sort by

22 publications mentioning dre-mir-9-4

Open access articles that are associated with the species Danio rerio and mention the gene name mir-9-4. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 231
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-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-214, hsa-mir-200b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, 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-96, hsa-mir-200c, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-130b, hsa-mir-376a-1, mmu-mir-376a, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, hsa-mir-429, mmu-mir-429, hsa-mir-450a-1, mmu-mir-450a-1, dre-mir-429a, 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-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-96, 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-130b, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, hsa-mir-450a-2, dre-let-7j, hsa-mir-376a-2, mmu-mir-450a-2, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Some of the miR-9 and miR-200-class targets upregulated in the mutant OE (Qk, Foxf2) are mesenchymally-expressed rather than OE-expressed, while other targets were actually downregulated in the absence of Dlx5 (Akap6, Elmod1, Snap25) (Table 1C). [score:15]
We found eight miRs differentially expressed, six down-regulated (miR-9, miR-141, miR-200a, miR-200b, miR-429 and miR-376a) and two up-regulated (miR-450a-5p and miR130b*) in the Dlx5 [−/−] OE (Fig.  1a). [score:9]
In summary, since miR-9 and miR-200-class are down-modulated in the absence of Dlx5, while Foxg1 protein level is up-regulated, and since the 3′ UTR of the Foxg1 mRNA is a predicted target of these miRs, we can infer that the Dlx5-miR-Foxg1 regulation is most likely a direct one. [score:8]
Thus, Dlx5 is likely to regulate the expression of miR-9.3 directly, and the expression of miR-200a/ b/ miR-429 indirectly. [score:8]
To determine whether the forced expression of DLX5 may result in an upregulation of miR-9 and miR-200-class RNAs, SH-SY5Y cells were transfected with myc-tagged wild-type DLX5 or Q178P mutant DLX5 expression vectors, and the relative abundance of miR-9 and miR-200 was quantified by Real-Time qPCR. [score:8]
Two possible explanations: either changes in the abundance of miR-9 and miR-200-class cause changes in the abundance of target RNAs that are too modest to pass the imposed cut-off value, or these miRs preferentially affect translation and not stability of the target mRNAs. [score:7]
For chromatin immunoprecipitation (ChIP) we used the human SHSY-5Y neuroblastoma cells, which express low endogenous levels of Dlx5, miR-9 and miR-200, transfected with 5 μg of DLX5-myc-tag expression vector (from Open-Biosystem) or with the same vector in which the Q178P mutation (Shamseldin et al., 2012) was introduced (BioFab, Rome, sequence verified). [score:6]
A significant enrichment of miR-9 and miR-200-class target sequences was detected in the 3′ UTR of genes up-regulated in the Dlx5 [−/−] OE (Table 1A, B). [score:6]
To downmodulate endogenously expressed miR-9 and miR-200 we used the commercially available Ambion anti-miR inhibitors (Life Technologies). [score:5]
myc-tagged version of either the WT or the Q178P mutant DLX5 were expressed in the SH-SY5Y human neuroblastoma cells, which express DLX5, miR-9 and miR-200 endogenously. [score:5]
We also show that Dlx5 promotes expression of miR-9 and miR-200 class, thereby tends to repress Foxg1 protein translation. [score:5]
• Altered expression of miR-9 and -200 might contribute to the Kallmann disease. [score:5]
miR-9 expression is medio-laterally graded, being most intense in the cortical hem; it contrasts with the Foxg1 expression in a reciprocal gradient. [score:5]
2.9To downmodulate endogenously expressed miR-9 and miR-200 we used the commercially available Ambion anti-miR inhibitors (Life Technologies). [score:5]
miR-9 over -expression in developing forebrain at E11.5 resulted in ectopic Reelin + cells over the cortex beyond the marginal zone, while conversely the inhibition of endogenous miR-9 function caused the regression of Wnt3a positive cortical hem and reduction of Reelin+, p73+ and NeuroD1+ cells (Shibata et al., 2008). [score:5]
The expression of pre -miR-9 induced a 6-fold reduction in Foxg1 protein level, while expression of anti -miR-9 induced a 2-fold increase in Foxg1 level (Fig.  3a,b). [score:5]
•Dlx5 controls the expressions of miR9 and miR-200, which target the Foxg1 mRNA • miR-9 and -200 are needed for olfactory neurons differentiation and axon extension • miR-9 and -200 are required for the genesis and position of GnRH neurons. [score:5]
We observed a reduction of miR-9, miR-141 and miR-429 signal in the Dlx5 [−/−] OE, compared to the WT (Fig.  1c), while hybridization with two positive controls, Sp8 (expressed in the OE) and Sox5 (expressed in chondrogenic condensations), yielded an equivalent positive signal in both genotypes, indicating adequate RNA preservation. [score:4]
Indeed Foxg1 has been experimentally shown to be negatively regulated by miR-9. The mouse miR-9 targets Foxg1 mRNAs for proper generation of Cajal–Retzius neurons in the medial pallium (Shibata et al., 2008). [score:4]
3.3 miR-9 is wi dely expressed in the forebrain and olfactory sensory system of the mouse embryo and has been implicated in neural development (La Torre et al., 2013; Shibata et al., 2011; C. Zhao et al., 2013). [score:4]
Next we intersected the predicted miR-9 and miR-200-class targets with the coding mRNAs found to be differentially expressed in the Dlx5 [−/−] OE compared to the WT (Garaffo et al., 2013). [score:4]
miR-9 is wi dely expressed in the forebrain and olfactory sensory system of the mouse embryo and has been implicated in neural development (La Torre et al., 2013; Shibata et al., 2011; C. Zhao et al., 2013). [score:4]
With these two tools, we predicted the most reliable miR-9 targets, and functionally classified the top scoring ones, to search for significantly enriched categories. [score:3]
The 3′ UTR of tetrapod and zebrafish Foxg1 mRNAs hosts miR-9 and miR-200 target sequences. [score:3]
