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19 publications mentioning rno-mir-148b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-148b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 251
As shown in Figure 4C, the expression of Wnt/β-catenin signaling and the downstream proteins were obviously down-regulated when Wnt1 siRNA was applied, and miR-148b inhibitor could not increase the expression of these proteins (p < 0.01, vs. [score:10]
Mature neurons in SVZ were marked with NeuN staining, according our results, LV-148b inhibitor up-regulated the number of mature neurons at day 14, indicating neurogenesis was improved in SVZ and this process could at least partially explain the effects of miR-148b inhibitor on neurological function recovery after stoke. [score:8]
The next day, animals were randomly divided into the following three groups (n = 10/group): Lentivirus miR-148b inhibitor (LV-148b -inhibitor, CMV-ZsGREEN1-148b-miRNAinhibitor-PGK-puromycin, 3.0 × 10 [6] IU in 3 μL saline, Genomeditech, China), LV-GFP or saline vehicle control. [score:7]
To detect the effect of miR-148b in neurological functional recovery after ischemic stroke in vivo, we inhibited the miR-148b expression level in rats by Lentivirus miR-148b inhibitor injection. [score:7]
Quantitate RT-PCR demonstrated the expression level of miR-148b was significantly reduced in LV-148b inhibitor injection group (Figure 6C), which indicating the miR-148b inhibitor transduction succeed. [score:7]
MicroRNA-148b is frequently down-regulated in gastric cancer and acts as a tumor suppressor by inhibiting cell proliferation. [score:7]
miR-148b mimic, MiRNA-148b mimic negative control (miR-148b mimic-con), MiRNA-148b inhibitor, and MiRNA-148b inhibitor negative control (miR-148b inhibitor-con) were synthesized by RiboBio Co. [score:7]
Ischemic SVZ cells cultured in growth medium were transfected with miR-148b inhibitor and miR-148b inhibitor negative control (miR-148b inhibitor-con), respectively. [score:7]
Western blot further demonstrated the expression of NG2 (neural/glial antigen 2) and DCX was also increased significantly in miR-148b inhibitor transfected NSCs than inhibitor negative control transfected cells (Figures 4C,D). [score:7]
of Wnt-1, β-catenin, DCX and NG2 expression and their quantitative data in ischemic NSCs transfected with miR-148b inhibitor, miR-148b inhibitor-con and siRNA Wnt-1. mean ± SE, [*] p < 0.05, [**] p < 0.01. [score:7]
To confirm the directly targeting relationship of miR-148b and Wnt1, we constructed luciferase expression vectors harboring wild type or mutant Wnt1 3′UTR binding site (WNT1-3UTR and WNT1-3UTR-m; Figure 2). [score:6]
As shown above, down-regulated miR-148b in ischemic SVZ cells enhanced expression levels of Wnt1, β-catenin, and Cyclin D1, which indicated an activation of Wnt/β-catenin pathway. [score:6]
On the contrary, cells transfected with miR-148b inhibitor substantially decreased the expression of miR-148b by 0.31 ± 0.06 and 0.29 ± 0.04 times compared with blank and miR-148b inhibitor control transfected cells, respectively (Figure 3B). [score:6]
The infarction volume of rats transfected with lentivirus miR-148b -inhibitor showed significantly reduced and the functional test results suggested miR-148b inhibitor improve the neurological functional recovery after ischemic injury. [score:5]
Also, miR-148b suppressed hepatic cancer stem cell by targeting neuropilin-1 (Liu et al., 2015). [score:5]
8.4 ± 1.2% in miR-148b inhibitor-con group, p < 0.05) and GFAP -positive cells (37.8 ± 3.1% in miR-148b inhibitor group vs. [score:5]
of Wnt-1, β-catenin, Cyclin D1, NeuroD1, and Prox1 expression contents and their quantitative data in ischemic NSCs transfected with miR-148b mimic, miR-148b inhibitor and their negative controls. [score:5]
LV-GFP group); (C) The relative miR-148b expression level in LV-148b and LV-GFP inhibitor injected rat brains SVZ (n = 5/group. [score:5]
Immunofluorescent staining showed a robustly up-regulated BrdU -positive cell percentage as 56.5 ± 9.1% compared with miR-148b inhibitor-con group (41.6 ± 8.5%, p < 0.01; Figure 4A). [score:5]
According to our data, the expression of NeuroD1, Prox1, and Cyclin D1 were obviously increased after Wnt/β-catenin signaling activated by miR-148b inhibitor, which partly explained the action mechanism of miR-148b on neurogenesis. [score:5]
In the present study, the expression of miR-148a and miR-148b both increased in ischemic rat brain SVZ, we speculate that reduction of blood flow and oxygen input may induce miR-148a/b expression. [score:5]
