therapeutic target of CRC. [score:3]
Therefore, we next determined whether overexpression of miR-409-3p in CRC cells could affect cell proliferation. [score:3]
By wound distance analysis, the movement ability of CRC cells was inhibited by miR-409-3p. [score:3]
miR-409-3p targets the 3′-UTR of NLK. [score:3]
Furthermore, we elucidated the correlation between miR-409-3p expression and clinicopathologic factors. [score:3]
As a negative regulator of NLK, miR-409-3p has a naturally potential value in personalized medicine. [score:2]
c Schematic graph of the putative binding sites of miR-409-3p in the NLK 3′UTR and the mutation in miR-409-3p -binding sites. [score:2]
The results showed that cell growth was inhibited in cells transfected with miR-409-3p mimics compared with the cells transfected with control mimics (Figure  2a, b). [score:2]
The genes predicted by all the used programs were considered candidate targets of miR-409-3p. [score:2]
a Relative expression of miR-409-3p in 45 CRC patients tumor tissues compared with adjacent non-tumor tissues. [score:2]
In pervious studies, dysregulation of miR-409-3p has been reported in many cancers, including gastric cancer [8, 9], prostate cancer [10] and bladder cancer [11]. [score:2]
The results were shown in Figure  3a, miR-409-3p overexpression cell lines SW480 [miR-409-3p] restoration slowly closed the scratch wounds compared with the control 48 h after scratching, in contrast to the control SW480 [NC mimics] cells which were significantly efficient in wound healing. [score:2]
The relative luciferase activity of the NLK-3′UTR [wt] reporter was markedly suppressed by miR-409-3p mimics compared with that of NLK-3′UTR [mut] in a miR-409-3p dependent manner (Figure  7d). [score:2]
This result strongly indicates that 3′UTR of NLK carries the direct binding seed of miR-409-3p. [score:2]
Strikingly, the peritoneal nodules were significantly inhibited in miR-409-3p mimics transfected group compared with control group (Figure  6). [score:2]
The results suggested that the functions of miR-409-3p in CRC were worthy to study further. [score:1]
The number of colonies from SW480 [miR-409-3p] and SW1116 [miR-409-3p] cells was fewer than that from the control groups (SW480 [NC mimics] and SW1116 [NC mimics], * P < 0.05, Figure  2e, f). [score:1]
miRNA-409-3p mimics and negative control mimics were purchased from GenePharma (Shanghai, China). [score:1]
In order to further assess the influence of miR-409-3p on CRC cells, we further explored its effects on cell migration and invasion, a key ability of tumor progression and metastasis. [score:1]
miR-409-3p mimics or control mimics oligos were transfected into CRC cells respectively. [score:1]
a Representative histograms depicting apoptosis of SW480 cells transfected with miR-409-3p mimics or control. [score:1]
b Representative histograms depicting apoptosis of SW1116 cells transfected with miR-409-3p mimics or control. [score:1]
a Representative photographs of migratory or invasive SW480 [NC mimics] and SW480 [miR-409-3p] cells on the membrane (magnification, ×100). [score:1]
c Representative photographs of migratory or invasive SW1116 [NC mimics] and SW1116 [miR-409-3p] cells on the membrane (magnification, ×100). [score:1]
To confirm the contribution of miR-409-3p in vivo, we carried out peritoneal spreading in mice mo dels. [score:1]
Luciferase reporters were constructed containing either a wild-type NLK 3′UTR sequence containing the miR-409-3p binding site (NLK-3′UTR [wt]), or a mutated 3′UTR (NLK-3′UTR [mut]) (Figure  7c). [score:1]
The results showed that the number of colonies from CRC cells transfected with miR-409-3p mimics was significantly fewer than that from the control group (Figure  2c, d). [score:1]
However, the clinical significance and functions of miR-409-3p in human CRC were not entirely clear. [score:1]