The results presented here indicate that loss of Dlx5 causes a down-modulation of miR-9 and of miR-200-class, which results in the over -expression of the Foxg1 protein. [score:3]
We also show that miR-9 and miR-200-class target (amongst others) the foxg1 mRNA, through which they likely exert their functions. [score:3]
Here we show that mouse and fish foxg1 mRNA is a target of miR-9 and miR-200 class, both of which are down-modulated in the Dlx5 null embryonic OE. [score:3]
Fig. 2), and Foxg1 mRNA has been proposed as a valid target of miR-9 (Shibata et al., 2008). [score:3]
The sequence of miR-9 and mi-200-class shows a high degree of identity between mouse and zebrafish (95% to 100%), as well as high similarity in their expression territories in early embryos ((Choi et al., 2008; Wienholds et al., 2005) and public databases). [score:3]
To overexpress miR-9 and miR-200 exogenously we used commercially available Ambion pre-miR precursors (Life Technologies). [score:3]
3.6To functionally demonstrate a role of miR-9 and miR-200-class for olfactory development, and the involvement of Foxg1 in this regulation in vivo, the zebrafish mo del was again used. [score:3]
To determine whether miR-9 and miR-200-class play a role in GnRH neuronal differentiation and migration, we used the GnRH3:GFP transgenic zebrafish strain, in which the GFP reporter is expressed under the transcriptional control of a fragment of the z- GnRH3 promoter. [score:3]
Searching for functionally relevant targets of miR-9 and miR-200 clsss in the OE. [score:3]
These results indicate that higher expression of foxg1 has similar effects as Dlx5, miR-9 and - 200 depletions on olfactory differentiation, in vivo. [score:3]
We also determined the level of endogenous Foxg1 mRNA, by Real-Time qPCR, upon expression of pre -miR-9 or anti- miR-9, and observed, respectively, a 2-fold decrease and a 2.5-fold increase in the relative Foxg1 mRNA abundance (data not shown). [score:3]
We raised the hypothesis that, in the absence of Dlx5 and reduced levels of miR-9 and - 200-class, Foxg1 protein level is increased due to higher stability/translation of the Foxg1 mRNA. [score:3]
3.7To determine whether miR-9 and miR-200-class play a role in GnRH neuronal differentiation and migration, we used the GnRH3:GFP transgenic zebrafish strain, in which the GFP reporter is expressed under the transcriptional control of a fragment of the z- GnRH3 promoter. [score:3]
We screened for miR expression in ORNs, comparing wild-type vs Dlx5 mutant tissues, and identified miR-9 and miR 200-class as the molecular link between Dlx5 and Foxg1. [score:3]
For miR-9 we detected only three enriched categories: regulation of cell differentiation, cell junction assembly and neuron development (Suppl. [score:3]
To functionally demonstrate a role of miR-9 and miR-200-class for olfactory development, and the involvement of Foxg1 in this regulation in vivo, the zebrafish mo del was again used. [score:3]
The over -expression of DLX5 induced a 2.5–3 fold increase in the abundance of miR-9 in this system, while the Q178P mutant DLX5 did not (Fig.  2d). [score:3]
The knock-down of miR-9 in zebrafish embryos, via injection of a MO previously shown to be specific and effective (Leucht et al., 2008) (sequence in Suppl. [score:2]
Thus, both miR-9 and miR-200 negatively regulate Foxg1 protein level. [score:2]
Genomic regulation of miR-9 and miR-200 by Dlx5. [score:2]
In this work we define the role of miR-9 and miR-200-class in the development of the olfactory system, with functions ranging from ORN differentiation to axon guidance, glomerulus formation and GnRH neuron migration. [score:2]
Examining olfactory development more thoroughly we now can implicate the miR-9 and miR-200-class networks in a more complex phenotype reminiscent of the Kallmann syndrome (see below). [score:2]
miR-9 and miR-200-class regulate Foxg1. [score:2]
To determine whether miR-9 and miR-200-class may modulate Foxg1 protein level, the effect of introduction of pre-miR-9 or depletion of endogenous miR-9 on Foxg1 protein level was assayed by Western blot analysis in SH-SY5Y cells, which express DLX5, miR-9, miR-200-class and Foxg1 endogenously. [score:2]
We injected anti- miR-9 and anti- miR200 (or control) MOs in WT zygotes, then at 48 hpf we extracted total -RNA from these and carried out Real-Time qPCR analyses. [score:1]
3.2The three loci miR-9.1, -9.2 and - 9.3, located on chromosomes 3, 13 and 17 respectively, generate identical mature miR when transcribed, referred to as “ miR-9”. [score:1]
Depletion of miR-9 and miR-200-class in zebrafish results in delayed ORN differentiation. [score:1]
The most altered miR was miR-9, with a fold change of -2, while the other miRs showed a fold-change between − 1.9 and + 1.3. [score:1]
Depletion of miR-9 and miR-200-class in zebrafish results in altered GnRH neuron genesis and position. [score:1]
Table III), led to a significant and dose -dependent reduction of the endogenous miR-9, relative to control -injected ones, accompanied by a 3.5-fold increase of the endogenous z- foxg1 mRNA (Fig.  5d, e). [score:1]
z-foxg1 mRNA level increased by three-folds when either miR-9 or miR-200-class were depleted (Figs.  5e and 6f). [score:1]
3.4The 3′ UTR of the mammalian and fish Foxg1 mRNA contains seed sequences for miR-9 and miR-200 (Suppl. [score:1]
Hybridization was carried out with DIG -labelled riboprobes that specifically detect the mature form of mouse miR-9 and miR-141 (Exiqon) in according with manufactory instruction. [score:1]
Thus, our results provide the first evidence of the participation of miR-9 and miR-200-class in these early events. [score:1]
As a further confirmation, we carried out in situ hybridization on sections of WT and Dlx5 [−/−] embryonic OE, at the age E12.5, to detect miR-9, miR-141 and miR-429, using specific mouse DIG -labelled probes. [score:1]
Upon injection of the anti- miR-9 MO, only approximately 45% of the embryos were found to be CFP + (72% in the control injected), and in these we observed a clear reduction of the CFP + signal. [score:1]