Nevertheless, over -expression of miR-148b suppressed Wnt/β-catenin pathway activity. [score:5]
Immunofluorescent staining analysis revealed that suppress of miR-148b resulted in a significant increase in the number of Tuj1 -positive cells (12.2 ± 1.9% in miR-148b inhibitor vs. [score:5]
MicroRNA-148b suppresses cell growth by targeting cholecystokinin-2 receptor in colorectal cancer. [score:4]
Three downstream proteins of Wnt/β-catenin pathway, Cyclin D1, NeuroD1 and Prox1 were also detected and showed significantly downregulated in miR-148b mimic transfected NSCs (p < 0.05, n = 3; Figures 3C,D). [score:4]
MiR-148/152 family members are down-regulated in various cancer cell lines, which indicates the members in this family potential effect in regulating cell cycle, proliferation, and apoptosis (Yu et al., 2009; Song et al., 2011, 2012). [score:4]
MiRNA-148b suppresses hepatic cancer stem cell by targeting neuropilin-1. Biosci. [score:4]
miR-148b directly targeted Wnt1 gene. [score:4]
In the present study, ischemic NSCs with decreased miR-148b showed significantly higher percentage of BrdU [+] cells and DCX expression level, indicating self-renewing progenitor population was raised. [score:3]
The expression of miR-148b was increased by 5.92 ± 0.44 and 5.58 ± 0.38 times higher than blank (vehicle control) and miR-148b mimic-con, respectively (Figure 3A). [score:3]
miR-148b inhibitor decreased the ischemic lesion volume and improved neurological recovery in MCAo rats. [score:3]
org, we searched predicted target genes of miR-148b. [score:3]
The expression of miR-148/152 family could be altered by exposure to certain physical and chemical factors (Chen et al., 2013). [score:3]
This study indicated a novel mechanism for the miR-148b attenuated neuroprotection by inhibiting Wnt/ β-catenin signaling, which may become a potential therapeutic option for ischemic stroke. [score:3]
In conclusion, we reported for the first time the suppression role of miR-148b in SVZ NSCs. [score:3]
After EGF and FGF-2 were withdrawn, new born neurons (Tuj1 [+] cells) were increased with silenced miR-148b, meanwhile, Type B cells (GFAP [+] cells) and OPCs marker NG [2] expression were increased. [score:3]
miR-148b inhibitor). [score:3]
These results indicating Wnt/β-catenin signaling mediated the neurogenesis inhibitory effect of miR-148b on SVZ NSCs. [score:3]
Wnt1 is a miR-148b target gene. [score:3]
Primary ischemic SVZ cells were transfected with miR-148b inhibitor/inhibitor negative control and cultured in differentiation medium for another 5 days. [score:3]
These data revealed miR-148b expression implied the recovery outcome in ischemic stroke. [score:3]
miR-148b was reported to regulate the differentiation of mesenchymal stem cells in the process of early osteogenesis (Schoolmeesters et al., 2009), and involved in mouse adipogenesis via regulating PPARγ (John et al., 2012). [score:3]
The expression of miR-148b was significantly increased in ischemic rodent brain SVZ. [score:3]
These data indicated miR-148b could target Wnt1 mRNA in HEK 293T cells. [score:3]
26.5 ± 6.4% in miR-148b inhibitor negative control group, p < 0.05; Figures 4A,B). [score:3]
In our study, we first tested the impact of ischemia on miR-148b, then explored the regulation of miR-148b on NSCs neurogenesis and the mechanism beneath in vitro. [score:2]
In order to demonstrate the neurogenesis regulating ability of miR-148b could affect stroke outcome, the neurological protection effect of miR-148b also be studied in vivo. [score:2]
Point mutations of 3′UTR of Wnt1 gene (Wnt1-3′UTR-m) in miR-148b binding site were made as UGCACUG to UGCCGGG (Figure 2). [score:2]
These results further demonstrated that Wnt1/ β-catenin signaling was regulated by miR-148b in SVZ NSCs. [score:2]
Quantitate RT-PCR analysis indicated the expression levels of both miR-148a and miR-148b in ischemic SVZ were obviously increased compared with sham group (Figure 1B). [score:2]
Several studies showed miR-148/152 family members regulate not only proliferation but also differentiation process in stem cells (Yu et al., 2012; Fujiwara and Ozaki, 2016). [score:2]
miR-148b regulated Wnt/β-catenin signaling in SVZ NSCs. [score:2]
Western blot data showed the expression of Wnt1 and β-catenin were significantly decreased (p < 0.05, n = 3) in miR-148b mimic group compared with blank and miR-148b mimic-con group. [score:2]
