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19 publications mentioning dre-mir-200a

Open access articles that are associated with the species Danio rerio and mention the gene name mir-200a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 187
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-9-4, 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-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]
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]
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]
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]
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]
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]
•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]
2.9To downmodulate endogenously expressed miR-9 and miR-200 we used the commercially available Ambion anti-miR inhibitors (Life Technologies). [score:5]
To downmodulate endogenously expressed miR-9 and miR-200 we used the commercially available Ambion anti-miR inhibitors (Life Technologies). [score:5]
On the contrary, DLX5 overexpression did not induce changes in miR-200 expression, either in SH-SY5Y (Fig.  2d) or in GN11 (neuroendocrine) or in U2OS (osteosarcoma) cells (data not shown). [score:5]
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]
Alternatively the expression of miR-200a/ b/ miR-429 could require additional transcription (co)factors not present in these cells. [score:3]
To overexpress miR-9 and miR-200 exogenously we used commercially available Ambion pre-miR precursors (Life Technologies). [score:3]
miR-200a, miR-200b, miR-141 and miR-429 share the same seed sequence and likely target the same mRNAs; for this reason they are grouped in a single miR class (named miR-200-class). [score:3]
The 3′ UTR of tetrapod and zebrafish Foxg1 mRNAs hosts miR-9 and miR-200 target sequences. [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]
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]
Searching for functionally relevant targets of miR-9 and miR-200 clsss in the OE. [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]
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]
Instead, we could easily monitor the number and position of early GFP -expressing neurons, and noted that upon depletion of miR-200 class they appear reduced in number but normally clustered. [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]
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]
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]
In the same cells, the expression of pre -miR-200 led to a 3.9-fold decrease in Foxg1 proteins level (Fig.  3c). [score:3]
The most abundant miRs expressed in the developing mouse OE are: the miR-200-class (- 200a, - 200b, - 200c, - 141 and - 429), miR-199, miR-152, miR-214, miR-205, miR-183, miR-182 and miR-96 (Choi et al., 2008). [score:3]
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]
Another indication comes from a study in zebrafish, showing a role of miR-200-class for olfactory development (Choi et al., 2008). [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]
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]
miR-9 and miR-200-class regulate Foxg1. [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]
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]
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]
It has also been shown that miR-200 represses neural induction of human embryonic stem cells, via modulation of Pax6 and Zeb transcription factors (Du et al., 2013). [score:1]
Since miR-200a, miR-200b, miR-141 and miR-429 share very similar seed sequences (Suppl. [score:1]
miR200a and miR200b could not be tested by in situ hybridization due to high sequence conservation between all members of the miR-200-class. [score:1]
To complement the previous (static) data with live images of the migrating GnRH3 neurons, we carried out few time-lapse video recordings on untreated (4) and z- miR-200-class MO injected (4) embryos at earlier ages (36–52 hpf), in order to observe the first appearance of these neurons. [score:1]
We depleted the miR-200 class in fish zygotes, by injecting a mix of anti -miR-200 MO previously described and found to efficiently down-modulate several miR of the class-200 and to affect ORN differentiation (Choi et al., 2008). [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 abundance of z-hoxa-7a and z-hoxa-10b mRNAs did not greatly change, indicating that the differentiation delay observed upon depletion of miR-200-class is specific. [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]
z-foxg1 mRNA level increased by three-folds when either miR-9 or miR-200-class were depleted (Figs.  5e and 6f). [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]
3.4The 3′ UTR of the mammalian and fish Foxg1 mRNA contains seed sequences for miR-9 and miR-200 (Suppl. [score:1]
Depletion of miR-9 and miR-200-class in zebrafish results in altered GnRH neuron genesis and position. [score:1]
Previous results in which zebrafish embryos were injected with anti- miR-200 class MOs found a delayed ORN differentiation, but axonal organization and GnRH neuron migration was not assessed (Choi et al., 2008). [score:1]
com/request/, while the anti- z-miR-200 MO mix was as previously published (Choi et al., 2008). [score:1]