b Average number of migratory or invasive SW480 [NC mimics] and SW480 [miR-409-3p] cells. [score:1]
d Average number of migratory or invasive SW1116 [NC mimics] and SW1116 [miR-409-3p] cells (* P < 0.05, ** P < 0.01). [score:1]
d SW1116 cells were transfected with miR-409-3p mimics or NC mimics then seeded onto 6-well plates. [score:1]
miR-409-3p CRC NLK Tumorigenesis Colorectal carcinoma (CRC) is one of the prevalent cancer types, ranking the third of all cancer-related deaths worldwide. [score:1]
A recent investigation on a large cohort of over 2,000 CRC patients indicated that NLK might promote the aggressiveness of CRC, which is consistent with the expression profile of miR-409-3p in the present study. [score:1]
Therefore, the mechanism underlying the control of miR-409-3p level in colorectal cells is expected to be addressed in the future study. [score:1]
SW480 cells were transfected with miR-409-3p mimics or NC mimics then seeded onto 6-well plates. [score:1]
We then performed luciferase reporter assays to verify a direct interaction between miR-409-3p and the 3′UTR of NLK. [score:1]
To investigate the mechanism of miR-409-3p on CRC cell proliferation inhibitory effects, we performed apoptosis analysis by flow cytometry. [score:1]
A recent study demonstrated that miR-409-3p could be used for early detection of CRC [12]. [score:1]
miR-409-3p has not yet been well explained in CRC. [score:1]
Whereas, miR-409-3p level was not associated with other clinicopathologic features, including age, sex (P > 0.05). [score:1]
a The putative binding sites of miR-409-3p in NLK 3′-UTR region were predicted. [score:1]
miR-409-3p induces CRC cells apoptosis. [score:1]
As shown in Figure  3, the number of migratory and invasive SW480 cells transfected with miR-409-3p mimics was significantly less than the control group (* P < 0.05. [score:1]
Figure 2The effect of miR-409-3p on the proliferation of CRC cells. [score:1]
The transportation of miR-409-3p was implicated in early CRC detection [12]. [score:1]
CRC cells transfected with miR-409 mimics or control mimics were selected and intraperitoneally injected into nude mice, These mice were euthanized 8 weeks after the injection, and the tumor lesions in the peritoneal cavity were counted. [score:1]
MicroRNA-409 dysregulation has been detected in many cancers, including gastric cancer [8, 9], prostate cancer [10] and bladder cancer [11]. [score:1]
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2
[+] score: 38
Among the ten miRNAs validated by qRT-PCR, we found that mmu-miR-487b-5p, mmu-miR-709, mmu-miR-182-5p, mmu-miR-214-3p and mmu-miR-467a-3p were up-regulated in HCC-activated Tregs, mmu-miR-142-5p, mmu-miR-30b-5p, mmu-miR-409-3p and mmu-miR-129-5p were down-regulated (P < 0.01), while miR-344e-5p did not change significantly, as shown in Figure 1C. [score:7]
There were four up-regulated miRNAs (mmu-miR-709, mmu-miR-467a-3p, mmu-miR-182-5p and mmu-miR-25-5p) and seven down-regulated miRNAs (mmu-miR-615-3p, mmu-miR-409-3p, mmu-miR-680, mmu-miR-129-5p, mmu-miR-151-5p, mmu-miR-142-5p and mmu-miR-30b-5p), as the values presented in Table 1. Then we performed unsupervised hierarchical clustering of the eleven miRNAs. [score:7]
In control Tregs, mmu-miR-487b-5p, mmu-miR-214-3p, mmu-miR-30b-5p and mmu-miR-129-5p showed significant down-regulation while mmu-miR-409-3p showed significant up-regulation (Figure 2C, left). [score:7]
Compared with control Tregs, although mmu-miR-487b-5p and mmu-miR-129-5p showed similar down-regulation in HCC-activated Tregs, mmu-miR-409-3p was actually significantly down-regulated; mmu-miR-214-3p and mmu-miR-30b-5p did not exhibit significant changes (Figure 2C, right). [score:6]