To explore the potential involvement of miR-148 in ischemic SVZ, sub-ventricular zone was isolated from sham-operation (Sham) and MCAo applied rat brains (Figure 1A). [score:1]
Based on it, we infer miR-148b might affect the neurogenesis of NSCs and affect post-stroke recovery. [score:1]
The microRNA-148/152 family: multi-faceted players. [score:1]
We also tested the effect of miR-148b on neurological functional recovery in vivo. [score:1]
Then, we tested the effect of miR-148b on NSCs differentiation. [score:1]
All the data implied that MiRNA-148b regulated proliferation and differentiation of NSCs in SVZ after ischemic stroke via Wnt/β-catenin signaling. [score:1]
These data indicated that miR-148b reversely correlated with proliferation and differentiation potential SVZ NSCs. [score:1]
A potential miR-148b broadly conserved sequence was found to be seed matched with 3′UTR of Wnt1 mRNA (Figure 2A). [score:1]
All these results revealed miR-148b participate in cancer cell self-renewal and differentiation. [score:1]
First, we tested the effect of miR-148b on SVZ NSCs proliferation. [score:1]
To further explore the effects of miR-148b on neurogenesis in vivo, Paraffin coronal sections were used for DCX, NeuN, and GFAP staining. [score:1]
miR-148b mediated the proliferation and differentiation of SVZ NSCs via Wnt/β-catenin signaling. [score:1]
To test the interaction between miR-148b and 3′ UTR of Wnt1 gene, 293T cells (ATCC) were co -transfected with miR-148b mimics (100 ng/10 [6] cells) or miR-148b mimic negative control (miR-148b mimic-con, 100 ng/10 [6] cells) and Wnt1-3′UTR (100 ng/10 [6] cells) or Wnt1-3′UTR-m (100 ng/10 [6] cells) by using lipofectamine-2000 transfection reagent (Life technologies, USA). [score:1]
MiRNA-148b belongs to miRNA-148/152 (miR-148/152) family, which has been elucidated to involved in various biological processes (Chen et al., 2013). [score:1]
Figure 3Effects of miR-148b on Wnt/β-catenin signaling activity. [score:1]
More work is needed in the future to illustrate the effect of miR-148b in neuroprotection and neuro-restoration. [score:1]
Briefly, a segment of the 3′UTR of wild type Wnt1 gene (Wnt1-3′UTR) encompassing the miR-148b binding site was cloned in a pEZX-MT06 vector with Firefly/Renilla duo Luciferase reporter driven by a CMV promoter (Genecopoeia, USA). [score:1]
In contrast, miR-148b mimics did not reduce luminescence activity when miR-148b seed sequences at 3′ UTR of Wnt1 gene was mutated (Figure 2B). [score:1]
These results are consistent with the earlier demonstration that miR-148b reversely correlated with Wnt/β-catenin pathway activity (Liu et al., 2015). [score:1]
Hence, we cannot exclude the possibility that anti-miR-148b could induce a neuroprotection process via Wnt/β-catenin signaling. [score:1]
Due to the low enrichment of miR-148a in SVZ, we focused our study on miR-148b. [score:1]
However, the enrichment of miR-148a in sham and ischemic brains were significantly lower than miR-148b, and the following study was focused on miR-148b. [score:1]
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2
[+] score: 30
For example, the precursor sequences of the up-regulated miRNAs (miR-21, miR-10b) and down-regulated miR-148b* observed in our study are located at 17q23, 3q23 and 12q13. [score:7]
In detail, five miRNAs were significantly up-regulated (miR-21, miR-34c-3p, miR-470*, miR-10b, let-7i*) and two miRNAs significantly down-regulated in SP of HCC cells (miR-200a*, miR-148b*). [score:7]
To further confirm the differentially expressed miRNA, some known target genes expression of those validated miRNAs excluded miR-470* and miR-148b were detected in sorted SP cells and compared by using qRT-PCR between fetal liver cell and HCC cells. [score:6]
of the down-regulated miR-200a*, and miR-148b* in SP of HCC cells had the fold changes 0.1 ± 0.04, and 0.4 ± 0.08, respectively (P < 0.01). [score:4]
Ten miRNAs were underexpressed, including miR-200a* and miR-148b*. [score:3]
A subset of miRNAs was also identified and shown to be significantly underexpressed in our study, including miR-200a and miR-148b*. [score:3]
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3
[+] score: 19
For example, the regulation of NF-κB activation in vivo by PRKCZ (network 1) [32] is related to the downregulated miR-148b, and the downregulation of miR-133b and miR-341 is related to PTPRF (Figure 7, networks 1 and 4), the overexpression of which induces apoptosis independently of p53 through a caspase cascade that does not affect cell adhesion [33]. [score:10]