Similarly, the depletion of miR-200-class (N = 23) resulted in a reduced number of GFP + neurons in 22% of GFP + embryos with the phenotype “reduced number” and 50% of the cases showing the phenotype “scattered position” (Fig.  7). [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]
In Danio rerio (zebrafish) the miR-200-class is required for the proliferation, differentiation and survival of ORNs (Choi et al., 2008). [score:1]
Upon injection of the anti-miR-200 MO mix, only about 24% of examined embryos turned out CFP + (vs. [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]
The miR-200a, - 200b and - 429 loci are closely located on chromosome 4, while miR-141 and -200c are closely located on chromosome 6. miR-376a is clustered with 16 other miRs on chromosome 12. [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]
miR-9 and miR-200 mediate the Dlx5-Foxg1 cascade. [score:1]
Depletion of miR-9 and miR-200-class in zebrafish results in delayed ORN differentiation. [score:1]
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]
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2
[+] score: 177
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-191, mmu-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-let-7d, 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, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, 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, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, mmu-mir-429, mmu-mir-449a, 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-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-140, dre-mir-141, dre-mir-152, 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, dre-let-7j, mmu-mir-449c, mmu-mir-449b, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-124b
These results argue that lfng and zfhx1 can be efficiently downregulated by the miR-200 family alone, whereas foxg1 and neuroD, although likely genuine targets, may require the combined action of several miRNA species in addition to miR-200 action, in order to be efficiently downregulated. [score:9]
Our data show that expression patterns of genes expressed throughout the brain and in areas devoid of miR-200 family expression were comparable between wild-type and triple MO morphants, indicating that widespread neural defects were absent in the morphant fish (Figure 7D). [score:7]
Intriguingly, miR-200 family members are coordinately expressed from different loci, yet members express different 5′ seed heptamers, changes in which are thought to alter the binding specificity to target mRNA (Doench and Sharp, 2004; Lewis et al., 2005). [score:7]
Knocking down the expression of mature miR-200 family members led to impairment of mature olfactory marker expression and expansion of the early marker, foxg1, in the olfactory primordium. [score:6]
Expression of the miR-200 family can be detected in olfactory placodes as early as E9.5, which is the first identifiable stage of olfactory development, with continued expression within the MOE anlage in the posterodorsal aspect of the olfactory pit at E11.5 (Figure 2B). [score:6]
In addition, in situ hybridization analyses (Figure 7C) show that a mixture of all three morpholinos (Triple MO mix: miR-141 MO, miR-200b MO, and miR-429 MO) was sufficient to simultaneously inhibit the expression of all five mature zebrafish miR-200 family members to threshold levels of detection. [score:5]
We conclude that foxg1, zfhx1, and lfng are likely to be genuine targets for miR-200 family members in both mouse and zebrafish olfactory systems, while neuroD might only be a target in the fish. [score:5]
Antisense morpholino experiments in zebrafish reveal that the inhibition of expression of a single miRNA family, miR-200, largely phenocopies the defect in terminal olfactory differentiation resulting from lack of Dicer function in mouse olfactory progenitor cells. [score:5]
Exogenous miR-200 duplex RNA was able to reduce expression of the lfng and zfhx1 reporters, while miR-200 duplexes did not affect GFP expression levels for the foxg1 and neuroD reporters (Figure 8B). [score:5]
Finally, 8 of 24 miRNA probes, including miR-200a and miR-200b, as well as miR-96, miR-141, miR-182, miR-183, miR-191, and miR-429, revealed robust expression in the MOE and VNO neuroepithelium, with weaker expression in the adjacent respiratory epithelium (Figure 2A, right column, and Table S3). [score:5]
Embryos injected with either miR-141/miR-200a or miR-200b/miR-429 pairs of antisense morpholinos showed lack of expression of the corresponding miR-200 members with a given 5′ seed but did not display any change in OMP expression relative to wild-type controls (data not shown). [score:5]
Moreover, increased foxg1 expression observed in the zebrafish morpholino experiments and in the mouse conditional Dicer microarray experiments (Table S3) also suggests that foxg1 may be a genuine miR-200 family target. [score:5]
As predicted from sequence analyses and thermal stability calculations, miR-141 MO specifically inhibited miR-200a and miR-141, miR-200b MO specifically inhibited miR-200b and miR-200c, and miR-429 MO specifically inhibited miR-429 (Figure S4B). [score:5]
In situ hybridization analyses using LNA antisense probes to detect mature miRNAs indicated that 4 ng per embryo per miR-200 family member was the minimal dose required to knock down miRNA expression to threshold levels of detection (data not shown). [score:4]
Taken together, these results indicate that in the absence of miR-200 family expression during olfactory placodal development, zebrafish olfactory progenitors are unable to undergo normal terminal differentiation and, instead, undergo apoptosis. [score:4]