Control) P -valuemmu-miR-25-5p2.210.04mmu-miR-7091.980.02mmu-miR-467a-3p1.820.04mmu-miR-182-5p1.540.05mmu-miR-129-5p0.290.02mmu-miR-6800.340.02mmu-miR-615-3p0.360.00mmu-miR-409-3p0.440.02mmu-miR-30b-5p0.510.05mmu-miR-151-5p0.610.03 mmu-miR-142-5p 0.63 0.04By TargetScan, we found that mmu-miR-25-5p, mmu-miR-615-3p, mmu-miR-151-5p and mmu-miR-680 had few target genes directly relating with Tregs in MeSH database, so we excluded the four miRNAs for further exploration. [score:6]
Compared with the healthy controls, the expression levels of hsa-miR-182-5p, hsa-miR-214-3p, hsa-miR-129-5p and hsa-miR-30b-5p were significantly up-regulated in Tregs from HCC patients while the hsa-miR-409-3p and hsa-miR-142-5p did not show significant changes (Figure 3). [score:5]
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3
[+] score: 34
Among these upregulated miRNAs were miR-10a, which is a candidate tumor suppressor and suppresses apoptosis in leukemia [39], miR-409 that suppresses tumor cell invasion and metastasis in gastric cancer [40], and miR-206 and miR-345, which are frequently downregulated in various types of cancers and are believed to act as tumor suppressors [41], [42]. [score:15]
As shown in Figure 9C, there was excellent concordance in the data from the miRNA profiling and qPCR, the expression of miR-21, miR-26a, miR-24, miR-30b and miR-29a was down-regulated by EF24 treatment both in vitro and in vivo, while the expression of miR-345, miR-409, miR-10a and miR-206 was upregulated by EF24 treatment. [score:11]
Only four miRNAs (miR-10a, miR-409, miR-206 and miR-345) were upregulated both in vitro and in vivo, which reportedly act as tumor suppressors or inhibitors of cell cycle progression. [score:8]
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4
[+] score: 27
To explore the functional link between altered miRNA expression and AD development, we predicted the potential targets of two representative miRNAs, miR-331-3p and miR-409-5p, which were the top -elevated and top-reduced miRNAs in both groups, by three prediction methods (miRDB, miRanda and TargetScan). [score:8]
Although the target of miR-409-5p remained to be validated to provide further mechanistic insight, the early onset of its expression alteration suggests that miR-409-5p may play a role in the induction phase of AD, making it a potential target for early diagnosis and treatment of AD in huamn patients. [score:7]
MiR-331-3p and miR-409-5p were predicted to each target 1138 and 745 genes (that are predicted in all three methods), Further analysis using GO database showed that the top biological processes affected by the predicted target genes are phosphate metabolic process and regulation of transcription (GO:0006796 and GO:0045449). [score:6]
Among multiple miRNAs that were found to be dysregulated in AD brains, miR-409-5p showed constantly decreased expression level in AD brains from 4 months to 12 months of age, which is consistent with previous findings [25]. [score:4]
Among them, nine miRNAs (miR-99b-5p, miR-7b-5p, miR-7a-5p, miR-501-3p, miR-434-3p, miR-409-5p, miR-331-3p, miR-138-5p and miR-100-5p) showed consistent changes in both groups. [score:1]
The level of miR-409-5p was lower since 6 months of age in AD brains. [score:1]
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5
[+] score: 27
Some reports have shown a correlation between miR-409 overexpression and epithelial-mesenchymal transition and tumour growth in prostate cancer progression 27 28, while others report an onco-suppressive action of miR-409 and demonstrate its down-regulation in gastric and lung cancers 29 30. [score:8]
The miR-409-5p, despite a less significant variation in the first week of withdrawal (Fig. 3e), was the one showing the highest expression value after the long term therapy discontinuation, with almost the same expression value throughout acute and chronic phase response. [score:5]