In control embryos, we counted an average of 13 (+/− 2) GnRH3::GFP + neurons/embryo at 72 hpf, while in miR-9 and miR-200 MO injected embryos the average number was, respectively, 5 (+/− 1) and 6 (+/− 1) (Suppl. [score:1]
Anti- z-miR-9 MO was designed with the on-line dedicated tool https://oligodesign. [score:1]
Using reporter zebrafish strains to visualize the embryonic olfactory axons (Miyasaka et al., 2005; Sato et al., 2005; Yoshida et al., 2002) or the GnRH + neurons (Abraham et al., 2008, 2009, 2010), we show that miR-9 and miR-200-class play a role in ORN differentiation and axonal organization. [score:1]
To test whether the DLX5 protein physically occupies the Dlx5 sites near the miR-9.3 and miR-200a/ b/ miR-429 loci, Chromatin Immuno-Precipitation (ChIP) analysis on these sites was performed. [score:1]
We previously verified that the depletion of miR-9 and miR-200-class in zebrafish embryos leads to higher level of z-foxg1 mRNA (no Ab efficiently recognizes the z-foxg1 protein). [score:1]
The 3′ UTR of the mammalian and fish Foxg1 mRNA contains seed sequences for miR-9 and miR-200 (Suppl. [score:1]
The majority of anti -miR-9 injected embryos displayed a normal placode organization, a normal pattern of olfactory axon fasciculation, extension and connectivity, and normal glomeruli formation. [score:1]
Starting from profile data obtained from a mouse mo del of Kallmann syndrome, we functionally examined this pathway in zebrafish showing that miR-9 and miR-200-class are required for normal differentiation of the ORNs, for the extension and connectivity of the olfactory axons, and for the migration of the GnRH neurons from the nasal primordium to the forebrain. [score:1]
This possibility is clearly consistent with the results reported by Shibata et al. (2008), in which they show that the depletion of miR-9 resulted in abnormally high levels of Foxg1 proteins, and this caused a delayed differentiation of the Cajal–Retzius neurons in the cortex. [score:1]
We predicted one Dlx5 binding site near the miR-9.2 locus, located about 1.5 kb downstream, three sites near the miR-9.3 locus, located about 4, 5 and 6 kb downstream, and two sites near the miR-200a–200b-429 locus, located about 5 kb upstream (Fig.  2a). [score:1]
The three loci miR-9.1, -9.2 and - 9.3, located on chromosomes 3, 13 and 17 respectively, generate identical mature miR when transcribed, referred to as “ miR-9”. [score:1]
No Dlx5 binding site was predicted within a 50 kb range from the miR-9.1, miR-141, miR-200c and miR-376a loci. [score:1]
We used the same MOs indicated above to deplete miR-9 and miR-200 class in GnRH3::GFP zygotes, and examined the effect on the number and position of the GFP + neurons associated to the terminal nerves, between 36 and 72 hpf. [score:1]
These data indicate that the depletion of miR-9 results in a delayed or absent differentiation of the OMP + type ORN, with only a minimal effect of the Trpc2 + type neurons, and minimal consequences on axon/glomeruli organization. [score:1]
This provides an indication that the differentiation delay observed upon depletion of miR-9 is specific for the olfactory and anterior brain regions. [score:1]
miR-9 and miR-200 mediate the Dlx5-Foxg1 cascade. [score:1]
[1 to 20 of 76 sentences]
2
[+] score: 106
miR-9 and miR-30a inhibited TBX5 expression at the transcriptional and translational levels independentlyIt was determined that both miR-9 and miR-30a were present at detectable levels in cardiac tissues (Figure 3a), and the expression of the two miRNAs was 3.7 to 4.9 times higher in cardiac tissues from CHD cases compared with that of cardiac tissues from the non-CHD controls (Figure 3b). [score:8]
MiR-9 reduced the transcription of TBX5 mRNA by 57% (Figure 3c, left), and the miR-9 inhibitor up-regulated TBX5 mRNA expression 1.88-fold (Figure 3d, left). [score:8]
miR-9 and miR-30a inhibited TBX5 expression at the transcriptional and translational levels independently. [score:7]
Because miR-9 and miR-30a had similar inhibition patterns on the luciferase expression vector with the TBX5 3′UTR (Supplementary Figure S2), we measured whether TBX5 transcription or translation in cultured HEK 293T cells could be regulated by miR-9 and miR-30a. [score:6]
Despite a potential miRNAs expression disparity between adults and children, such a large difference in miR-9 and miR-30a expression might still represent the potential contributions of the two miRNAs in CHD development, which would require more robust studies to confirm in the future. [score:6]
It was confirmed that miR-30a did not affect the concentration of TBX5 mRNA, but reduced its protein concentration, while miR-9 downregulated both transcription and translation of TBX5. [score:6]
On the other hand, the allelic expression disparity was diminished by the use of each specific inhibitor for miR-9 or miR-30a individually or in tandem (Figure 2d). [score:5]
These results suggested that miR-9 primarily regulates endogenous transcription of TBX5, and that miR-30a regulates translation of the TBX5 mRNA. [score:5]
miR-9 and miR-30a inhibited TBX5 expression by interacting with the TBX5 c. *1101C>T variant. [score:5]
miR-9 and miR-30a inhibited TBX5 expression by interacting with the TBX5 c. *1101C>T variantIn the flanking region of the TBX5 3′UTR variant rs6489956, there are 16 software-predicted miRNAs including five upstream miRNAs, seven downstream miRNAs and four on-site miRNAs (Figure 2a). [score:5]
Additionally, miR-9 or miR-30a inhibitors could increase TBX5 protein expression separately or together (Figure 3d, right). [score:5]
The fluorescence sensor assay in zebrafish embryos demonstrated that the miR-9/30a precursor repressed the expression of egfp-tbx5-3′-UTR-C and more apparently the expression of egfp-tbx5-3′-UTR-T in vivo (Figure 4f). [score:4]
The specific inhibition of miR-9 and miR-30a for TBX5 caused by the 3′ UTR variant c. *1101C>T was demonstrated by a psiCHECK luciferase reporter assay as well as the rescue experiments from miRNA inhibitors. [score:4]
If it is true that miR-30a and miR-9 expression level changes are minimal after the heart has formed, our data suggest that miR-30a and miR-9 are likely contributors to the occurrence of CHDs. [score:3]