We conclude that mature zebrafish miR-200 family members can be specifically and efficiently knocked down in various combinations in the developing olfactory system using antisense morpholinos without confounding “off-target” effects. [score:4]
Due to the molecular and cellular similarity of mouse and zebrafish olfactory development processes and the high degree of conservation between the miR-200 miRNAs in the respective organisms, we reasoned that physiologically meaningful targets were likely to be conserved between the zebrafish and mouse genomes. [score:4]
Preliminary data suggest that lunatic fringe (lfng) and zinc-finger homeobox 1 (zfhx1), two key factors associated with Notch and BMP pathways, respectively, as well as foxg1, a transcription factor required for normal olfactory development, may be relevant miR-200 targets. [score:4]
However, miR-141 and -200a express different 5′ seed heptamers from miR- 200b, -200c, and -429 and are thus likely to form two functional subgroups within the miR-200 family (Figure 2C; Doench and Sharp, 2004; Lewis et al., 2005). [score:3]
A subset, including the miR-200 family, shows high olfactory enrichment and expression patterns consistent with a role during olfactory neurogenesis. [score:3]
In the adult, the expression pattern of all miR-200 family members is restricted to the immature and mature neuronal cell layers of the MOE and is excluded from the basal and sustentacular cell layers (Figure 2B). [score:3]
The strong, specific, and coordinated expression of miR-200 members in the MOE anlage and in the mature and immature MOE is consistent with a potential role of this miRNA family during MOE neurogenesis. [score:3]
In order to further validate the physiological requirement for miR-200's action on these targets, we generated GFP reporters containing the full-length 3′ UTRs for zebrafish neuroD, foxg1, zfhx1, and lfng (Giraldez et al., 2006). [score:3]
As shown in Figure 3C, miR-200a is wi dely expressed throughout the developing MOE neuroepithelium in embryonic day 13.5 (E13.5) wild-type mice. [score:3]
Notch and TGFβ Signaling Pathways and Foxg1 Are Candidate Targets of the miR-200 Family. [score:3]
In addition, other predicted miR-200 family targets may also contribute to the olfactory phenotypes observed in morphant fish and the Foxg1-Cre;Dicer [loxP/loxP] mutant mice. [score:3]
In addition, our preliminary microarray and GFP-sensor experiments suggest that foxg1 itself, as well as lunatic fringe (lfng) and zinc-finger homeobox 1 (zfhx1), two key factors associated with Notch and BMP pathways, respectively, may be genuine miR-200 targets. [score:3]
From the over 100 distinct miRNAs identified in olfactory tissues, the most abundant miRNAs isolated from our study include species that are wi dely expressed in many neural tissues (miR-124a and let-7 variants), as well as a highly restricted family of miRNAs (miR-200). [score:3]
Recently, independent reports have demonstrated that the miR-200 family is highly expressed in skin epidermal cells (Yi et al., 2006). [score:3]
By contrast, we identified 12 miRNAs corresponding to 9 families (miR-199, miR-140, miR-152, miR-214, miR-205, miR-200, miR-183, miR-182, miR-96) that displayed highly enriched expression in the olfactory system (Figure 1A). [score:3]
To gain further insights into the role of the miR-200 family in mediating olfactory differentiation, we used a bioinformatic approach to predict and validate potential miR-200 targets. [score:3]
Thus, the regulatory step involving the miR-200 family, and shown here to be essential for olfactory neurogenesis, may be employed by other systems of epithelial origin to ensure the proper mediation of critical signaling cascades during development. [score:3]
Accordingly, we decided to focus our efforts on potential functions mediated by the miR-200 family, which is among the most highly and most specifically miRNA subset expressed in the developing olfactory system. [score:3]
All individual members of the miR-200 family display similar expression patterns. [score:3]
We designed three morpholino antisense oligonucleotides predicted to each target the mature sequence of one or a few members of the miR-200 family (Figure S4A). [score:3]
Morpholinos targeting the miR-200 family were generated as described in. [score:3]
Moreover, as shown in the mouse, miR-200 family members display early expression in zebrafish (Wienholds et al., 2005) and appear highly enriched in olfactory tissues by the time olfactory placodes arise at 26 hpf (Figure 7A). [score:3]
In marked contrast, miR-200a expression is undetectable in the MOE of E13.5 Foxg1-Cre [+/−]; Dicer [loxP/loxP] mutants, despite the fact that the main olfactory epithelium is still present at this stage, as revealed by Foxg1 staining in adjacent sections (Figure 3C). [score:3]
The function of miR-200 during olfactory development is likely to be conserved throughout evolution, as judged from the absolute conservation of miR-200 orthologs between mouse and zebrafish with respect to the relative genomic clustering position, the conserved seed region sequences, the conserved size of the family, and the conserved arm of the hairpin that generates the mature miRNA (Figure S3). [score:2]
The morpholino knockdown experiments show that miR-200 family members are likely to act redundantly, even though they display different 5′ seed regions. [score:2]
