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24 publications mentioning mmu-mir-367

Open access articles that are associated with the species Mus musculus and mention the gene name mir-367. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 219
Here, we report that ICH downregulated miR-367 expression but upregulated IRAK4 expression in primary microglia. [score:11]
Erythrocyte lysates upregulated IRAK4 expression but downregulated miR-367 expression in microglia. [score:11]
Fig. 1Erythrocyte lysates upregulated IRAK4 expression but downregulated miR-367 expression in microglia. [score:11]
These results indicate that miR-367 likely suppresses IRAK4 expression by directly binding target sites in the IRAK4 3′-UTR. [score:8]
We also demonstrate that miR-367 suppressed IRAK4 expression by directly binding its 3′-untranslated region. [score:8]
Previously, we used a miRNA microarray to detect the expression profiles of cellular miRNAs, and our unpublished observations found that the expression level of miR-367 was significantly downregulated in microglia treated with erythrocyte lysates. [score:8]
Lastly, we found that over -expression of miR-367 significantly inhibited IL-6, IL-1β, and TNF-α expression in brain tissues, reduced water content and neurological injury after ICH. [score:7]
The 3′-UTR of IRAK4 mRNA contains a putative miR-367 target sequence based on the target prediction program TargetScan (www. [score:7]
Microglia transfected with miR-367 had dramatically reduced IRAK4 expression (Fig.   2b), which suggests that miR-367 inhibits erythrocyte lysate -induced IRAK4 expression in microglia. [score:7]
To further explore the potential target proteins of miR-367, we utilized the bioinformatic tool, TargetScan, and found that IRAK4 was the main target. [score:7]
In addition, we also found that upregulated miR-367 attenuated inflammatory mediator expression of erythrocyte lysate -treated microglia (Fig.   4b). [score:6]
Previously, we found that the expression level of miR-367 was significantly downregulated in microglia treated with erythrocyte lysates. [score:6]
We found that upregulated miR-367 attenuated NF-κB and inflammatory mediator expression of erythrocyte lysate -treated microglia. [score:6]
Our results indicate that miR-367 downregulation leads to increased IRAK4 expression of microglia after ICH. [score:6]
Our present data identified that miR-367 was a crucial regulator of TLRs downstream NF-κB signaling by direct targeting IRAK4. [score:5]
We found that administration of miR-367 significantly improved the miR-367 level in vivo, and miR-367 could significantly inhibit IRAK4, NF-κB p65, IL-6, IL-1β, and TNF-α expression in brain tissues after ICH (Fig.   6a, b). [score:5]
In addition, our results indicate that miR-367 could inhibit expression of proinflammatory cytokines, reduce brain edema, and improve neurological functions in ICH mice. [score:5]
Co -expression with miR-367 mimics significantly suppressed the activity of a firefly luciferase reporter containing wild-type IRAK4 3′-UTR but had no effect on a reporter with a mutated IRAK4 3′-UTR (Fig.   3b). [score:5]
The 3′UTR of IRAK4 mRNA contained conserved miR-367 binding sites, and we showed that miR-367 directly regulated IRAK4 expression through these 3′UTR sites. [score:5]
Fig. 3IRAK4 is a direct target of miR-367 in microglia. [score:4]
miR-367 regulates IRAK4 expression in microglia. [score:4]
IRAK4 is a direct target of miR-367 in microglia. [score:4]
The results demonstrated that upregulated miR-367 attenuated NF-κB p65 mRNA and protein levels in the nuclei of erythrocyte lysate -treated microglia (Fig.   4a). [score:4]
Related studies showed that miR-367 promoted pancreatic cancer invasion in vitro and metastasis in vivo through downregulating Smad7 [40]. [score:4]
Fig. 5IRAK4 mediated the suppressed inflammatory response induced by miR-367 in erythrocyte lysate -treated microglia. [score:3]
In this study, we identified an inverse relationship between miR-367 and IRAK4 expression. [score:3]
The results suggest that miR-367 may be a promising therapeutic target for the treatment of human pancreatic cancer. [score:3]
These results demonstrated that miR-367 and IRAK4 expression of microglia have an inverse correlation after erythrocyte lysates treatment. [score:3]
These data showed that miR-367 could inhibit inflammation response in vivo. [score:3]
On the contrary, miR-367 expression significantly decreased after erythrocyte lysates treatment (Fig.   1). [score:3]
The region of the IRAK4 mRNA 3′UTR predicted to be targeted by miR-367 as indicated. [score:3]
Our finding also suggests that miR-367 might represent a potential therapeutic target for ICH. [score:3]
miR-367 inhibits inflammation response in vivo. [score:3]
We found that transfection of miR-367 improved miR-367 mRNA expression (Fig.   2a). [score:3]
To generate the miR-367 expression vector, the miR-367 gene was amplified from mouse genomic DNA and cloned into the pcDNA3.0 vector (Invitrogen Corp. [score:3]
miR-367 inhibited NF-κB activation and proinflammatory mediators production. [score:3]
Therefore, the miR-367 represents a potential therapeutic target for ICH. [score:3]
These data showed that miR-367 could inhibit inflammation response in vivo, meliorate the neurological symptoms, and improve brain function after ICH. [score:3]
MiR-367 inhibited NF-ĸB activation and downstream proinflammatory mediator production. [score:2]