However, our study elucidated that the sporadic CHDs could be attributed to the combined contribution of the common regulatory variations in the TBX5 gene, as well as the epigenetic factors such as miR-30a or miR-9. The possible mechanism of underlying the association of TBX5 non-coding variants with increased CHD risk may be explained by the sensitive nature of the dosage effect of TBX5 on heart development. [score:3]
The endogenous expression of miR-9 and miR-30a was detected in all of the 30 human cardiac samples (Figure 3a). [score:3]
It was found that only 2 out of these 16 miRNAs, namely, miR-9 and miR-30a, can cause a significant disparity in the expression of the two allelic reporters in HEK 293T cells co -transfected with the psiCHECK-C/T plasmid (Figure 2b). [score:3]
Both miR-9 and miR-30a could decrease TBX5 translation (Figure 3c, right). [score:3]
For the upstream miR-9, although the variant rs6489956 appears not to directly affect miR-9 binding (Supplementary Figure S1), it might impair the miRNAs complex that interacts with the TBX5 motif containing variant rs6489956, as previously described [25]. [score:2]
In order to test the interaction effect of TBX5 3′UTR variant and miR-30a or miR-9 in vivo, we explored their function on heart development using zebrafish mo del system. [score:2]
It was determined that both miR-9 and miR-30a were present at detectable levels in cardiac tissues (Figure 3a), and the expression of the two miRNAs was 3.7 to 4.9 times higher in cardiac tissues from CHD cases compared with that of cardiac tissues from the non-CHD controls (Figure 3b). [score:2]
Therefore, the mechanisms by which miR-9 and miR-30a regulate TBX5 were confirmed both in vitro and in vivo. [score:2]
TBX5 3′UTR variant rs6489956 interacted with miR-30a or miR-9 in zebrafishIn order to test the interaction effect of TBX5 3′UTR variant and miR-30a or miR-9 in vivo, we explored their function on heart development using zebrafish mo del system. [score:2]
While co-injection of TBX5 3′UTR variant with miR-30a or miR-9 into tbx5 loss-of-function embryos significantly reduced the rescue effects, especially in T allele and miR-30a or miR-9 coinjected embryos (Figure 4e). [score:1]
We set up 11 groups for microinjection and did imaging analysis at 48 h post fertilization (hpf): wild-type (WT) control, standard MO control (5 ng), tbx5 MO (5 ng), tbx5 MO (2.5 ng), tbx5 MO (0.5 ng), MO (5 ng)+C allele mRNA (100 pg), MO (5 ng)+T allele mRNA (100 pg), MO (5 ng)+C allele mRNA (100 pg)+hsa-mi9 (100 pg), MO (5 ng)+T allele mRNA (100 pg)+hsa-miR-9 (100 pg), MO (5 ng)+C allele mRNA (100 pg)+hsa-miR-30a (100 pg) and MO (5 ng)+T allele mRNA (100 pg)+hsa-miR-30a (100 pg). [score:1]
Human miR-30a, mir-9 and a negative control were purchased from Thermo Fisher Scientific (Waltham, MA, USA). [score:1]
TBX5 3′UTR variant rs6489956 interacted with miR-30a or miR-9 in zebrafish. [score:1]
Both bioinformatic predictions and functional analyses showed that both miR-30a and miR-9 have a higher affinity to the minor T allele. [score:1]
We further identified two miRNAs, miR-9 and miR-30a, that interacted with this variant. [score:1]
The functional variant TBX5 c. *1101C>T (rs6489956) was found to significantly increase CHD risk in Han Chinese by interacting with miR-30a and miR-9 (OR=1.83. [score:1]
[1 to 20 of 30 sentences]
3
[+] score: 75
Other miRNAs from this paper: dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-mir-219-1, dre-mir-219-2, dre-mir-221, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, 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-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-92b, dre-mir-96, dre-mir-100-1, dre-mir-100-2, 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-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-135c-1, dre-mir-135c-2, dre-mir-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-153a, dre-mir-181c, dre-mir-200a, dre-mir-218a-1, dre-mir-218a-2, dre-mir-219-3, dre-mir-375-1, dre-mir-375-2, dre-mir-454a, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-181a-2, dre-mir-34b, dre-mir-34c, dre-mir-222b, dre-mir-138-2, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-128-3
Our results show miRNAs have a wide variety of different expression profiles in neural cells, including: expression in neuronal precursors and stem cells (for example, miR-92b); expression associated with transition from proliferation to differentiation (for example, miR-124); constitutive expression in mature neurons (miR-124 again); expression in both proliferative cells and their differentiated progeny (for example, miR-9); regionally restricted expression (for example, miR-222 in telencephalon); and cell-type specific expression (for example, miR-218a in motor neurons). [score:15]
The absence of temporally restricted expression and presence of spatially restricted expression is consistent with the main targets of this miRNA being restricted to those regions lacking miR-9 expression. [score:9]
Additionally, within the retina miR-9 is expressed in maturing cells of the CMZ (which are likely to still be proliferative) but expression is maintained only in amacrine cells of the inner nuclear layer (INL in Figure 2d). [score:5]
For instance, miR-9 is broadly expressed in both proliferative and differentiated cells in many of its expression domains. [score:5]
In addition to miRNAs with expression restricted to either proliferating or differentiating cells, miR-9, miR-135c, miR-153a, miR-219 and members of the let-7 family (let-7a, let-7b and let-7c) show expression in both proliferating and differentiating cells of the larval brain (Figures 1c,f; 2, 3, 9, 12, 18, and 22-24, and Tables A, B and C in7). [score:5]
Additional data file 2 is a figure showing miR-9 expression in the 3 dpf zebrafish brain. [score:3]
miR-9 expression in the 5 days post-fertilization (dpf) zebrafish brain. [score:3]
Additional data file 4 is a figure showing miR-9 expression in the adult zebrafish brain. [score:3]
Click here for file miR-9 expression in the 3 days post-fertilization (dpf) zebrafish brain. [score:3]