The intriguing specificity and intensity of expression of the miR-200 family members in the MOE prompted us to pursue an in-depth investigation of their distribution during embryonic development and in the adult. [score:2]
These results indicate that the functional loss of the miR-200 family precludes normal differentiation of olfactory progenitor cells into mature olfactory neurons and thus phenocopies an important aspect of the Dicer knockout phenotype observed both in mice and zebrafish. [score:2]
The miR-200 family is therefore among the first neuronal miRNA families in vertebrates with a loss-of-function phenotype. [score:1]
We used the MicroCosm system that interfaces the miRanda prediction software with miRBase, the accepted database of miRNA classification, to confirm that mouse orthologs of zebrafish neuroD, foxg1, zfhx1, and lfng have conserved miR-200 seeds in their 3′UTRs (Griffiths-Jones et al., 2006) (Figure 8A). [score:1]
In mouse, the miR-200 family is composed of five family members (miR-141, -200a, -200b, -200c, -429) clustered into two loci of chromosomes 4 and 6 (Figure 2C). [score:1]
These results suggest that the loss of miR-200 family function disrupts terminal differentiation of olfactory progenitor cells, thus phenocopying an important aspect of the defects observed in mouse Foxg1-Cre; Dicer [loxP/loxP] mutant MOE. [score:1]
We subsequently performed immunohistochemical identification of proliferating and apoptotic cells in order to determine whether miR-200 morphant olfactory phenotypes are accompanied by increased cellular apoptosis, as observed in Dicer null mouse olfactory placodes. [score:1]
In order to test the specificity of each morpholino (MO) sequence, we systematically injected one-cell zebrafish embryos with either miR-141 MO, miR-200b MO, or miR-429 MO and performed in situ hybridization against all five miRNAs of the miR-200 family. [score:1]
To evaluate the contribution of specific miRNAs, we focused on the miR-200 family, which is highly and specifically expressed in the developing olfactory system. [score:1]
By contrast, miR-200 morphant olfactory epithelia presented significantly increased numbers of apoptotic cells relative to wild-type controls (mean ± SEM, WT 12.55 ± 1.46, n = 11; mutant 30.67 ± 2.59, n = 12, p < 0.01, Student's t test) (Figure 7F), as detected by TUNEL staining. [score:1]
One of these families, miR-200 family comprising miR-200a, miR-200b, miR-200c, miR-429, and miR-141, also highly detected by microarray, was among the most frequently cloned species in all olfactory tissues examined (Table S2). [score:1]
How does the miR-200 family mediate its control of olfactory neurogenesis? [score:1]
miR-200 Family Members Are Required for the Proper Differentiation of Olfactory Progenitor Cells. [score:1]
We next wished to determine whether the distinct 5′ seeds contributed differentially to the physiological function of the miRNA-200 family. [score:1]
Loss of function of the miR-200 family phenocopies the terminal differentiation defect observed in absence of all miRNA activity in olfactory progenitors. [score:1]
Finally, we eliminated the function of all miR-200 family members by injecting embryos simultaneously with the Triple MO mix. [score:1]
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[+] score: 92
Given that recent studies have reported that the microRNA-200 family and miR-205 regulate EMT by targeting ZEB-1 and SIP-1, we examined whether the expression of members of the microRNA-200 family and miR-205 were up-regulated prior to repression of ZEB-1 and SIP-1 expression in ERβ1 -expressing cells [16]. [score:13]
By inducing the degradation of EGFR, ERβ1 sustains ERK1/2 inactive, up-regulates miR200a-b and miR-429, down-regulates ZEB1/2 and induces the expression of E-cadherin. [score:9]
The inhibition of EMT correlates with an ERβ1 -mediated up-regulation of miR-200a/b/429 and the subsequent repression of ZEB1 and SIP1, which results in increased expression of E-cadherin. [score:8]
Transfection of the cells with miR200a-b-429 inhibitors resulted in a more than two-fold increase in luciferase activity compared with the negative control inhibitor suggesting that a greater than 50% inhibition of the miR200a-b-429 function had been achieved by the miR200a-b-429 inhibitors (Figure 2F). [score:8]
ERβ1 was found to induce the expression of E-cadherin by inhibiting its transcriptional repressors ZEB1/2 and up -regulating the miR-200a, miR-200b and miR-429, which correlate with the epithelial breast cancer phenotype (Figure 6E). [score:6]
As expected, treatment of the cells with EGF restored the phosphorylation of ERK1/2, decreased the cell-cell contact observed in the ERβ1 -expressing cells and abolished the ERβ1 -mediated up-regulation of miR-200a-200b-429 and the increased levels of E-cadherin (Figure 3D-F, 3G). [score:6]
Cells were transfected with microRNA inhibitors at a final concentration of 300 nM (100 nM of each of miR-200a, miR-200b and miR-429 2'-O-Methylmodified oligonucleotides, Dharmacon, Waltham, MA USA) or a negative control inhibitor (300 nM). [score:5]
Inhibition of miR200a-b-429 partially reversed the ERβ1 -mediated epithelial phenotype and caused a 50% reduction in the expression of E-cadherin (Figure 2F). [score:5]