The variation of miR-98, miR-200b and miR-409 plasmatic expression was validated at different time-point of HT1 disease. [score:5]
The pattern of HT1 -induced up-regulation of miR-409 was different from the two other miRNAs, with significant variations starting at 4 weeks. [score:4]
Although no functional study has been conducted to establish its role in liver injury progression, our result unveils for the first time an important deregulation of miR-409 circulating levels in the HT1 pathological process. [score:2]
Graph represents 3 individual per time point and median levels of miR-98-5p (c), miR-200b-3p (d) and miR-409-5p (e) in healthy controls and in NTBC-withdrawn mice (i. e. 1 week off, 4 weeks off and 8 weeks off). [score:1]
To confirm the modulation of specific miRNAs during progression of the HT1 -induced liver pathology in fah [−/−] mice after NTBC removal, three miRNAs (namely miR-200b-3p, miR-98-5p and miR-409-5p) were selected for validation by RT-qPCR (Table 2, highlighted miRNAs). [score:1]
Modulation of plasma levels of miR-98, miR-200b and miR-409 after NTBC withdrawal. [score:1]
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6
[+] score: 16
However, miR-409-3p, Let-7i and miR-30c already exhibited a significant down-regulation while miR-148b was the only up-regulated miRNA in hippocampus at this age (Fig 3C). [score:7]
Interestingly, miR-9 maintained its down-regulation in older mice and miR-409-3p was the only miRNA to be consistently down-regulated in APP23 from a very young age right through to older animals. [score:7]
Individual TaqMan assays (Applied Biosystems) were used to analyse the expression of the following mature mouse miRNAs: miR-181c, miR-9, miR-20b, miR-21, miR-30c, miR-148b, miR-361, miR-409-3p and Let-7i. [score:2]
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7
[+] score: 16
TIFA, with an up-regulated gene transcriptional level (Supplementary Figure S1B), was predicted to be a target gene of miR-409-5p and miR-128-3p; and these miRNAs all showed decreased expression upon MC-LR treatment (Supplementary Table S2). [score:8]
In this study, we also observed up-regulated expression of SGTB, targeted by miR-133a-3p, miR-181a-5p, miR-409-5p, and miR-542-3p, at both the transcriptional and protein levels in Sertoli cells following exposure to MC-LR (Supplementary Figure S1B and Fig. 5B). [score:8]
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8
[+] score: 9
MiRNA target site/Species Human Mouse Cow Dog Chicken FrogTargeting Twist2 miR-15b-3p + − + + − − − miR-33-5p + + + + − + − miR-137-3p + + + + − + − miR-145a-5p + + + + − − + miR-151-5p + + + + − + − miR-214-5p + + + + − − − miR-326-3p + + + + − − − miR-337-3p + + + + − + − miR-361-5p + + + + − − − miR-378a-5p + + + + − − − miR-381-3p + + + + − + − miR-409-3p + + + + − − − miR-450b-5p + + + + − + − miR-508-3p + + + + − − − miR-543-3p + + + + − − − miR-576-5p + + + + − − − miR-580 + + + + − − − miR-591 + + + + − − − MicroRNAs underlined were tested in this study. [score:5]
The following miRNAs were tested for their potential to repress Twist1 translation in the human lung carcinoma cell line H1299: miR-33, miR-145a, miR-151, miR-326, miR-337, miR-361, miR-378a, miR-381, miR-409 and miR-543 (Fig. 1). [score:3]
The miRBase accession numbers for miRNAs are: mmu-miR-33 (MI0000707), mmu-miR-145a (MI0000169), mmu-miR-151 (MI0000173), mmu-miR-326 (MI0000598), mmu-miR-337 (MI0000615), mmu-miR-361 (MI0000761), mmu-miR-378a (MI0000795), mmu-miR-381 (MI0000798), mmu-miR-409 (MI0001160) and mmu-miR-543 (MI0003519). [score:1]
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9
[+] score: 5