miR-9 expression in the adult zebrafish brain. [score:3]
Click here for file miR-9 expression in the adult zebrafish brain. [score:3]
For example, miR-9 is expressed in telencephalic, diencephalic and tectal periventricular proliferative zones as well as the mature neurons that arise from these domains (Figure 1c,f; 2 and 3, and Table A in7). [score:3]
miR-9 expression in the 3 days post-fertilization (dpf) zebrafish brain. [score:3]
Click here for file miR-9 expression in the 5 days post-fertilization (dpf) zebrafish brain. [score:3]
Additional data file 3 is a figure showing miR-9 expression in the 5 dpf zebrafish brain. [score:3]
Likewise, miR-9 is expressed wi dely in periventricular zones and in many differentiated cells throughout the adult brain as in the larval brain (for instance, compare Vv in Figure 1i with Sv in Figure 1c; 2-4, and Tables A and F in7). [score:3]
miR-137 (Figure 5i) and miR-9 (Figure G in) show expression in groups of dorsal lateral habenular cells of the adult brain. [score:3]
[1 to 20 of 17 sentences]
4
[+] score: 47
For instance, miR-9-2 is highly expressed in the developing retina (Figure 2C, white asterisk), miR-9–4 showed early expression in the posterior brain regions (Figure 2E, white arrowhead) and miR-9-6 showed a distinctive strong expression in the hypothalamus (Figure 2H, white arrow). [score:7]
However, differences in fine patterns of expression were detected between different miR-9 family members most notably at prim6. [score:3]
Figure 2. Expression pattern revealed by in situ hybridization of mature miR-9 and pri-miRNA transcripts during prim6 stage. [score:3]
Expression of these pri-miRNA precedes the appearance of detectable levels of mature miR-9 in these brain regions, as seen at 48hpf (Supplementary Figure S3C). [score:3]
In zebrafish embryos, miR-9 expression is detected around 20 hpf (30 somites stage) in the telencephalon, and later spreads to a more posterior region of the brain (38). [score:3]
Furthermore, we demonstrated that our predicted pri-miRNAs are bona fide transcripts by validating seven paralogous copies of miR-9, by describing their processing and by identifying their expression patterns. [score:3]
The expression pattern of mature miR-9, determined by miR-9 antisense LNA probe, is restricted to telencephalon during prim6 stage (Figure 2A). [score:3]
The differential distribution of miR-9 pri-miRNAs might generate different level of mature miR-9 in different brain areas relative to its mRNA targets, and might thus impact its functional output. [score:3]
The miR-9 family is highly conserved and a crucial regulator of embryonic neurogenesis in vertebrates (37). [score:2]
Coolen M. Katz S. Bally-Cuif L. miR-9: a versatile regulator of neurogenesis Front. [score:2]
Similarly, analysis of miR-9–1/6 products indicated that the 5′-ends mapped in close vicinity (1 base offset) to the predicted Drosha cleavage site (red arrow; Figure 6C and  D). [score:1]
To validate the annotated pri-miRNA promoters, we selected the miR-9 family with seven paralogous copies. [score:1]
Validation of pri-miRNAs transcription start site regions and pre-miRNA processing sites of the miR-9 family. [score:1]
In contrast, 5′ RACE PCR of miR-9-4 did not reveal any discrete TSS in the upstream region (Figure 2K) consistent with the lack of alternative intronic CAGE tags, further suggesting that miR-9-4 is processed from its host gene as predicted by CAGE analysis. [score:1]
Spatiotemporal distribution of each miR-9 pri-miRNA was determined by ISH probes (Supplementary Figure S3B), and was highly reminiscent of the mature miR-9 LNA probe, mostly restricted to the telencephalon at prim6 (Figure 2B- I) and at later stages including the posterior brain (Supplementary Figure S3C), thus validating these transcripts as miR-9 precursors. [score:1]
Antisense DIG labeled RNA probes for each miR-9 transcripts were synthesized and in situ hybridization performed using standard protocols (36). [score:1]
Leucht C. Stigloher C. Wizenmann A. Klafke R. Folchert A. Bally-Cuif L. MicroRNA-9 directs late organizer activity of the midbrain-hindbrain boundary Nat. [score:1]
Except for miR-9-1, CAGE-seq detected miR-9 pri-miRNA TSSs at 16 hpf (14 somites stage) (Supplementary Figure S3A) before mature miR-9 becomes detectable by in situ hybridization. [score:1]
Distinct CAGE tags mapped to the promoter of annotated pri-miRNA transcripts of miR-9 (Supplementary Figure S2). [score:1]
Figure 6.3′ RACE PCR amplification of miR-9-(1/4/5/6). [score:1]
Z and RNAPII peaks at pre-miRNAs suggesting local promoter activity, however CAGE-seq and 5′ RACE PCR of two pre-miR-9 candidates did not support production of capped RNA at these predicted local promoter regions (Figure 2J and  K). [score:1]
Multiple non-specific bands and/or a smear were obtained for miR-9-4 that did not have alternative intronic CAGE tags. [score:1]
We have noticed H3K4me3 -modified histones are present on pre-miRNA sites of individual miR-9 in zebrafish and human (Figure 4A, B; Supplementary Figure S2). [score:1]
Analysis of miR-9–4/5 products indicated that the 5′-ends mapped exactly to the annotated Drosha cleavage site (red arrow; Figure 6A and  B), further suggesting that it is first processed from the host intron and subsequently capped. [score:1]
Similarly, 3′ RACE PCR on four pre-miR-9 candidates revealed no local promoter activity, but indication of Drosha cleavage. [score:1]
[1 to 20 of 25 sentences]
5
[+] score: 37
The expression of the miR-9 family of genes is dynamically regulated [42] during differentiation and development, and the human miR-9 family has three members: hsa-mir-9-1, -2, and -3. In the human genome, hsa-mir-9-2 and hsa-mir-9-3 are intergenic miRNAs, and hsa-mir-9-1 is found in the second intron of C1orf61. [score:5]
Our predictions included 29 ST miRNA genes/miRNA gene clusters, 19 of which have known functions in development (Additional file 5 and Table S3) as well as the miR-9 family, which are the validated GRB target miRNAs. [score:4]