These results suggested that miR-367 was a novel inflammatory regulator in ICH. [score:2]
The miR-367 mimics or miR-367 control (2 μg/2 μl) were added to 1.25 μl of Entranster™ in vivo transfection reagent. [score:1]
a A IRAK4 3′UTR fragment containing wild-type or mutant miR-367 -binding sites was cloned downstream of the luciferase reporter gene. [score:1]
Mice were received an intracerebral ventricular injection of miR-367 mimics or miR-367 control 10 min after ICH and sacrificed 48 h after ICH. [score:1]
In the experiment, microglia were stimulated with erythrocyte lysates, and then miR-367, IRAK4, NF-ĸB activation and downstream proinflammatory mediator production were analyzed. [score:1]
We detected the effects of miR-367 on the NF-κB pathway of erythrocyte lysate -treated microglia. [score:1]
Microglia was transfected with miR-367 mimics or miR-367 control. [score:1]
We found that administration of miR-367 significantly reduce water content and neurological injury (Fig.   6c, d). [score:1]
miR-367 attenuated inflammatory response of microglia via IRAK4. [score:1]
We further transfected microglia with miR-367 mimics or miR-367 control, and then treated the microglia with erythrocyte lysates. [score:1]
We further detected the effects of miR-367 on the NF-κB pathway of erythrocyte lysate -treated microglia. [score:1]
miR-367 reduces brain damage in ICH. [score:1]
b Microglia was transfected with miR-367 mimics or miR-367 control, and then was treated with PBS or erythrocyte lysates. [score:1]
In conclusion, our study demonstrates that miR-367/IRAK4 pathway plays an important role in microglial activation and neuroinflammation in ICH. [score:1]
Microglia (1 × 10 [5]) was stimulated with 10 μl PBS or erythrocyte lysates for 48 h. a IRAK4 and miR-367 mRNA expression levels were evaluated by quantitative RT-PCR. [score:1]
These analyses showed that miR-367 could ameliorate the neurological symptoms and improve brain function after ICH. [score:1]
To determine the contribution of miR-367 to neurological function, i. c. v. injection of miR-367 control or mimics were administered 10 min after ICH. [score:1]
After 24 h, cells were harvested, and miR-367 expression was evaluated by RT-PCR. [score:1]
In conclusion, we identified a strong correlation between miR-367 and IRAK4, and the effect of miR-367 on microglial activation after ICH. [score:1]
a Microglia was transfected with miR-367 mimics or miR-367 control. [score:1]
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[+] score: 15
Changes in miRNA expression at 3 h ranged from 11-fold down-regulation (miR-224) to 3.8-fold up-regulation (miR-367), and at 24 h from 7-fold down-regulation (miR-222) to 20.6-fold up-regulation (miR-135a*; Figure 2). [score:15]
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[+] score: 13
As shown in previous work [18], the 290 ~ 295 paralogous clusters (clusters 17 ~ 92, 106b ~ 25, 106a ~ 363 and 302b ~ 367) were all highly upregulated in reprogramming (Figure 2; Additional file 3); however, the miRNA 17 ~ 92 and 106b ~ 25 clusters were among the most significantly upregulated miRNAs in the first (MEF to Thy1-) transition, while the 106a ~ 363 and 302b ~ 367 clusters were not significantly upregulated at any single transition (except miR-367-3p at the Thy1- to SSEA1+ transition), but were highly significantly upregulated overall, and in general exhibited a pattern similar to the 290 ~ 295 cluster. [score:13]
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[+] score: 13
The expression levels and fold-changes of 35 most abundantly expressed miRNAs of T3/HDF and T3/CMHDF, as well as those of 31 miRNAs of T3/MEF and T3/CMMEF, cells are summarized in Table 2. These results indicate that nine hES cell-specific miRNAs (miR-302a, 302b, 302c, 302 d, 367, 371, 372, 373 & 200c) were abundantly expressed in T3/HDF and T3/CMHDF cells, and that miR-367 and miR-373 had little more than 2-fold variations between these two cell populations. [score:7]
Recently, we reported that the expression of hES cell-specific miRNAs miR-302 d, miR-372 and miR-367 and miR-200c, as well as miR-199a, were strongly up-regulated by activin A [6]. [score:6]
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[+] score: 10
As shown in Figure 4I, expression of miR-302a, miR-302b, miR-302d and miR-367 was identified in p100−/− cells, and such ectopic expression led to a dramatically inhibition of cyclin d1 3′-UTR activity in p100−/− cells (Figure 4J). [score:7]
Since there is no putative binding site of miR-367 in cyclin d1 3′-UTR luciferase reporter, we anticipated that miR-302d might be a major player in inhibiting cyclin d1 3′-UTR activity. [score:3]
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[+] score: 10
Significant upregulation of OCT4, Sox2, and Nanog mRNAs and OCT4A protein in the miR-302s -transfected ADSCs, despite the low transfection efficiency, shows that miR-302s play a role in regulating the expression of these genes independent of miR-367. [score:7]
However, it has been shown that the expression of OCT4 gene is not induced after transfection of mouse embryonic fibroblasts with miR-302s without miR-367 which is in contrast to our findings [40]. [score:3]
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[+] score: 7
Recently, ectopic expression of Rab23 could reverse the migration and invasion inhibitory activity of miR-367 suggesting that Rab23 is also a target gene of miR-367 [68, 69]. [score:7]
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[+] score: 6