In addition, reduction of endogenous ERβ1 expression in MDA-MB-231 and Hs578T cells by ERβ siRNA led to a decrease in the expression of miR-200a, miR-200b and miR-429 (Figure 2E; Additional file 8, Figure S4B). [score:5]
We transfected the ERβ1 -expressing MDA-MB-231 cells with inhibitors of miR-200a, miR-200b and miR-429 and assessed the level of functional knockdown of miR200a-b-429 by a reporter assay, in which the complementary sequence of miR200a-b-429 was introduced in the 3' UTR of a luciferase reporter gene. [score:5]
ERβ1 regulates the expression of miR-200a, miR-200b and miR-429. [score:4]
We also examined how important is the up-regulation of miR-200a-b-429 for the ERβ1 -mediated repression of EMT. [score:4]
The family of microRNAs 200 (miR-200a, miR-200b, miR-200c, miR-141 and miR-429) and the miR-205A regulate the expression of the transcriptional repressors of E-cadherin ZEB-1 and ZEB-2 and, consequently, the levels of E-cadherin in breast cancer cells and tissues. [score:4]
This process requires repression of the expression of members of miR-200 family. [score:3]
miR-200 and ZEB1/2 are involved in ERβ1 -mediated regulation of E-cadherin. [score:2]
The level of functional knockdown of miR-200a-b-429 was examined by a miR-200a-b-429-regulated reporter assay. [score:2]
The figure shows the regulation of miR-200a, miR-200b and miR-429 by ERβ1 in Hs578T cells. [score:2]
The complementary sequences for miR-200a, miR-200b and miR-429 were cloned in the 3' end of the luciferace gene into the PGL3-promoter vector (Promega, San Luis Obispo, CA USA). [score:1]
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[+] score: 65
Other miRNAs from this paper: dre-mir-429a, dre-mir-141, dre-mir-200b, dre-mir-200c, dre-mir-429b
So RT-PCR was performed to check the expression of these predicted target genes after ectopic expression of miR-200 family members. [score:7]
Using the Targetscan bioinformatics algorithm, we found that several genes in the growth hormone endocrine axes, such as growth hormone (GH), growth hormone receptor a (GHRa), growth hormone receptor b (GHRb) and insulin-like growth factor 2a (IGF2a) were potential candidate targets of miR-200 family members (Fig. 2A and Fig. S1). [score:5]
However, injection of miR-141/429a inhibitors did not cause any observable developmental defects in zebrafish embryos, that was the same phenotype as injection of morpholinos of miR-200 family members 35 36. [score:4]
miR-200 s repress expression of multiple GH/IGF axis genes during embryo development. [score:4]
As a direct downstream of p53, miR-200 miRNAs have been known as inhibitors of tumor cell proliferation and growth 23. [score:4]
In zebrafish embryo, miR-200 family members regulate body growth by directly repressing critical GH/IGF axis genes, GH, GHRa, GHRb and IGF2a. [score:3]
miR-141/429a repressed the luciferase activity of GH 3′ UTR-pmirGLO, whereas mutation of either predicted miR-200a/141 or miR-200b/200c/429a/429b binding site attenuated this repression, and mutation in both binding sites abrogated this repression (Fig. 5A). [score:3]
As a tumor suppressor, the miR-200 family has anti-growth and anti-differentiation function in cancer cells 41 42. [score:3]
3′UTR fragments of target genes (GH, GHRa, GHRb, IGF2a), which contain one or more putative miR-200 binding sites were inserted into the pmir-GLO plasmid (Promega). [score:3]
Genomic organization and expression pattern of zebrafish miR-200 family members. [score:3]
To check the expression of miR-200 family members during normal embryonic development, we synthesized cDNA with a mixture of stem-loop RT primers of miR-141/200a, miR-429a/429b and miR-200b/200c, respectively. [score:3]
Characterization and expression pattern of miR-200 family members during zebrafish embryo development. [score:2]
Mut 1/mut 2 and mut 3 in GHRb 3′UTR correspondingly represented mutations of miR-200b/200c/429 and miR-200a/141 binding sites. [score:2]
And mut 1 + 2/mut 1 + 3 and mut 1 + 2 + 3 represented double and triple mutations for the miR-200 binding sites. [score:2]
Then, the binding sites of miR-200a/141 (CAGTGTT) and miR-200b/200c/429 (CAGTATT) in the constructed wild-type plasmids were replaced with TGACGCG and TCAGTCG by site-directed mutagenesis 57, respectively. [score:2]
For GH, mut1 and mut2 represented mutations of miR-200b/200c/429 and miR-200a/141 binding sites. [score:2]
miR-200 s regulate somatic growth in zebrafish embryo. [score:2]
How to cite this article: Jing, J. et al. A feedback regulatory loop involving p53/miR-200 and growth hormone endocrine axis controls embryo size of zebrafish. [score:2]
Mo del for the feedback regulatory loop involve p53/miR-200 and GH/IGF axis. [score:2]
250 ng PGL3-miR-200 promoter plasmid or PGL3-Basic empty vector was transfected into HEK-293 T cell using 25 ng pRL-TK vector (Promega) as a control. [score:1]
All the miR-200 family members were divided into three functional subgroups, miR-200b/200c, miR-200a/141 and miR-429a/429b, while miR-200b, -200c, -429a and -429b have the same seed sequence. [score:1]
Conserved miR-200–binding sites in GH and GHRb 3′ UTR are indicated and mutated separately. [score:1]
In zebrafish, the miR-200 family is composed of six family members (miR-200a, -200b, -200c, -141, -429a, -429b) clustered into two loci of chromosomes 6 and 23 (Fig. 1A). [score:1]
Furthermore, various PLG3-miR-200 promoter construct vector (wild-type or mutant) was co -transfected with 500 ng pcDNA3.1 (+)-p53-ORF plasmid. [score:1]