The miR-9 family of miRNAs is a known, experimentally verified GRB target [17] and therefore a prime example for illustrating how the genomic features we analyzed could serve to annotate miRNAs under long-range regulation. [score:4]
The analysis of the mir-9 miRNA family members (dre-mir-9-5 and ) dre-mir-9-1) in zebrafish has shown that they are regulated by the same type of enhancers as protein-coding GRB target genes [17]. [score:4]
In summary, the genomic features of regions around members of the miR-9 family display characteristics equivalent to those of protein-coding GRB target genes, lending further support to the use of these features for predicting novel miRNA targets of long-range regulation. [score:4]
Furthermore these predictions include miRNAs of the miR-9 family, which are the only experimentally verified GRB target miRNA genes. [score:3]
However, it was shown that two regions with enhancer activity located ~10 kb downstream of dre-mir-9-1, the zebrafish ortholog of hsa-mir-9-1, and ~100 kb downstream of dre-mir-9-5, the zebrafish ortholog of hsa-mir-9-2, gave the reporter gene an expression pattern similar to that of zebrafish miR-9, but not the zebrafish myocyte enhancer factors [17]. [score:3]
The mir-9 family of miRNAs is highlighted since it contains know examples of GRB target miRNAs that were captured using our two prediction features: 1) localization in regions of high HCNE density and 2) association with a bivalent promoter. [score:3]
Furthermore these predictions include miRNAs of the miR-9 family, which are the only experimentally verified GRB target miRNAs. [score:3]
Given this functional similarity as well as recent zebrafish transgenesis assays showing that the miR-9 family is indeed regulated by with enhancer activity, we hypothesized that this type of miRNA regulation is prevalent. [score:2]
Therefore, all miR-9 family members can be classified as ST miRNAs and are likely to have their own promoters. [score:1]
Figure 4 Case study of the miR-9 family. [score:1]
[1 to 20 of 12 sentences]
6
[+] score: 34
miR-124 is expressed by differentiated neurons while miR-9 was reported, in zebrafish, to be up-regulated in the regions where adult neurogenesis occurs (Kapsimali et al., 2007). [score:6]
miR-9, however, was not up-regulated in the germinal layer of the OT (arrow), indicating that miR-9 is not associated with neuroepithelial progenitors. [score:4]
Here, we report that miR-9 is highly expressed in the radial glia in telencephalon and OT but not in the neuroepithelial precursors of the OT. [score:3]
The expression pattern of miR-9 in the telencephalon was complementary to that of miR-124 and was concentrated in the neurogenic niches (Fig. 3C,D). [score:3]
Confocal microscopy (Fig. 3E,F) revealed partial colocalization of miR-9 and EdU 4 h postinjection, indicating that miR-9 is expressed in mitotically active neuronal progenitors. [score:3]
This result is in line with the expression domains reported in adult zebrafish brain (Kapsimali et al., 2007) and suggests that miR-9 controls the activity of the neurogenic radial glia, while miR-124 is necessary for differentiation of postmitotic neurons. [score:3]
This area corresponds to the location of radial glia (Fig. 5, see below), where expression of miR-9 is particularly high (Fig. 3H). [score:3]
MicroRNAs are emerging as important regulators of neurogenesis and in particular miR-9 and miR-124 (Leucht et al., 2008; Cheng et al., 2009; Yoo et al., 2009). [score:2]
Magnification of the region boxed in E is shown in panel F. (G, H) In situ hybridization labeling in the optic tectum for miR-9 (G) and miR-124 (H). [score:1]
Single-channel visualizations of in situ hybridization for miR-124 and miR-9 in the telencephalic structure (Fig. 3B,D,F) are shown in Fig. S6 (Supporting Information, A/B, D/E, G/H, respectively). [score:1]
Note the exclusion of miR-124 and miR-9 as well from the germinal layer (arrow) and the complementary labeling pattern of miR-124 and miR-9 in the radial glia (arrowheads). [score:1]
Fig. S6 In situ hybridization for miR-124 and miR-9 (separated and merged channels). [score:1]
The microRNAs, miR-9 and miR-124, are known to control neurogenesis and neuronal differentiation (Leucht et al., 2008; Cheng et al., 2009; Yoo et al., 2009; Bonev et al., 2011). [score:1]
A preliminary study of small RNA sequencing (M. Baumgart, M. Grothe, M. Platzer, A. Cellerino, paper in preparation) revealed that the sequences of mature miR-124 and miR-9 in N. furzeri are identical to the sequences of Danio rerio. [score:1]
Fig. 3 In situ hybridization for miR-124 and miR-9 (A–H) in the telencephalic and tectal structures of 7-week-old Nothobranchius furzeri (young adult), and double-staining for doublecortin (DCX)/PCNA andDCX/5-ethynil-2′deoxyuridin (EdU) (I-T). [score:1]
[1 to 20 of 15 sentences]
7
[+] score: 18
The miR-9 is abundantly expressed in developing neurogenic cell that regulates neuron differentiation [31]. [score:4]
The 3 ng/embryo of control mimic (5’-UCACAACCUCCUAGAAAGAGUAGA-3’), 1.5 and 3 ng/embryo miR-145 mimic (5’-GUCCAGUUUUCCCAGGAAUCCCU-3’), 3 ng/embryo miR-9 mimic (5’-UCUUUGGUUAUCUAGCUGUAUGA-3’), 0.03ng/embryo miR-206 mimic (5′-UGGAAUGUAAGGAAGUGUGUGG-3’), 3 ng/embryo miR-731 mimic (5’-AAUGACACGUUUUCUCCCGGAUCG-3’), 3 ng/embryo miR-217 mimic (5’-UACUGCAUCAGGAACUGAUUGG-3’) and 1.5 and 3 ng/embryo miR-145 inhibitor (Dharmacon, Thermo) were injected into one-cell stage embryos. [score:3]
From miRNAs prediction of GrnA, miR-9, miR-206, miR-731, and miR-217 on 3’ UTR were predicted by TargetScan (http://www. [score:3]
Because the 3’UTR of GrnA is 487 nucleotides in size, there are only putative four miRNAs, including miR-9, miR-206, miR-731 and miR-217 predicted by TargetScan. [score:3]
The EGFP expression of Tg (fabp10: EGFP) fish showed no significantly changes in liver size in miR-9 mimic-, miR-206 mimic-, miR-731 mimic- and miR-217 mimic -injected fish, but the miR-145 mimic -injected fish has a smaller liver size (Fig 1B). [score:3]
Liver morphology at 4 dpf was observed after injecting control mimic, miR-145 mimic, miR-9 mimic, miR-206 mimic, miR-731 mimic and miR-217 mimic in Tg(fabp10: EGFP) embryos. [score:1]