Among which we found that three miRNAs (miR-363, miR-367, miR-25) were commonly upregulated while six (miR-33a, miR-33b, miR-92a, miR-92b, miR-137, miR-32) were downregulated in IL-6 -treated GBC-SD cell line samples compared to the representative controls (Figure 4A and Figure 4B). [score:6]
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[+] score: 6
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, rno-mir-223, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
From the top ten downregulated miRNAs at this transition, six miRNAs (miR-367, miR-302a, miR-302c, miR-372, miR-302b, and miR-302d) have been shown to encourage proliferation and are highly expressed in undifferentiated cells and cancer stem cells [43], [44], [45], [46], [47], [48]. [score:6]
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[+] score: 5
The miR-302 gene encodes a cluster of five microRNAs (miRNAs) (miR-302a/b/c/d and miR-367) that are highly expressed in human embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs), and mouse embryonal carcinoma cells (e. g., P19 cells) and moderately expressed in mouse ESCs [1– 3]. [score:5]
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[+] score: 5
Surprisingly, all these top miRNAs, including miR-302b, miR-367, miR-294, and miR-292, do not directly target any core factors (Fig.   4a- 4d). [score:4]
a, b, c, d, the shortest paths from miR-302b, miR-367, miR-294, and miR-292-5p respectively to the pluripotent core factors. [score:1]
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[+] score: 4
It has been shown that a set of three miRs (miR-302s, miR-369s and miR-200c) selected from numerous miRs expressed exclusively in induced pluripotent stem cells (iPSCs)/ESCs, elicited reprogramming [13]; a significant role for miR-367 was also shown [12]. [score:3]
Thus, miR -based reprogramming may be beneficial, given that a combination of miR-302s and miR-367 could carry out reprogramming without apparent c-Myc alterations [8, 9, 11, 20, 21]. [score:1]
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[+] score: 3
Here, by sequence matching using bioinformatics analyses, we found quite a few of candidate miRNAs that target Bcl-2, including miR-429, miR-30, miR-22, miR-25, miR-32, miR-92, miR-363, miR-367, miR-99, miR-27, miR-128, etc. [score:3]
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[+] score: 3
Supplementary Figure 2 showed that CXCR4 3′UTR was efficiently targeted by miR-302a, b, c, d but not by miR-367. [score:3]
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[+] score: 3
The miR-302-367 cluster is comprised of miR-302b, miR-302c, miR-302a, miR-302d and miR-367, which are expressed specifically in pluripotent ESCs and mEC cells 23. [score:3]
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[+] score: 3
For example, the expression of a miR302/367 cluster (comprised of 5 miRNAs) by miR367 activation initiates the process two-fold more effectively than OCT4/SOX2/KLF4/MYC-derived methods and precludes genes breaks or transgene reactivation (Anokye-Danso et al. 2011). [score:3]
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[+] score: 2
LncRNA CASC2 have been demonstrated as playing crucial regulatory roles in a few of cancers, and functioned as endogenous RNA by sponging miRNAs, such as miR-18a [26], miR-367 [27], miR-21 [28], etc. [score:2]
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[+] score: 1
In addition, miR-367, which is a distantly related member of the miR-302 cluster [36], was 37 [th] in the mouse list and 17 [th] in the human list. [score:1]
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[+] score: 1
These include mir-24-2, mir-30c-2, mir-125a, mir-130a, mir-196, mir-215, mir-218-2, and mir-367. [score:1]
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[+] 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-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, mmu-mir-299b, 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
For instance, miR-208, miR-302 (a-d), miR-367 were not detected (at >10 cpm on average) in the heart tissue; miR-134 and miR-208a were not detected in skeletal muscles; miR-483 in liver; or miR-483 and miR-377 in bone [36]. [score:1]
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[+] score: 1
We also found a homologue of human miR-367. [score:1]
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[+] score: 1
Phylogenetic analysis support the miR-base classification that miR-1 belongs to the miR-1/206 family including hsa-miR-206 and the Drosophila dme-miR-1, an indication of the high evolutionary conservation of this family (shown in Supplementary, Fig. S2A by alignments and phylogenetic quartette puzzling trees); hsa-miR-25 belongs to the evolutionary conserved miR-25/92 family [39] including Drosophila miR-92a+b/310/311/312/313, shown in Fig. S2B, and shares only the seed sequence with other miRs like miR-4325 or miR-367. [score:1]
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[+] score: 1
Another member of the cluster, mir-367, was not detected because of the lack of the "CATG" site. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, 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-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
In the mouse genome, we only found 53 miRNA genes completely located in SDs and two (mmu-mir-367, mmu-mir-669g) partially overlap with SDs. [score:1]
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