In the promoters of zebrafish miR-200 clusters, two putative response elements (RE1 and RE2 as a half-site) were identified from miR-200b/a/429a and miR-200c/141/429b promoters, respectively 33. [score:1]
The potential p53–binding sites in miR-200 promoters were responsible for promoter activity. [score:1]
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[+] score: 59
Values are the mean ± S. E. F, shown are qRT-PCR data of zeb1a, zeb1b, and cdh1 mRNA expression in miR-200 family -deficient embryos relative to SCMO -injected control embryos at 2- and 6-somite stage (n = 5 per condition). [score:3]
We measured the expression of miR-141 and miR-200b, located in the two different miR-200 family clusters, in zeb1b -overexpressing embryos and zeb1a/b morphants by qRT-PCR. [score:3]
zeb1a, zeb1b, and cdh1 expression in control embryos was set to 1. Values are mean ± S. E. We also performed in silico analyses of the zebrafish miR-200 clusters and the 3′-UTRs of zeb1a and zeb1b (Fig. 7 A). [score:3]
To investigate their functional relevance, we generated miR-200 morphants by injection of a triple anti-miR-200 MO mix (miR-141 MO, miR-200b MO, and miR-429 MO) that was shown to efficiently knockdown all five members of the miR-200 family (23) and controlled our knockdown experiment for the absence of expression of these by whole-mount ISH of 2-day-old embryos (data not shown). [score:3]
Zebrafish miR-200a and miR-200b have similar but not identical seed sequences and are together sufficient to post-transcriptionally repress Zeb1b expression by binding to their miR response elements (MREs) in the zeb1b 3′-UTR (23) (Fig. 7 A). [score:3]
zeb1a, zeb1b, and cdh1 expression in control embryos was set to 1. Values are mean ± S. E. We also performed in silico analyses of the zebrafish miR-200 clusters and the 3′-UTRs of zeb1a and zeb1b (Fig. 7 A). [score:3]
Finally, our results show that zebrafish Zeb1 proteins control miR-200 family member expression. [score:3]
A recent study revealed the importance of Zeb1/miR-200 regulation for the development of the mouse palate, which requires coordinated cellular rearrangements driven by EMT (60). [score:3]
To verify the efficacy of anti-miR-200 family MOs, one-cell stage embryos were injected with an anti-miR-200 MO mix (miR-141, -200b, -429) or SCMO, fixed at 48 h post fertilization (hpf), and assayed for miR-141, 200a/b/c, and -429 expression by whole-mount ISH. [score:2]
The Regulatory Feedback Loop of Zeb1 and miR-200 Is Functional but Has Only Minor Impact on Zebrafish Gastrulation. [score:2]
D, shown are live control and miR-200 family knockdown embryos at the indicated stages. [score:2]
Choi P. S. Zakhary L. Choi W. Y. Caron S. Alvarez-Saavedra E. Miska E. A. McManus M. Harfe B. Giraldez A. J. Horvitz H. R. Schier A. F. Dulac C. (2008) Members of the miRNA-200 family regulate olfactory neurogenesis. [score:2]
Bracken C. P. Gregory P. A. Kolesnikoff N. Bert A. G. Wang J. Shannon M. F. Goodall G. J. (2008) A double -negative feedback loop between ZEB1-SIP1 and the microRNA-200 family regulates epithelial-mesenchymal transition. [score:2]
Interestingly, our data show that the miR-200 family -based feedback loop controlling Zeb1 activity is functional but does not effectively contribute to control of the Zeb1-E-cadherin regulatory system during zebrafish gastrulation and segmentation stages (Fig. 8). [score:2]
Together with previously published data (23) showing miR-200 regulation of zeb1b, this reveals that the double -negative feedback loop is conserved in evolution from zebrafish to mammals. [score:2]
An additional level of adhesion regulation is established by the ZEB1/miR-200 feedback loop that controls cellular plasticity in cancer cells (14). [score:2]
In the triple anti-miR-200 MO injection, 4 ng of each MO were co -injected into the yolk at the one-cell stage. [score:1]
We analyzed the 3′-UTRs of zeb1a and zeb1b for potential MREs for the miR-200 family (Fig. 7 A, left side). [score:1]
The stem-loop sequences of miR-200b and miR-200a are separated only by a 49-base pair spacer sequence, whereas the spacer between miR-200a and miR-429 comprises 1569 base pairs. [score:1]
E, shown is quantification of epiboly progress in SCMO -injected embryos and miR-200 family -deficient embryos shown in D (shield, n = 25 embryos each; 75%-epiboly, n = 34 embryos each; 90% epiboly, n = 33 embryos each). [score:1]
Left side, shown is a scheme of the genomic organization of the zeb1b 3′UTR and the putative zeb1a 3′-UTR with their miR-200 family MREs. [score:1]
This finding and previously published data by Choi et al. (23) together reveal that the reciprocal ZEB1/miR-200 feedback loop, which plays an essential role in defining the EMT status and cellular plasticity of human cancer cell lines, is also conserved in teleosts. [score:1]
Recently we and others have shown that this morphological plasticity of cancer cells is mediated by a double -negative feedback loop between ZEB1 and the miR-200 family members (13, 14). [score:1]
The zeb1a 3′UTR contains 4, and the zeb1b 3′UTR 10 miR-200 family MREs. [score:1]
C, a comparative genomic analysis of the miR-200 family members in human (hsa) and zebrafish (dre) indicates extensive conservation with respect to the mature miR and the seed sequences. [score:1]
Studies in human cancer cell lines revealed that ZEB1 and the miR-200 family are linked in a reciprocal negative feedback loop (13, 14). [score:1]