The miRNA predictions of GrnA included miR-9, miR-206, miR-731, miR-217 on 3’UTR and miR-145 on CDS region (Fig 1A). [score:1]
[1 to 20 of 7 sentences]
8
[+] score: 16
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-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, 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-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, 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-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-17a-1, dre-mir-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, 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-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
microRNA-9 suppresses the proliferation, invasion and metastasis of gastric cancer cells through targeting cyclin D1 and Ets1. [score:5]
MicroRNA-9 regulates neurogenesis in mouse telencephalon by targeting multiple transcription factors. [score:3]
A feedback regulatory loop involving microRNA-9 and nuclear receptor TLX in neural stem cell fate determination. [score:2]
MicroRNAd regulates the TLX/microRNA-9 cascade to control neural cell fate and neurogenesis. [score:2]
MicroRNA-9: functional evolution of a conserved small regulatory RNA. [score:1]
miR-9 is also a brain-enriched miRNA (Landgraf et al., 2007) and it is evolutionary conserved from flies to human (Yuva-Aydemir et al., 2011). [score:1]
miR-9. Conclusion and perspectives. [score:1]
MicroRNA-9 directs late organizer activity of the midbrain-hindbrain boundary. [score:1]
[1 to 20 of 8 sentences]
9
[+] score: 15
Other miRNAs from this paper: dre-mir-181b-1, dre-mir-181b-2, dre-mir-181a-1, 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-9-1, dre-mir-9-2, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-16b, dre-mir-16c, dre-mir-29a, dre-mir-101a, dre-mir-144, dre-mir-153b, dre-mir-181c, dre-mir-462, dre-mir-457b, dre-let-7j, dre-mir-181a-2, dre-mir-1388, dre-mir-7147, ipu-let-7a-7, ipu-let-7a-1, ipu-let-7a-3, ipu-let-7a-5, ipu-let-7a-6, ipu-let-7a-4, ipu-let-7a-2, ipu-let-7b-2, ipu-let-7b-1, ipu-let-7c-1, ipu-let-7c-2, ipu-let-7d-2, ipu-let-7d-1, ipu-let-7e-2, ipu-let-7e-1, ipu-let-7f, ipu-let-7g-1, ipu-let-7g-2, ipu-let-7h, ipu-let-7i, ipu-let-7j-1, ipu-let-7j-2, ipu-mir-101a, ipu-mir-1388, ipu-mir-144, ipu-mir-153b, ipu-mir-16b, ipu-mir-181a-1, ipu-mir-181a-2, ipu-mir-181a-3, ipu-mir-181a-4, ipu-mir-181a-5, ipu-mir-181b-2, ipu-mir-181b-1, ipu-mir-181c, ipu-mir-462, ipu-mir-9-4, ipu-mir-9-2, ipu-mir-9-6, ipu-mir-9-1, ipu-mir-9-3, ipu-mir-9-7, ipu-mir-9-5, ipu-mir-7147, ipu-mir-29a, ipu-mir-16c, ipu-mir-203c, ipu-mir-129b, ipu-mir-7553, ipu-mir-7556, ipu-mir-7562, ipu-mir-7568, ipu-mir-7569, ipu-mir-7570, ipu-mir-7571, ipu-mir-7572, ipu-mir-7573, ipu-mir-7574, ipu-mir-7575, ipu-mir-7576, ipu-mir-7577, ipu-mir-457b, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d
Another highly expressed miRNA family was ipu-miR-9 (807,317reads), an important miRNAs that show brain-specific expression in mammals and fish [33]– [34]. [score:5]
Leucht et al. found that the organizing activity and progenitor state of the midbrain-hindbrain boundary (MHB) are co-regulated by miR-9 during late embryonic development of zebrafish. [score:3]
Functional studies demonstrate that miR-9 can target several components of the Fgf signaling pathway, thereby promoting the organizing activity of the MHB. [score:3]
Some highly expressed miRNAs, like ipu-miR-462 and ipu-miR-9, were poorly represented by their star sequences. [score:3]
In addition, zebrafish miR-9 promotes progression of neurogenesis in the MH, defining the MHB progenitor pool [34]. [score:1]
[1 to 20 of 5 sentences]
10
[+] score: 12
Other miRNAs from this paper: dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-210, dre-mir-214, dre-mir-219-1, dre-mir-219-2, dre-mir-221, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, dre-mir-429a, 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-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-21-1, dre-mir-21-2, dre-mir-25, dre-mir-30e-2, dre-mir-101a, dre-mir-103, dre-mir-107a, dre-mir-122, 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-126a, dre-mir-129-2, dre-mir-129-1, dre-mir-130b, dre-mir-130c-1, dre-mir-130c-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-135c-1, dre-mir-135c-2, dre-mir-140, dre-mir-142a, dre-mir-142b, dre-mir-150, dre-mir-152, dre-mir-462, dre-mir-196a-2, dre-mir-196b, dre-mir-202, dre-mir-203b, dre-mir-219-3, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-mir-455-1, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-135b, dre-mir-135a, dre-mir-499, dre-mir-738, dre-mir-429b, dre-mir-1788, dre-mir-196c, dre-mir-107b, dre-mir-455-2, dre-mir-222b, dre-mir-126b, dre-mir-196d, dre-mir-129-3, dre-mir-129-4
Some miRNAs were mainly expressed during development, namely dre-miR-430 family, dre-miR-135c and dre-miR-9. The former was absent in the adult fish while dre-miR-135c and dre-miR-9 had decreased expression in mature organs with exception of the brain. [score:6]
For example, the miR-430 family, dre-miR-135c and dre-miR-9 were mainly expressed during development, but the miR-430 family was absent in adult fish, while dre-miR-135c and dre-miR-9 showed decreased expression in mature organs with exception of the brain. [score:6]
[1 to 20 of 2 sentences]
11
[+] score: 9
Furthermore, although the misexpression of Notch signaling components or miR-9 shifts the balance between proliferation and quiescence, these effects are independent of gata3 expression [53••]. [score:5]
This is based on the findings that the Notch signaling is a major determinant of stem cell quiescence [49], its gradient in the pallium is regulated by a transcription factor Fezf2 [50•], and microRNA miR-9 is a downstream effector of Notch signaling during development and homeostatic state of the adult fish brain [51, 52]. [score:3]
In homeostatic constitutive neurogenesis Fezf2 [50], Notch3 [49], miR-9 [53], and Estrogen [54] favor quiescence of neural stem cells where Notch1 [49] promotes proliferation Upon traumatic injuries, acute inflammation induces the plasticity of neural stem cells through LTC4 [42], Gata3 [41], and Cxcr5 [40] signaling, and Id1 [44] restores quiescence of neural stem cells. [score:1]