More interestingly, the downregulation of the BCL-2-inhibiting microRNAs miR-1, miR-138, and miR-148b is broadly consistent with the increase in the number of BCL-2 -positive cells present 3 days after injury ([76]; however, see [77]), although microRNA downregulation extends throughout the 7-day period after injury, which is typically a time when the number of BCL-2 -positive cells is progressively reduced. [score:9]
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4
[+] score: 18
Other miRNAs from this paper: rno-mir-214
It is possible that suppressing miR-214 concurrently elevates miR-148b and decreases noggin expression, thus enhancing bone repair by alleviating the negative regulation. [score:6]
Orso F miR-214 and miR-148b targeting inhibits dissemination of melanoma and breast cancerCancer Res. [score:5]
miR-148b can effectively enhance ASCs osteogenesis [43] by targeting noggin [44], a BMP2 antagonist that negatively regulates BMP2 -induced osteoblast differentiation and bone formation [3]. [score:4]
Li, K. -C. et al. Improved calvarial bone repair by hASCs engineered with Cre/loxP -based baculovirus conferring prolonged BMP-2 and MiR-148b co -expression. [score:2]
Furthermore, miR-214 and miR-148b antagonize the effects of each other in cancer cells [42]. [score:1]
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5
[+] score: 16
Cluster analysis of over-expressed miRNAs (Figure S1A) and under-expressed miRNAs (Figure S1B) indicated that some deregulated miRNAs might play their roles in groups, such as up-regulated miR-10b and miR-21 and down-regulated miR-200a* and miR-148b*. [score:12]
Two important miRNAs that were down-regulated in SP-HCCs, miR-200a* and miR-148b*, have been described in HCC tissues [26] and ovarian cancers [47]. [score:4]
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6
[+] score: 11
MiR-148-3p, mir-17-5p, miR-181a-5p, miR-19b-3p and miR-24-3p were predicted to control the expression of the following target genes: Interleukin 6 signal transducer IL6ST (gp130). [score:5]
In contrast, there was no change in the expression of mir148-3p or mir19b-3p (Fig 5). [score:3]
Amongst the 5 miRNAs (miR148-3p, miR17-5p, miR181a-5p, miR19b-3p and miR24-3p) targeting multiple genes from our 70 genes list, mir17-5p, which is increased with stress was confirmed by qRT-PCR. [score:3]
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7
[+] score: 8
miRNA Target Genes Pathways miR-128 ABCB9, BTG1, DSCR1, RASD1 ABC transporters General miR-136 GRN, PPP1R9B miR-147 HOXA1, PTGFRN miR-148 EGR3, SCN3A miR-181b IGF1R, NKX6-1 Adherens junction, Maturity onset diabetes of the, Focal adhesion, **Long term depression miR-196a ABCB9, CPB2, IRS1, MAPK10 ABC transporters General, Complement and coagulation cas, Adipocytokine signaling pathwa, Insulin signaling pathway, Type II diabetes mellitus, Fc epsilon RI signaling pathwa, Focal adhesion, **GnRH signaling pathway, **MAPK signaling pathway, Toll like receptor signaling p, Wnt signaling pathway miR-203 SARA1 miR-20 BTG1, SARA1, YWHAB Cell cycle miR-21 TPM1 mir-216 GNAZ **Long term depression miR-217 RHOA Adherens junction, Axon guidance, Focal adhesion, Leukocyte transendothelial mig, Regulation of actin cytoskelet, TGF beta signaling pathway, T cell receptor signaling path, Tight junction, Wnt signaling pathway miR-31 ATP2B2, DNM1L, EGR3, PPP1R9B, YWHAB **Calcium signaling pathway, Cell cycle miR-7 SLC23A2 miR-7b HRH3, NCDN, SLC23A2 **Neuroactive ligand receptor in b: miRNAs and their targets (from TargetScan and miRanda). [score:8]
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8
[+] score: 8
Similarly, the expression of oncogenic miRNAs like miR-21, miR-10b, let-7i, miR-34c, were increased more than 2 fold in EpCAM [+] liver cancer cells; whereas miR-125b, miR-200a, miR-148b were most down-regulated. [score:6]
In addition, the miR-200a and miR-148b were significantly underexpressed in EpCAM [+] liver cancer cells compared to fetal liver cells (P<0.05) [22]. [score:2]
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9
[+] score: 6
In the context of development, higher detected levels of miRNA in colostrum whey are interesting because miR-143, miR-148b-3p, and miR-141 are known to regulate intestinal function [41], [42] and miR-107 and miR-370 are known to modulate carbohydrate and lipid metabolism [27], [33]. [score:3]
Among miRNAs that were present at higher levels in colostrum whey, let-7i, miR-148b-3p, miR-27b, and miR-125b-3p affect the function of antigen-presenting cells, and miR-15b, miR-24, miR-92a, miR-181a, miR-181c, and miR-181d affect T cell development and function [29], [30], [35]. [score:2]