A, shown is a schematic representation of the reciprocal Zeb1a/b-miR-200 feedback loop. [score:1]
So far little is known about Zeb1/miR-200 feedback loop functions during gastrulation. [score:1]
In summary, our in vivo and in silico data in combination with the data by Choi et al. (23) indicate that the reciprocal negative feedback loop between ZEB1 and the members of the miR-200 family is conserved through evolution. [score:1]
miR-200 morphant gastrulae displayed only a small delay of epiboly progression (Fig. 7, D and E), whereas deep cell layer thinning appeared unaffected (data not shown). [score:1]
Our results together with previously published data (23) demonstrate that the Zeb1/miR-200 double -negative feedback loop is conserved in teleosts. [score:1]
Finally, we show that Zeb1b represses transcription of miR-141 and -200b, two members of the miR-200 family. [score:1]
Burk U. Schubert J. Wellner U. Schmalhofer O. Vincan E. Spaderna S. Brabletz T. (2008) A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells. [score:1]
MOs against the miR-200 family are as published (23): anti-miR-141 (5′-GCA TCG TTA CCA GAC AGT GTT A-3′), anti-miR-200b (5′-GTC ATC ATT ACC AGG CAG TAT TA-3′), and anti-miR-429 (5′-ACGGCATTACCAGACAGTATTA-3′). [score:1]
FIGURE 7. Analysis of the potential reciprocal Zeb1a/b-miR-200 negative feedback loop. [score:1]
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[+] score: 14
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-9-4, 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-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
The expression of these miRNAs in peripheral sensory neural cells overlaps with miR-200a (Additional data file 16), although miR-200a lacks the CNS and cranial ganglia expression sites common to miR-183, miR-182 and miR-96 (Table E in7). [score:5]
Additional data file 16 is a figure showing miR-200a expression in the zebrafish brain. [score:3]
miR-200a expression in the zebrafish brain. [score:3]
Click here for file 6 miR-200a expression in the zebrafish brain. [score:3]
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7
[+] score: 13
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-9-4, 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-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
miR-200 negatively regulates the expression of Sox2 and E2F3, a pluripotency factor and a cell cycle regulator, respectively (Johnson and Walker, 1999; Peng et al., 2012). [score:5]
The lack of Sox2 and E2F3 regulation by miR-200 results in reduced cell cycle exit and neuronal differentiation of ventral midbrain/hindbrain (vMH) NPs while, overexpression of miR-200 in primary vMH NPs results in the opposite effect (Peng et al., 2012) indicating that these interactions control the proliferative state of vMH NPs (Figure 2). [score:4]
Interestingly, both TFs Sox2 and E2F3 activate miR-200 transcription which establish a negative feedback loop between miR-200 and its target genes that guaranty NPs cell cycle exit and differentiation in the midbrain/hindbrain region (MHR) (Peng et al., 2012). [score:3]
A unilateral negative feedback loop between miR-200 microRNAs and Sox2/E2F3 controls neural progenitor cell-cycle exit and differentiation. [score:1]
[1 to 20 of 4 sentences]
8
[+] score: 13
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-200c, hsa-mir-200a, dre-mir-200b, dre-mir-200c
Further study of the miR-200 family, the regulatory miRNAs targeting ZEB1 and modulating the expression of β-catenin [20], revealed that miR-200b was downregulated in A549-LG cells (Fig.   5b). [score:9]
Ahn SM Smad3 regulates E-cadherin via miRNA-200 pathwayOncogene. [score:2]
Smad3 modulates EMT in a TGF-β-independent manner through the regulation of miR-200 clusters [43]. [score:2]
[1 to 20 of 3 sentences]
9
[+] score: 11
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-9-4, 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-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
For example, in mouse [14], miR-10b is highly expressed in spinal cord; miR-124 is wi dely expressed in brain tissues; miR-200b, miR-128a, miR-128b, miR-429 are specifically expressed in olfactory bulb; miR-200a is highly expressed in olfactory bulb; miR-7b is highly expressed in hypothalamus. [score:11]
[1 to 20 of 1 sentences]
10
[+] score: 10
MiR-200b belongs to the miR-200 family and together with other family members miR-200a and miR-429, it is clustered in an intergenic region on human chromosome 1. MiR-200b is expressed in the epithelium during palatogenesis in the mouse, including in the midline epithelial seam (MES), and its expression gradually decreases as fusion proceeds (Shin et al., 2012a, b). [score:5]
MiR-200b belongs to the miR-200 family and together with other family members miR-200a and miR-429, it is clustered in an intergenic region on human chromosome 1. MiR-200b is expressed in the epithelium during palatogenesis in the mouse, including in the midline epithelial seam (MES), and its expression gradually decreases as fusion proceeds (Shin et al., 2012a, b). [score:5]
[1 to 20 of 2 sentences]
11
[+] score: 8
Korpal M. Lee E. S. Hu G. Kang Y. The miR-200 family inhibits epithelial-mesenchymal transition and cancer cell migration by direct targeting of E-cadherin transcriptional repressors ZEB1 and ZEB2J. [score:6]
Jing J. Xiong S. Li Z. Wu J. Zhou L. Gui J. F. Mei J. A feedback regulatory loop involving p53/miR-200 and growth hormone endocrine axis controls embryo size of zebrafishSci. [score:2]