[1 to 20 of 3 sentences]
12
[+] score: 9
Also, the neuronal enriched miR-128 regulates Reelin and Dcx and migratory potential of neuronal cells through distinct mechanisms [35], while miR-9 regulates the Fgf signaling by inhibiting Fgf8, Fgfr1 and Canopy1 and exerts a proneurogenesis effect by inhibiting expression of antineurogenic bHLH [33]. [score:9]
[1 to 20 of 1 sentences]
13
[+] score: 6
Inhibition of three miRNAs, let-7, miR-125, and miR-9, caused similar defects in retinal development shown in Dicer1 conditional knock-out mice, further confirming that miRNAs are essential for early retinal development [23]. [score:6]
[1 to 20 of 1 sentences]
14
[+] score: 6
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, rno-mir-148b, 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-9-3, 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
In them, four miRNAs (miR-9, miR-124, miR-128a and miR-128b) were previously reported to be specifically expressed in the cortex and hippocampus in rat [18]. [score:3]
Moreover, miR-200b is enriched in zebrafish olfactory bulb; miR-124 and miR-9 expression are detected throughout adult brain [16]. [score:3]
[1 to 20 of 2 sentences]
15
[+] score: 3
Other miRNAs from this paper: dre-mir-10a, dre-mir-10b-1, dre-mir-183, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, 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-mir-1-2, dre-mir-9-1, dre-mir-9-2, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-20a, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-101a, dre-mir-101b, 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-145, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-mir-499, ola-mir-430a-1, ola-mir-430c-1, ola-mir-430b-1, ola-mir-430c-2, ola-mir-430c-3, ola-mir-430d-1, ola-mir-430a-2, ola-mir-430c-4, ola-mir-430d-2, ola-mir-430a-3, ola-mir-430a-4, ola-mir-430c-5, ola-mir-430d-3, ola-mir-430b-2, ola-mir-430c-6, ola-mir-430c-7, ola-mir-20a-1, ola-mir-92a-2, ola-mir-9a-2, ola-mir-101a, ola-mir-9b-1, ola-mir-499, ola-let-7a-1, ola-mir-9a-3, ola-mir-183-1, ola-let-7a-2, ola-mir-29b-1, ola-mir-29a, ola-mir-124-1, ola-mir-124-2, ola-mir-9a-4, ola-mir-101b, ola-let-7a-4, ola-mir-10d, ola-mir-9a-1, ola-mir-92b, ola-mir-9b-2, ola-mir-1-2, ola-mir-124-3, ola-mir-15a, ola-mir-10b, ola-mir-92a-1, ola-mir-20a-2, ola-mir-17, ola-mir-29b-2, ola-mir-29c, ola-mir-183-2, ola-let-7a-3, ola-mir-9a-5, ola-mir-145, dre-mir-29b3
The expression of the following miRNAs in the brain was confirmed by in situ hybridisation using LNA probes (Exiqon): miR-9, miR-124 [63] and miR-15a, miR-20a [64]. [score:3]
[1 to 20 of 1 sentences]
16
[+] score: 3
Thus, miR-9 facilitates the transition of progenitors toward cell-cycle exit at late stages of embryonic development [127], to enable the nervous system to generate an increased number of neurons at this stage [128]. [score:2]
Indeed, microRNA-9 defines an intermediate, ambivalent state by repression of both the progenitor marker Her6 as well as the post-mitotic marker Elavl3, formerly known as HuC. [score:1]
[1 to 20 of 2 sentences]
17
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-18a, hsa-mir-21, hsa-mir-27a, hsa-mir-96, hsa-mir-99a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30b, mmu-mir-99a, mmu-mir-124-3, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-181a-2, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-21a, mmu-mir-27a, mmu-mir-96, mmu-mir-135b, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, hsa-mir-200a, hsa-mir-135b, dre-mir-182, dre-mir-183, dre-mir-181a-1, 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-9-1, dre-mir-9-2, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-15a-1, dre-mir-15a-2, dre-mir-18a, dre-mir-21-1, dre-mir-21-2, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30b, dre-mir-96, 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-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-135c-1, dre-mir-135c-2, dre-mir-200a, dre-mir-200b, dre-let-7j, dre-mir-135b, dre-mir-181a-2, dre-mir-135a, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
miRNAs appeared in the mammalian inner ear field in 2006, with the description of miR-9 as a potential regulator of the COL9A1 short isoform (Sivakumaran et al, 2006). [score:2]
[1 to 20 of 1 sentences]
18
[+] score: 2
Given that brain morphogenesis disruption by ethanol exposure resulted in abnormal neurobehavioral development in zebrafish larvae and juveniles, miRNAs were essential for the establishment of vertebrate neurobehavioral and skeletal systems (e. g., miR-9/9* and miR-153c) [10]. [score:2]
[1 to 20 of 1 sentences]
19
[+] score: 2
MicroRNA miR-9 modifies motor neuron columns by a tuning regulation of FoxP1 levels in developing spinal cords. [score:2]
[1 to 20 of 1 sentences]
20
[+] score: 1
B1: An interesting example from the network highlighted in orange showing interactions between of network highlighting miRNA: (a) hsa-mir-9; lncRNA: (d) ENST00000500197.2, (e) ENST00000509783.1, (f) ENST00000511014.1, (h) ENST00000505030.1, (i) ENST00000504246.1; mRNA: (b) ENST00000384838.1, (c) ENST00000262095.2, (g) ENST00000491143.1, (j) ENST00000226574 B2: Another interesting example from the network highlighted in blue showing interactions between miRNA: (1) hsa-miR-196a, (5) hsa-miR-196b*, (13)hsa- miR-196b; lncRNA: (4) ENST00000523790.1; (6) ENST00000489695.1, (12) ENST00000519935.1; mRNA: (2) ENST00000354032.4, (3) ENST00000384852.1, (7) ENST00000313173, (8) ENST0000024215, (9) ENST00000040584, (10) ENST00000304786.7, (11) ENST00000366839.4. [score:1]
[1 to 20 of 1 sentences]
21
[+] score: 1
A nuclear role for miR-9 and argonaute proteins in balancing quiescent and activated neural stem cell states. [score:1]
[1 to 20 of 1 sentences]
22
[+] score: 1
The induction of members of the miR-21, miR-29, and miR-146 families was in line with earlier microarray studies, which reported these along with some other miRNAs, like miR-9, miR-132, miR-147, and miR-155 as infection-inducible [13, 26, 43, 44]. [score:1]
[1 to 20 of 1 sentences]