The motif represents putative target of human mature miRNA hsa-miR-409-5p (v7.1 miRBase) 30 -0.47 -1.53 METABOLISM OF VITAMINS AND COFACTORS (REACTOME) Genes involved in metabolism of vitamins and cofactors 46 -0.46 -1.24 GLUTAMATE NEUROTRANSMITTER RELEASE CYCLE (REACTOME) Genes involved in glutamate neurotransmitter release cycle 15 -0.44 -1.29 PPARA 01 Genes having at least one occurrence of the transcription factor binding site V$PPARA_01 (v7.4 TRANSFAC) in the regions spanning up to 4 kb around their transcription start sites 32 -0.42 -1.37 INTEGRIN CELL SURFACE INTERACTIONS (REACTOME) Genes involved in integrin cell surface interactions 75 -0.41 -1.42 PTEN PATHWAY SA PTEN is a tumor suppressor that dephosphorylates the lipid messenger phosphatidylinositol triphosphate 17 -0.40 -1.40 RYAAAKNNNNNNTTGW UNKNOWN Genes having at least one occurrence of the highly conserved motif M151 RYAAAKNNNNNNTTGW in the region spanning up to 4 kb around their transcription start sites. [score:5]
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10
[+] score: 4
MiR-409-3p and miR-22-3p were down-regulated in the PFC tissues of the PR+BC untreated and crizotinib -treated PR+BC animals. [score:4]
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11
[+] score: 4
On that basis, we identified miRNAs (e. g. miR-409-5p, miR-433, miR-541, miR-742) that, in the adult retina, are clearly detected in the vitreal part of the Inner Nuclear Layer (INL) and are likely to be expressed in amacrine cells (blue arrows in the third column of Figure 4A; Database). [score:3]
For miR-409-5p, miR-433, miR-541 and miR-742 (top bracket; panel A) a weak staining is detectable in the inner neuroblastic layer (INBL; blue arrowheads) at P0. [score:1]
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12
[+] score: 3
miR-431, miR-714, miR-744, miR-877, miR-130b, miR-21, miR-323-3p, miR-325, miR-409-3p, miR-154*, and miR-681 were significantly increased 4 days post-sciatic nerve crush in pre-conditioned DRGs, while miR-190, miR-1, miR-33, miR-32, miR-153, miR-335-5p, miR-193, and miR-488 showed significantly decreased expression. [score:3]
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13
[+] score: 3
Our studies also showed that miR-127 and miR-409-3p were strongly expressed at all stages of human embryonic chondrocyte differentiation. [score:3]
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14
[+] score: 3
Likewise, miR-93-5p and miR-409-5p were 38- and 85-fold more highly expressed, respectively, in MIN6 cells than in human beta cells (Fig. 3A). [score:3]
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15
[+] score: 3
Three other miRNAs within this region (mmu-miR-673 and mmu-miR-370 flanking the core anti-Rtl1 cluster, and mmu-miR-409 at the distal end of the Mirg cluster) did not exhibit statistically significant differences in expression, suggesting that there may be tissue-specific cleavage of mature miRNAs from this region. [score:3]
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16
[+] score: 3
Thus, of 54 mouse and 47 human miRNAs expressed in all TECs, 22 were common to both species, whereas the overlap in cTEC-specific miRNAs was confined to miR-409–5p. [score:3]
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17
[+] score: 3
miR-409-3p was predicted to target α2 only. [score:3]
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18
[+] score: 1
Of these 116 miRNAs, miR-466d-3p (1520 fold), miR-449a (975 fold), miR-29a (479 fold), miR-146b (278 fold) and miR-409-3p (255 fold) were the top five miRNAs which had the highest fold changes across the dataset. [score:1]
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19
[+] score: 1
Genes that are involved in transcriptional processes, such as Polr3f, Polr2a, Polr3g and Polr2a were also mapped to the eQTL for miR-409, miR-681, miR-34 and miR-449. [score:1]
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