[1 to 20 of 2 sentences]
12
[+] 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-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-9-4, 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-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
miRNA expression in the zebrafish inner ear was first demonstrated by mir-200a and mir-183 expression in the sensory epithelia (Wienholds et al, 2005). [score:5]
A few miRNAs were identified in the enrichment analysis, such as miR-181a, miR114, miR-200a and miR-27, suspected as being active miRNAs in the regeneration. [score:1]
[1 to 20 of 2 sentences]
13
[+] score: 5
Other miRNAs from this paper: dre-mir-34a, dre-mir-200b, dre-mir-200c
Potential contributions of miR-200a/-200b and their target gene–leptin to the sexual size dimorphism in yellow catfish. [score:3]
A feedback regulatory loop involving p53/miR-200 and growth hormone endocrine axis controls embryo size of zebrafish. [score:2]
[1 to 20 of 2 sentences]
14
[+] score: 4
Aging regulates cardiac miRNAs expression in Nothobranchius furzeriThe accumulation of oxidative stress and miR-200 family modulation prompted us to characterize the age -dependent regulation of the cardiac miRNome in Nfu. [score:3]
The oxidative stress damage was determined both by confocal analysis of total nitrotyrosinated proteins [45] and by evaluation of miR-200 family member expression levels [46], both increasing when ROS accumulates. [score:1]
[1 to 20 of 2 sentences]
15
[+] score: 4
A number of these hypoxia-regulated miRNAs are demonstrated to contribute to cellular responses to hypoxia by modulating critical downstream targets, including let-7 [29], miR-429 [30], miR-195 [31], miR-210 [32, 33], miR-322 [34], miR-200a [35], miR-199a [36, 37] and miR-150 [38]. [score:4]
[1 to 20 of 1 sentences]
16
[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-31, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-221, hsa-mir-23b, hsa-mir-27b, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-200c, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-30e, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-10b-1, dre-mir-181b-1, dre-mir-181b-2, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-204-1, dre-mir-181a-1, dre-mir-221, dre-mir-222a, 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-7e, dre-mir-7a-3, dre-mir-10b-2, dre-mir-20a, dre-mir-21-1, dre-mir-21-2, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-26b, dre-mir-27a, dre-mir-27b, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-30e-2, dre-mir-101b, dre-mir-103, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-148, dre-mir-181c, dre-mir-200c, dre-mir-203b, dre-mir-204-2, dre-mir-338-1, dre-mir-338-2, dre-mir-454b, hsa-mir-181d, dre-mir-212, dre-mir-181a-2, hsa-mir-551a, hsa-mir-551b, dre-mir-31, dre-mir-722, dre-mir-724, dre-mir-725, dre-mir-735, dre-mir-740, hsa-mir-103b-1, hsa-mir-103b-2, dre-mir-2184, hsa-mir-203b, dre-mir-7146, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-204-3, dre-mir-24b, dre-mir-7133, dre-mir-128-3, dre-mir-7132, dre-mir-338-3
26 +2.14 miR-132 +1.83 (1.71e-3) +0.52 miR-2184 -2.63 (2.54e-5) -2.25 -2.50 miR-222a +1.54 (1.13e-2) +3.24 miR-24 -1.36 (1.9e-2) -1.41 -0.73 miR-454b +1.14 (4.93e-2) +0.14 miR-133a -1.72 (2.67e-3) -4.25 -5.07 miR-101b -2.52 (3.44e-5) -3.43 miR-338 -2.23 (1.90e-4) -2.90 -1.57 miR-26b -1.91 (1.84e-3) -3. 67 miR-204 -2.60 (4.76e-5) -0.57 -2.36 miR-203b -1.77 (3.45e3 -0.21 miR-10b -1.36 (2.90e-2) -1.78 miR-725 -1.29 (3.23e-2) -1.62 Zebrafish + Axolotl Zebrafish SymbolZebrafish log [2] Fold-change (p-value)Axolotl log [2] Fold-change SymbolZebrafish log [2] Fold-change (p-value) miR-27a +1.57 (7.96e-3) +2.15 miR-27b +1.38 (2.44e-2) miR-29b -2.05 (1.28e-2) -0.97 miR-143 +1.31 (2.89e-2) miR-30e +1.18 (4.80e-2) miR-200c -1.85 (1.72e-3) miR-200a -1.74 (3.66e-3) miR-23a -1.35 (2.05e-2) 10. [score:1]
26 +2.14 miR-132 +1.83 (1.71e-3) +0.52 miR-2184 -2.63 (2.54e-5) -2.25 -2.50 miR-222a +1.54 (1.13e-2) +3.24 miR-24 -1.36 (1.9e-2) -1.41 -0.73 miR-454b +1.14 (4.93e-2) +0.14 miR-133a -1.72 (2.67e-3) -4.25 -5.07 miR-101b -2.52 (3.44e-5) -3.43 miR-338 -2.23 (1.90e-4) -2.90 -1.57 miR-26b -1.91 (1.84e-3) -3. 67 miR-204 -2.60 (4.76e-5) -0.57 -2.36 miR-203b -1.77 (3.45e3 -0.21 miR-10b -1.36 (2.90e-2) -1.78 miR-725 -1.29 (3.23e-2) -1.62 Zebrafish + Axolotl Zebrafish SymbolZebrafish log [2] Fold-change (p-value)Axolotl log [2] Fold-change SymbolZebrafish log [2] Fold-change (p-value) miR-27a +1.57 (7.96e-3) +2.15 miR-27b +1.38 (2.44e-2) miR-29b -2.05 (1.28e-2) -0.97 miR-143 +1.31 (2.89e-2) miR-30e +1.18 (4.80e-2) miR-200c -1.85 (1.72e-3) miR-200a -1.74 (3.66e-3) miR-23a -1.35 (2.05e-2) 10. [score:1]
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17
[+] score: 1
Fgf signaling controls pharyngeal taste bud formation through miR-200 and Delta-Notch activity. [score:1]
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18
[+] score: 1
Other miRNAs from this paper: hsa-mir-200b, hsa-mir-200c, hsa-mir-200a, dre-mir-200b, dre-mir-200c
Fgf signaling controls pharyngeal taste bud formation through miR-200 and Delta-Notch activity. [score:1]
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19
[+] score: 1
Other miRNAs from this paper: dre-mir-200b, dre-mir-200c
Fgf signaling controls pharyngeal taste bud formation through miR-200 and Delta-Notch activity. [score:1]
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