On the other hand, other miRNAs such as, let-7i, miR-143, miR-148b-3p, miR-15b, miR-17-5p, miR-24, miR-27b, miR-92a, miR-106b, miR-125b-5p, miR-181a, miR-181c, miR-181d, miR-200c, miR-375, miR-107, miR-141, and miR-370, were present at higher levels in colostrum whey than in mature milk whey (Fig. 6). [score:1]
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10
[+] score: 6
Additionally, another evidence collected from the current inverstigation demonstrate that the microRNA -mediated regulation is not limited to the 3’UTR, the functionality of target sites in the CDS also confirmed by previous studies [57– 59], such as miR-24 [58], miR-296, miR-470, miR-134 [60], miR-126 [43], miR-181a [59], miR-148 [57] and miR-519 [61] that target sequences within the mRNA coding region have been reported to repress the biosynthesis of the encoded proteins in similar way. [score:6]
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11
[+] score: 5
MiR-148a and miR-148b, which are found in UC blood MSC-derived exosomes, reportedly regulate the proliferation of UC blood MSCs by upregulating NF-κB or hedgehog signalling [38]. [score:5]
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12
[+] score: 4
As development proceeds, the observed increases of miR-29c, miR-375, miR-148, and miR-200c may drive the observed decreased expression of Klf4 mRNA. [score:4]
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13
[+] score: 3
In relation to the potential role of Sry in regulating brain sexual differentiation, circSry consists of 16 potential binding sites for miR-148 (Hansen et al., 2013), which is abundant in neuronal and other cell types (Obernosterer et al., 2006; Morton et al., 2008; Eskildsen et al., 2011). [score:2]
One example as discussed previously is that circSry might act as a “miRNA sponge” by binding to ncRNAs and thereby rendering them inactive, as might occur for miR-148 in brain neuronal cells (Obernosterer et al., 2006; Morton et al., 2008; Eskildsen et al., 2011; Hansen et al., 2013). [score:1]
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14
[+] score: 3
Some of the diabetes -associated miRNAs were below the detection limit in our study, such as miR-9, miR-96 and miR-148, indicating that back-translation from humans to ZDF rats may be difficult for these markers. [score:3]
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15
[+] score: 2
Other miRNAs from this paper: rno-mir-21, rno-mir-25, rno-mir-26a, rno-mir-133a, rno-mir-148a
In a set of wheezing + LRI patients (n = 20) and age- and gender-matched LRI control children (n = 20), miR-21, miR-25, miR-26a, miR-133a and miR-148 showed potential statistical differences between the patient and control groups (p < 0.10) (Fig.   1a). [score:1]
b RT-qPCR results of miR-21, miR-25, miR-26a, miR-133a and miR-148 in plasma from 35 indifferent control, 35 LRI control and 70 wheezing + LRI children. [score:1]
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16
[+] score: 2
Indeed, when the data of the Yamaura’s study were compared with findings of the present study several miRNAs were regulated in common and included for blunt steatosis miR-10b and miR-183; similarly with NASH the miRNAs miR-17, miR148b-5p and miR-197 were commonly regulated thus providing independent evidence for their diagnostic utility in animal studies. [score:2]
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17
[+] score: 1
Among the 21 miRNAs altered at 24 hours, 5 (miR-144, miR-136, miR-148b-5p, miR-342-5p, miR-23a*) showed persistent changes by 7 days after CCI (Figure 1C, D). [score:1]
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18
[+] score: 1
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, 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-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
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19
[+] score: 1
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, 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-15a, rno-mir-193b
The terminal 5' exon of orthologous transcript NP_001101587.1 in rat is missing, locating miR-148b upstream of NP_001101587.1; (c) Rat miR-142 is located in the first exon of the alternatively spliced transcript Q9JIR0-2. The orthologous alternative transcripts in human and mouse lacks the 5' exon, placing human and mouse miR-142 upstream of the BZRAP1 transcript. [score:1]
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